Impaired processing speed and attention in first-episode drug naive schizophrenia with deficit syndrome.

PubMed

Chen, Ce; Jiang, Wenhui; Zhong, Na; Wu, Jin; Jiang, Haifeng; Du, Jiang; Li, Ye; Ma, Xiancang; Zhao, Min; Hashimoto, Kenji; Gao, Chengge

2014-11-01

Although first-episode drug naive patients with schizophrenia are known to show cognitive impairment, the cognitive performances of these patients, who suffer deficit syndrome, compared with those who suffer non-deficit syndrome is undetermined. The aim of this study was to compare cognitive performances in first-episode drug-naive schizophrenia with deficit syndrome or non-deficit syndrome. First-episode drug naive patients (n=49) and medicated patients (n=108) with schizophrenia, and age, sex, and education matched healthy controls (n=57 for the first-episode group, and n=128 for the medicated group) were enrolled. Patients were divided into deficit or non-deficit syndrome groups, using the Schedule for Deficit Syndrome. Cognitive performance was assessed using the CogState computerized cognitive battery. All cognitive domains in first-episode drug naive and medicated patients showed significant impairment compared with their respective control groups. Furthermore, cognitive performance in first-episode drug naive patients was significantly worse than in medicated patients. Interestingly, the cognitive performance markers of processing speed and attention, in first-episode drug naive patients with deficit syndrome, were both significantly worse than in equivalent patients without deficit syndrome. In contrast, no differences in cognitive performance were found between the two groups of medicated patients. In conclusion, this study found that first-episode drug naive schizophrenia with deficit syndrome showed significantly impaired processing speed and attention, compared with patients with non-deficit syndrome. These findings highlight processing speed and attention as potential targets for pharmacological and psychosocial interventions in first-episode schizophrenia with deficit syndrome, since these domains are associated with social outcomes. Copyright © 2014 Elsevier B.V. All rights reserved.

Heterogeneity of Developmental Dyscalculia: Cases with Different Deficit Profiles

PubMed Central

Träff, Ulf; Olsson, Linda; Östergren, Rickard; Skagerlund, Kenny

2017-01-01

Developmental Dyscalculia (DD) has long been thought to be a monolithic learning disorder that can be attributed to a specific neurocognitive dysfunction. However, recent research has increasingly recognized the heterogeneity of DD, where DD can be differentiated into subtypes in which the underlying cognitive deficits and neural dysfunctions may differ. The aim was to further understand the heterogeneity of developmental dyscalculia (DD) from a cognitive psychological perspective. Utilizing four children (8–9 year-old) we administered a comprehensive cognitive test battery that shed light on the cognitive-behavioral profile of each child. The children were compared against norm groups of aged-matched peers. Performance was then contrasted against predominant hypotheses of DD, which would also give insight into candidate neurocognitive correlates. Despite showing similar mathematical deficits, these children showed remarkable interindividual variability regarding cognitive profile and deficits. Two cases were consistent with the approximate number system deficit account and also the general magnitude-processing deficit account. These cases showed indications of having domain-general deficits as well. One case had an access deficit in combination with a general cognitive deficit. One case suffered from general cognitive deficits only. The results showed that DD cannot be attributed to a single explanatory factor. These findings support a multiple deficits account of DD and suggest that some cases have multiple deficits, whereas other cases have a single deficit. We discuss a previously proposed distinction between primary DD and secondary DD, and suggest hypotheses of dysfunctional neurocognitive correlates responsible for the displayed deficits. PMID:28101068

Heterogeneity of Developmental Dyscalculia: Cases with Different Deficit Profiles.

PubMed

Träff, Ulf; Olsson, Linda; Östergren, Rickard; Skagerlund, Kenny

2016-01-01

Developmental Dyscalculia (DD) has long been thought to be a monolithic learning disorder that can be attributed to a specific neurocognitive dysfunction. However, recent research has increasingly recognized the heterogeneity of DD, where DD can be differentiated into subtypes in which the underlying cognitive deficits and neural dysfunctions may differ. The aim was to further understand the heterogeneity of developmental dyscalculia (DD) from a cognitive psychological perspective. Utilizing four children (8-9 year-old) we administered a comprehensive cognitive test battery that shed light on the cognitive-behavioral profile of each child. The children were compared against norm groups of aged-matched peers. Performance was then contrasted against predominant hypotheses of DD, which would also give insight into candidate neurocognitive correlates. Despite showing similar mathematical deficits, these children showed remarkable interindividual variability regarding cognitive profile and deficits. Two cases were consistent with the approximate number system deficit account and also the general magnitude-processing deficit account. These cases showed indications of having domain-general deficits as well. One case had an access deficit in combination with a general cognitive deficit. One case suffered from general cognitive deficits only. The results showed that DD cannot be attributed to a single explanatory factor. These findings support a multiple deficits account of DD and suggest that some cases have multiple deficits, whereas other cases have a single deficit. We discuss a previously proposed distinction between primary DD and secondary DD, and suggest hypotheses of dysfunctional neurocognitive correlates responsible for the displayed deficits.

Gender-dependent behavioral and sensory effects of a commercial mixture of polychlorinated biphenyls (Aroclor 1254) in rats.

PubMed

Geller, A M; Oshiro, W M; Haykal-Coates, N; Kodavanti, P R; Bushnell, P J

2001-02-01

Developmental exposure to polychlorinated biphenyls (PCBs) has been associated with behavioral and cognitive deficits in humans and animal models. Perinatal exposure to PCBs has also been associated with sensory deficits in animal models. These effects were hypothesized to be mediated in part by ortho-substituted PCBs, which do not or weakly bind to the aryl hydrocarbon (Ah) receptor. The present studies were designed to determine whether perinatal exposure to Aroclor 1254, a commercial mixture of > 99% ortho-substituted PCBs, would affect cognitive and sensory function in Long-Evans rats. Adult male and female offspring of female rats fed Aroclor 1254 (Lot #124-191; doses of 0, 1, or 6 mg/kg/day; gestational day 6 through postnatal day 21; n = eight/group) were trained to perform a signal detection task capable of assessing sensory thresholds. Training included autoshaping and operant conditioning. Thresholds for detecting a 1-s light stimulus were determined under background illuminations ranging from 2 lux to complete darkness. Female rats exposed to Aroclor 1254 autoshaped more rapidly than control females, at a rate akin to control males. Control females had lower thresholds than control males at all levels of background illumination. These differences were abolished by Aroclor 1254, which reduced thresholds in males and increased thresholds in females. These data extend previous findings of gender-specific effects of PCBs on neurobehavioral development to measures of acquisition and sensory function.

A Multiple Deficit Model of Reading Disability and Attention-Deficit/Hyperactivity Disorder: Searching for Shared Cognitive Deficits

ERIC Educational Resources Information Center

McGrath, Lauren M.; Pennington, Bruce F.; Shanahan, Michelle A.; Santerre-Lemmon, Laura E.; Barnard, Holly D.; Willcutt, Erik G.; DeFries, John C.; Olson, Richard K.

2011-01-01

Background: This study tests a multiple cognitive deficit model of reading disability (RD), attention-deficit/hyperactivity disorder (ADHD), and their comorbidity. Methods: A structural equation model (SEM) of multiple cognitive risk factors and symptom outcome variables was constructed. The model included phonological awareness as a unique…

Frontal gamma noise power and cognitive domains in schizophrenia.

PubMed

Díez, Alvaro; Suazo, Vanessa; Casado, Pilar; Martín-Loeches, Manuel; Perea, María Victoria; Molina, Vicente

2014-01-30

The cognitive deficit profile is different among individuals with schizophrenia. We quantified the amount of electroencephalographic activity unlocked to stimuli onset (noise power) over frontal regions regarding deficit in cognitive domains. Forty-six patients with schizophrenia and 27 healthy controls underwent clinical, cognitive and electrophysiological assessments. Noise power studies may be considered complementary but not equivalent to induced power studies. We compared gamma and theta noise power magnitude during a P300 paradigm between subsets of patients divided according to cognitive deficit in key domains and controls. Patients displayed higher gamma noise power activity at Fz site and significantly lower performance in all cognitive domains when compared to controls. The subset of patients with cognitive deficit for working memory and problem solving/executive functions domains displayed significantly higher frontal-lateral noise power values in comparison to the subset of patients without cognitive deficit and controls. Patients with significant cognitive deficits in domains with greater frontal contribution are also characterized by an abnormally higher gamma band noise power over the frontal region. Our data may endorse various biological subsets within schizophrenia, characterized by the presence or absence of a significant cognitive deficit in frontal domains. © 2013 Published by Elsevier Ireland Ltd.

Gray matter morphological anomalies in the cerebellar vermis in first-episode schizophrenia patients with cognitive deficits.

PubMed

Wang, Jingjuan; Zhou, Li; Cui, Chunlei; Liu, Zhening; Lu, Jie

2017-11-22

Cognitive deficits are a core feature of early schizophrenia. However, the pathological foundations underlying cognitive deficits are still unknown. The present study examined the association between gray matter density and cognitive deficits in first-episode schizophrenia. Structural magnetic resonance imaging of the brain was performed in 34 first-episode schizophrenia patients and 21 healthy controls. Patients were divided into two subgroups according to working memory task performance. The three groups were well matched for age, gender, and education, and the two patient groups were also further matched for diagnosis, duration of illness, and antipsychotic treatment. Voxel-based morphometric analysis was performed to estimate changes in gray matter density in first-episode schizophrenia patients with cognitive deficits. The relationships between gray matter density and clinical outcomes were explored. Patients with cognitive deficits were found to have reduced gray matter density in the vermis and tonsil of cerebellum compared with patients without cognitive deficits and healthy controls, decreased gray matter density in left supplementary motor area, bilateral precentral gyrus compared with patients without cognitive deficits. Classifier results showed GMD in cerebellar vermis tonsil cluster could differentiate SZ-CD from controls, left supplementary motor area cluster could differentiate SZ-CD from SZ-NCD. Gray matter density values of the cerebellar vermis cluster in patients groups were positively correlated with cognitive severity. Decreased gray matter density in the vermis and tonsil of cerebellum may underlie early psychosis and serve as a candidate biomarker for schizophrenia with cognitive deficits.

Cognitive Deficits and Positively Biased Self-Perceptions in Children with ADHD

PubMed Central

McQuade, Julia D.; Tomb, Meghan; Hoza, Betsy; Waschbusch, Daniel A.; Hurt, Elizabeth A.; Vaughn, Aaron J.

2011-01-01

This study examined the relation between cognitive deficits and positive bias in a sample of 272 children with and without Attention Deficit Hyperactivity Disorder (ADHD; 7–12 years old). Results indicated that children with ADHD with and without biased self-perceptions exhibit differences in specific cognitive deficits (executive processes, working memory, broad attention, and cognitive fluency) compared to each other and to control children. Further, specific cognitive deficits emerged as partial mediators of the relation between ADHD diagnostic status and positive bias. Interestingly, some differences in results emerged based on the domain considered (academic, social, behavioral competence). Results lend initial support to the role of cognitive deficits in the positive bias of some children with ADHD. Implications for future research and intervention are discussed. PMID:20820902

Acupuncture Prevents the Impairment of Hippocampal LTP Through β1-AR in Vascular Dementia Rats.

PubMed

Xiao, Ling-Yong; Wang, Xue-Rui; Yang, Jing-Wen; Ye, Yang; Zhu, Wen; Cao, Yan; Ma, Si-Ming; Liu, Cun-Zhi

2018-02-13

It is widely accepted that the synaptic dysfunction and synapse loss contribute to the cognitive deficits of vascular dementia (VD) patients. We have previously reported that acupuncture improved cognitive function in rats with VD. However, the mechanisms involved in acupuncture improving cognitive ability remain to be elucidated. The present study aims to investigate the pathways and molecules involved in the neuroprotective effect of acupuncture. We assessed the effects of acupuncture on hippocampal long-term potentiation (LTP), the most prominent cellular model of memory formation. Acupuncture enhanced LTP and norepinephrine (NE) levels in the hippocampus. Inhibition of the β-adrenergic receptor (AR), but not the α-AR, was able to block the effects of acupuncture on hippocampal LTP. Furthermore, inhibition of β1-AR, not β2-AR, abolished the enhanced LTP induced by acupuncture. The expression analysis revealed a significant upregulation of β1-AR and unchanged β2-AR with acupuncture, which supported the above findings. Specifically, increased β1-ARs in the dentate gyrus were expressed on neurons exclusively. Taken together, the present data supports a beneficial role of acupuncture in synaptic plasticity challenged with VD. A likely mechanism is the increase of NE and activation of β1-AR in the hippocampus.

Cognitive Deficits in Breast Cancer Survivors After Chemotherapy and Hormonal Therapy.

PubMed

Frank, Jennifer Sandson; Vance, David E; Triebel, Kristen L; Meneses, Karen M

2015-12-01

Adjuvant treatments, specifically chemotherapy and hormonal therapy, have dramatically increased breast cancer survival, resulting in increased attention to the residual effects of treatment. Breast cancer survivors (BCS) frequently report that cognitive deficits are a particular source of distress, interfering with many aspects of quality of life. The literature on neuropsychological performance measures in BCS supports the reality of subtle cognitive deficits after both chemotherapy and hormonal therapy. This premise is supported by recent imaging studies, which reveal anatomical changes after chemotherapy as well as changes in patterns of neural activation while performing cognitive tasks. This review suggests that, even when performance on neuropsychological performance measures is within normal limits, BCS may be using increased cognitive resources in the face of reduced cognitive reserve. Potential interventions for cognitive deficits after adjuvant therapy include prescriptions for healthy living, pharmacotherapy, complementary therapy, and cognitive remediation therapy directed toward specific cognitive deficits or a combination of several strategies.

Cognitive Neuroscience of Attention Deficit Hyperactivity Disorder: Current Status and Working Hypotheses

ERIC Educational Resources Information Center

Vaidya, Chandan J.; Stollstorff, Melanie

2008-01-01

Cognitive neuroscience studies of Attention Deficit Hyperactivity Disorder (ADHD) suggest multiple loci of pathology with respect to both cognitive domains and neural circuitry. Cognitive deficits extend beyond executive functioning to include spatial, temporal, and lower-level "nonexecutive" functions. Atypical functional anatomy extends beyond…

Cognitive deficits in Korean women treated with chemotherapy for breast cancer.

PubMed

Jung, Mi Sook; Cimprich, Bernadine

2014-01-01

Cognitive deficits have been reported as detrimental side effects in chemotherapy-treated breast cancer patients and survivors. Korean women treated for breast cancer may experience unrecognized cognitive deficits related to their treatment. However, no research has examined cognitive test performance in chemotherapy-treated Korean breast cancer survivors. The objectives of this study were 2-fold: (1) to examine differences in occurrence and severity of cognitive deficits in Korean women treated with adjuvant chemotherapy for breast cancer as compared with a control group of women without breast cancer and (2) to examine the relationship of selected demographic and cultural factors with cognitive test performance. Sixty-four Korean women, 32 women treated for localized breast cancer and 32 healthy controls, were enrolled. Breast cancer participants were assessed with established cognitive measures within 4 months after chemotherapy, and healthy controls, within 6 months after negative screening mammography. The breast cancer group showed a significantly higher occurrence and greater severity of cognitive deficits than controls did. Importantly, older age, less education, greater collectivist tendency, and greater childrearing burden were reliably associated with poorer attention and working memory test performance. Cognitive deficits were found in chemotherapy-treated Korean women with moderate to large effect sizes compared with controls. Cultural characteristics contributed to worse cognitive performance. Healthcare providers should recognize that Korean women may be highly vulnerable to cognitive deficits. Cultural factors also need to be considered when assessing cognitive function and designing therapeutic interventions to counteract negative cognitive outcomes.

Subjective deficits of attention, cognition and depression in patients with narcolepsy.

PubMed

Zamarian, Laura; Högl, Birgit; Delazer, Margarete; Hingerl, Katharina; Gabelia, David; Mitterling, Thomas; Brandauer, Elisabeth; Frauscher, Birgit

2015-01-01

Patients with narcolepsy often complain about attention deficits in everyday situations. In comparison with these subjective complaints, deficits in objective testing are subtler. The present study assessed the relationships between subjective complaints, objectively measured cognitive performance, disease-related variables, and mood. A total of 51 patients with narcolepsy and 35 healthy controls responded to questionnaires regarding subjectively perceived attention deficits, sleepiness, anxiety and depression. Moreover, they performed an extensive neuropsychological assessment tapping into attention, executive functions, and memory. Patients rated their level of attention in everyday situations to be relatively poor. In an objective assessment of cognitive functioning, they showed only slight attention and executive function deficits. The subjective ratings of attention deficits significantly correlated with ratings of momentary sleepiness, anxiety, and depression, but not with objectively measured cognitive performance. Momentary sleepiness and depression predicted almost 39% of the variance in the ratings of subjectively perceived attention deficits. The present study showed that sleepiness and depression, more than objective cognitive deficits, might play a role in the subjectively perceived attention deficits of patients with narcolepsy. The results suggested that when counselling and treating patients with narcolepsy, clinicians should pay attention to potential depression because subjective cognitive complaints may not relate to objective cognitive impairments. Copyright © 2014 Elsevier B.V. All rights reserved.

A Cross-Sectional Study of the Relationship of Physical Activity with Depression and Cognitive Deficit in Older Adults.

PubMed

Paulo T, R S; Tribess, Sheilla; Sasaki, Jeffer Eidi; Meneguci, Joilson; Martins, Cristiane A; Freitas, Ismael F; Romo-Perez, Vicente; Virtuoso, Jair S

2016-04-01

The aim of this study was to examine the association of physical activity with depression and cognition deficit, separately and combined, in Brazilian older adults. We analyzed data from 622 older adults. Physical activity was assessed using the International Physical Activity Questionnaire. Depressive symptoms were assessed using the Geriatric Depression Scale, while cognitive deficit was assessed using the Mini-Mental State Examination. Multinomial logistic regressions were used to assess associations of depression and cognitive deficit with sociodemographic, health, and behavioral variables. Prevalence of physical inactivity (< 150 min of moderate-to-vigorous physical activity/ week), depression, and cognitive deficit were 35.7%, 37.4%, and 16.7%. Physical inactivity was associated with depression (OR: 1.83, 95% CI: 1.14-2.94) and with depression and cognitive deficit combined (OR: 4.23, 95% CI: 2.01-8.91). Physically inactive participants were also more likely to present limitations in orientation and language functions. Physical inactivity was associated with depression and also with depression and cognitive deficit combined in older adults.

Cognitive Deficits and Positively Biased Self-Perceptions in Children with ADHD

ERIC Educational Resources Information Center

McQuade, Julia D.; Tomb, Meghan; Hoza, Betsy; Waschbusch, Daniel A.; Hurt, Elizabeth A.; Vaughn, Aaron J.

2011-01-01

This study examined the relation between cognitive deficits and positive bias in a sample of 272 children with and without Attention Deficit Hyperactivity Disorder (ADHD; 7-12 years old). Results indicated that children with ADHD with and without biased self-perceptions exhibit differences in specific cognitive deficits (executive processes,…

An Overview of Non-pathological Geroneuropsychology: Implications for Nursing Practice and Research

PubMed Central

Graham, Martha A.; Fazeli, Pariya L.; Heaton, Karen; Moneyham, Linda

2011-01-01

One aspect of successful aging is maintaining cognitive functioning; that includes both subjective cognitive functioning and objective cognitive functioning even in lieu of subtle cognitive deficits that occur with normal, non-pathological aging. Age-related cognitive deficits emerge across several domains including attention, memory, language, speed of processing, executive, and psychomotor, just to name a few. A primary theory explaining such cognitive deficits is cognitive reserve theory; it posits that biological factors such as demyelination and oxidative stress interfere with neuronal communication which eventually produces observable deficits in cognitive functioning. Therefore, it is important to maintain or improve cognitive reserve in order to augment cognitive functioning in later life. This article provides a general overview of the principles of geroneuropsychology along with implications for nursing practice and research. PMID:22210304

Cognition, social cognition and functional disability in early-stage schizophrenia: A study from southern India.

PubMed

Kurtz, Matthew M; Gopal, Subhashini; John, Sujit; Thara, R

2018-04-24

In high-income countries a wealth of studies has revealed cognitive and social cognitive deficits in schizophrenia and a close relationship of these deficits to psychosocial functioning. Studies examining these illness features in middle and low-income countries are rare, particularly in early-stage samples. Sixty adult participants within 5 years of diagnosis with schizophrenia and 53 matched, healthy control were assessed with the MATRICS Consensus Cognitive Battery and the PEAT emotion identification task at study entry, and the WHODAS functioning scale one year later. Deficits on cognitive instruments ranged from d = 0.64-1.04 and were consistent with those reported in Western samples. Negative symptoms were linked to function longitudinally. Deficits in social cognitive skills and longitudinal links between cognition and functioning were not evident. These findings suggest a highly consistent magnitude of neurocognitive deficits in people with schizophrenia across widely varying cultures, but with limited evidence of social cognitive skill deficits using Western-based instruments. There was little evidence of a relationship between cognition and psychosocial disability in people with early-stage schizophrenia in this sample. Copyright © 2018 Elsevier B.V. All rights reserved.

Cortical morphology as a shared neurobiological substrate of attention-deficit/hyperactivity symptoms and executive functioning: a population-based pediatric neuroimaging study

PubMed Central

Mous, Sabine E.; White, Tonya; Muetzel, Ryan L.; El Marroun, Hanan; Rijlaarsdam, Jolien; Polderman, Tinca J.C.; Jaddoe, Vincent W.; Verhulst, Frank C.; Posthuma, Danielle; Tiemeier, Henning

2017-01-01

Background Attention-deficit/hyperactivity symptoms have repeatedly been associated with poor cognitive functioning. Genetic studies have demonstrated a shared etiology of attention-deficit/hyperactivity disorder (ADHD) and cognitive ability, suggesting a common underlying neurobiology of ADHD and cognition. Further, neuroimaging studies suggest that altered cortical development is related to ADHD. In a large population-based sample we investigated whether cortical morphology, as a potential neurobiological substrate, underlies the association between attention-deficit/hyperactivity symptoms and cognitive problems. Methods The sample consisted of school-aged children with data on attention-deficit/hyperactivity symptoms, cognitive functioning and structural imaging. First, we investigated the association between attention-deficit/hyperactivity symptoms and different domains of cognition. Next, we identified cortical correlates of attention-deficit/hyperactivity symptoms and related cognitive domains. Finally, we studied the role of cortical thickness and gyrification in the behaviour–cognition associations. Results We included 776 children in our analyses. We found that attention-deficit/hyperactivity symptoms were associated specifically with problems in attention and executive functioning (EF; b = −0.041, 95% confidence interval [CI] −0.07 to −0.01, p = 0.004). Cortical thickness and gyrification were associated with both attention-deficit/hyperactivity symptoms and EF in brain regions that have been previously implicated in ADHD. This partly explained the association between attention-deficit/hyperactivity symptoms and EF (bindirect = −0.008, bias-corrected 95% CI −0.018 to −0.001). Limitations The nature of our study did not allow us to draw inferences regarding temporal associations; longitudinal studies are needed for clarification. Conclusion In a large, population-based sample of children, we identified a shared cortical morphology underlying attention-deficit/hyperactivity symptoms and EF. PMID:27673503

Cortical morphology as a shared neurobiological substrate of attention-deficit/hyperactivity symptoms and executive functioning: a population-based pediatric neuroimaging study.

PubMed

Mous, Sabine E; White, Tonya; Muetzel, Ryan L; El Marroun, Hanan; Rijlaarsdam, Jolien; Polderman, Tinca J C; Jaddoe, Vincent W; Verhulst, Frank C; Posthuma, Danielle; Tiemeier, Henning

2017-03-01

Attention-deficit/hyperactivity symptoms have repeatedly been associated with poor cognitive functioning. Genetic studies have demonstrated a shared etiology of attention-deficit/hyperactivity disorder (ADHD) and cognitive ability, suggesting a common underlying neurobiology of ADHD and cognition. Further, neuroimaging studies suggest that altered cortical development is related to ADHD. In a large population-based sample we investigated whether cortical morphology, as a potential neurobiological substrate, underlies the association between attention-deficit/hyperactivity symptoms and cognitive problems. The sample consisted of school-aged children with data on attention-deficit/hyperactivity symptoms, cognitive functioning and structural imaging. First, we investigated the association between attention-deficit/ hyperactivity symptoms and different domains of cognition. Next, we identified cortical correlates of attention-deficit/hyperactivity symptoms and related cognitive domains. Finally, we studied the role of cortical thickness and gyrification in the behaviour-cognition associations. We included 776 children in our analyses. We found that attention-deficit/hyperactivity symptoms were associated specifically with problems in attention and executive functioning (EF; b = -0.041, 95% confidence interval [CI] -0.07 to -0.01, p = 0.004). Cortical thickness and gyrification were associated with both attention-deficit/hyperactivity symptoms and EF in brain regions that have been previously implicated in ADHD. This partly explained the association between attention-deficit/hyperactivity symptoms and EF (b indirect = -0.008, bias-corrected 95% CI -0.018 to -0.001). The nature of our study did not allow us to draw inferences regarding temporal associations; longitudinal studies are needed for clarification. In a large, population-based sample of children, we identified a shared cortical morphology underlying attention-deficit/hyperactivity symptoms and EF.

D-Serine and a glycine transporter inhibitor improve MK-801-induced cognitive deficits in a novel object recognition test in rats.

PubMed

Karasawa, Jun-Ichi; Hashimoto, Kenji; Chaki, Shigeyuki

2008-01-10

Compounds enhancing N-methyl-d-aspartate (NMDA) glutamate receptor function have been reported to improve cognitive deficits. Since cognitive deficits are considered to be the core symptom of schizophrenia, enhancing NMDA receptor function represents a promising approach to treating schizophrenia. In the present study, we investigated whether d-serine or a glycine transporter inhibitor N-[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl]sarcosine (NFPS), both of which enhance NMDA receptor function, could improve MK-801-induced cognitive deficits in rats, and compared their effects with those of the atypical antipsychotic clozapine and of the typical antipsychotic haloperidol. To assess cognitive function, we used a novel object recognition test in rats that measured spontaneous exploratory activity of a novel object when paired with a familiar object. We then evaluated the effects of the compounds on cognitive deficits induced by treatment with MK-801, the NMDA receptor antagonist. Pretreatment with clozapine (1, 5 mg/kg, i.p.) but not haloperidol (0.03, 0.1 mg/kg, i.p.) significantly improved MK-801-induced cognitive deficits. Pretreatment with D-serine at 800 mg/kg (i.p.) or NFPS (0.3, 1 mg/kg, i.p.) significantly improved MK-801-induced cognitive deficits under this test paradigm. These findings suggest that impaired preference for novel objects induced by MK-801 in the novel object recognition test could be a useful animal model for evaluating the efficacy of compounds targeting the cognitive deficits observed in schizophrenic patients. The results also suggest that enhancing NMDA receptor function is an effective way for treating the cognitive deficits associated with schizophrenia.

Prevention, Rehabilitation, and Mitigation Strategies of Cognitive Deficits in Aging with HIV: Implications for Practice and Research

PubMed Central

Vance, David E.

2013-01-01

Highly active antiretroviral therapy has given the chance to those living with HIV to keep on living, allowing them the opportunity to age and perhaps age successfully. Yet, there are severe challenges to successful aging with HIV, one of which is cognitive deficits. Nearly half of those with HIV experience cognitive deficits that can interfere with everyday functioning, medical decision making, and quality of life. Given that cognitive deficits develop with more frequency and intensity with increasing age, concerns mount that as people age with HIV, they may experience more severe cognitive deficits. These concerns become especially germane given that by 2015, 50% of those with HIV will be 50 and older, and this older cohort of adults is expected to grow. As such, this paper focuses on the etiologies of such cognitive deficits within the context of cognitive reserve and neuroplasticity. From this, evidence-based and hypothetical prevention (i.e., cognitive prescriptions), rehabilitation (i.e., speed of processing training), and mitigation (i.e., spaced retrieval method) strategies are reviewed. Implications for nursing practice and research are posited. PMID:23431469

Neurocognitive impairment in the deficit subtype of schizophrenia.

PubMed

Fervaha, Gagan; Agid, Ofer; Foussias, George; Siddiqui, Ishraq; Takeuchi, Hiroyoshi; Remington, Gary

2016-08-01

Schizophrenia is a heterogeneous disorder characterized by numerous diverse signs and symptoms. Individuals with prominent, persistent, and idiopathic negative symptoms are thought to encompass a distinct subtype of schizophrenia. Previous work, including studies involving neuropsychological evaluations, has supported this position. The present study sought to further examine whether deficit patients are cognitively distinct from non-deficit patients with schizophrenia. A comprehensive neurocognitive battery including tests of verbal memory, vigilance, processing speed, reasoning, and working memory was administered to 657 patients with schizophrenia. Of these, 144 (22 %) patients were classified as deficit patients using a proxy identification method based on severity, persistence over time, and possible secondary sources (e.g., depression) of negative symptoms. Deficit patients with schizophrenia performed worse on all tests of cognition relative to non-deficit patients. These patients were characterized by a generalized cognitive impairment on the order of about 0.4 standard deviations below that of non-deficit patients. However, when comparing deficit patients to non-deficit patients who also present with negative symptoms, albeit not enduring or primary, no group differences in cognitive performance were found. Furthermore, a discriminant function analysis classifying patients into deficit/non-deficit groups based on cognitive scores demonstrated only 62.3 % accuracy, meaning over one-third of individuals were misclassified. The deficit subtype of schizophrenia is not markedly distinct from non-deficit schizophrenia in terms of neurocognitive performance. While deficit patients tend to have poorer performance on cognitive tests, the magnitude of this effect is relatively modest, translating to over 70 % overlap in scores between groups.

Cognitive Deficits in Schizophrenia: Understanding the Biological Correlates and Remediation Strategies

PubMed Central

Tripathi, Adarsh; Shukla, Rashmi

2018-01-01

Cognitive deficits are one of the core symptoms of schizophrenia that evolve during the course of schizophrenia, after being originated even before the onset of illness. Existing pharmacological and biological treatment modalities fall short to meet the needs to improve the cognitive symptoms; hence, various cognitive remediation strategies have been adopted to address these deficits. Research evidences suggest that cognitive remediation measures improve the functioning, limit disability bettering the quality of life. The functional outcomes of cognitive remediation in schizophrenia are resultant of neurobiological changes in specific brain areas. Recent years witnessed significant innovations in cognitive remediation strategies in schizophrenia. This comprehensive review highlights the biological correlates of cognitive deficits in schizophrenia and the remedial measures with evidence base. PMID:29397662

Orexins Mediate Sex Differences in the Stress Response and in Cognitive Flexibility.

PubMed

Grafe, Laura A; Cornfeld, Amanda; Luz, Sandra; Valentino, Rita; Bhatnagar, Seema

2017-04-15

Women are twice as likely as men to experience stress-related psychiatric disorders. The biological basis of these sex differences is poorly understood. Orexins are altered in anxious and depressed patients. Using a rat model of repeated stress, we examined whether orexins contribute to sex differences in outcomes relevant to stress-related psychiatric diseases. Behavioral, neural, and endocrine habituation to repeated restraint stress and subsequent cognitive flexibility was examined in adult male and female rats. In parallel, orexin expression and activation were determined in both sexes, and chromatin immunoprecipitation was used to determine transcription factors acting at the orexin promoter. Designer receptors exclusively activated by designer drugs were used to inhibit orexin activation throughout repeated restraint to determine if the stress-related impairments in female rats could be reduced. Female rats exhibited impaired habituation to repeated restraint with subsequent deficits in cognitive flexibility compared with male rats. Increased orexin expression and activation were observed in female rats compared with male rats. The higher expression of orexin messenger RNA in female rats was due to actions of glucocorticoid receptors on the orexin promoter, as determined by chromatin immunoprecipitation. Inhibition of orexins using designer receptors exclusively activated by designer drugs in female rats throughout repeated restraint abolished their heightened hypothalamic-pituitary-adrenal responsivity and reduced stress-induced cognitive impairments. Orexins mediate the impairments in adaptations to repeated stress and in subsequent cognitive flexibility exhibited by female rats and provide evidence for a broader role for orexins in mediating functions relevant to stress-related psychiatric diseases. Copyright © 2016 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Perceived Cognitive Deficits in a Sample of Persons Living With Multiple Sclerosis.

PubMed

Henneghan, Ashley; Stuifbergen, Alexa; Becker, Heather; Kullberg, Vicki; Gloris, Nicole

2017-10-01

The aims of this study were to describe the nature and diversity of perceived cognitive deficits using the Perceived Deficits Questionnaire (PDQ), to assess the reliability of the PDQ, and to explore self-reported predictors of PDQ scores in a large community-based sample of persons with multiple sclerosis (MS). Persons with MS enrolled in a randomized controlled trial provided demographic data and completed the PDQ along with measures of cognitive and memory strategies, cognitive abilities, self-efficacy, and depressive symptoms and neuropsychological tests. Most of the 183 participants were non-Hispanic white women, approximately 49 years old, and diagnosed with MS 12.5 years prior. The most frequent cognitive complaints regarded trouble remembering telephone numbers, mind drifting, and forgetting why one came into a room. The PDQ scores were significantly related to self-rated cognitive abilities, depressive symptoms, self-efficacy, and use of cognitive strategies, but not to scores on neuropsychological performance tests. When controlling for other variables, self-rated cognitive abilities was the strongest, significant predictor of perceived cognitive deficits. Persons with MS most frequently experience deficits related to short-term memory and attention. The PDQ total is a reliable measure of perceived cognitive deficits in persons with MS, is feasible for use by nurses in clinical settings-can be administered in approximately 5 minutes, and is easily scored.

Cognitive deficits in individuals with methamphetamine use disorder: A meta-analysis.

PubMed

Potvin, Stéphane; Pelletier, Julie; Grot, Stéphanie; Hébert, Catherine; Barr, Alasdair M; Lecomte, Tania

2018-05-01

Methamphetamine has long been considered as a neurotoxic substance causing cognitive deficits. Recently, however, the magnitude and the clinical significance of the cognitive effects associated with methamphetamine use disorder (MUD) have been debated. To help clarify this controversy, we performed a meta-analysis of the cognitive deficits associated with MUD. A literature search yielded 44 studies that assessed cognitive dysfunction in 1592 subjects with MUD and 1820 healthy controls. Effect size estimates were calculated using the Comprehensive Meta-Analysis, for the following 12 cognitive domains: attention, executive functions, impulsivity/reward processing, social cognition, speed of processing, verbal fluency/language, verbal learning and memory, visual learning and memory, visuo-spatial abilities and working memory. Findings revealed moderate impairment across most cognitive domains, including attention, executive functions, language/verbal fluency, verbal learning and memory, visual memory and working memory. Deficits in impulsivity/reward processing and social cognition were more prominent, whereas visual learning and visuo-spatial abilities were relatively spared cognitive domains. A publication bias was observed. These results show that MUD is associated with broad cognitive deficits that are in the same range as those associated with alcohol and cocaine use disorder, as recently shown by way of meta-analysis. The prominent effects of MUD on social cognition and impulsivity/reward processing are based on a small number of studies, and as such, these results will need to be replicated. The functional consequences (social and occupational) of the cognitive deficits of methamphetamine will also need to be determined. Copyright © 2018 Elsevier Ltd. All rights reserved.

[Neurocognitive deficit and social cognition in schizophrenia].

PubMed

Rychkova, O V; Gurevich, G L

2012-01-01

To study the association between neurocognitive deficit and impairment of social cognition in schizophrenia, we assessed 30 patients and 30 healthy people (controls) using clinical, psychometric and psychological tests. Based on the results obtained in the study, authors could single out a specific block of impairment which was not associated with perceptive and gnostic deficits. The data confirmed the significant contribution of deficit neurodynamic and regulatory parameters in the impairment of social cognition in schizophrenia.

Broadening the cancer and cognition landscape: the role of self-regulatory challenges.

PubMed

Arndt, Jamie; Das, Enny; Schagen, Sanne B; Reid-Arndt, Stephanie A; Cameron, Linda D; Ahles, Tim A

2014-01-01

The potentially detrimental effects of cancer and related treatments on cognitive functioning have emerged as one of the key foci of cancer survivorship research, but little is known about how psychological variables other than depression influence these relationships. To illustrate the potential of social psychological perspectives, we examine how a self-regulatory analysis and specific self-regulatory challenges of contending with cancer-related expectancies and stereotypes provide conceptual frameworks for understanding some of the potential causes and consequences of cancer-related cognitive deficits. Literatures on cancer-related cognitive deficits, self-regulatory ego depletion, expectancy stereotypes, and their points of convergence are briefly reviewed. A review and conceptual integration of relevant literatures suggest that coping with cancer can impair self-regulatory capacity. There is an overlap between cognitive deficits associated with self-regulatory challenge and with cancer and its treatment, and restoring self-regulatory resources can attenuate cancer-related cognitive deficits. Examination of specific regulatory challenges of contending with expectancies and stereotypes related to treatment suggests insights that can inform when and among whom cognitive deficits may most likely emerge. Integrating social psychological ideas with a substantial knowledge base can illustrate novel research trajectories that can deepen our understanding of cancer-related cognitive deficits and their impact on psychosocial well-being. Copyright © 2013 John Wiley & Sons, Ltd.

Broadening the cancer and cognition landscape: The role of self-regulatory challenges

PubMed Central

Arndt, Jamie; Das, Enny; Schagen, Sanne B.; Reid-Arndt, Stephanie A.; Cameron, Linda D.; Ahles, Tim A.

2013-01-01

Objective The potentially detrimental effects of cancer and related treatments on cognitive functioning have emerged as key foci of cancer survivorship research, but little is known about how psychological variables other than depression influence these relationships. To illustrate the potential of social psychological perspectives, we examine how a self-regulatory analysis and specific self-regulatory challenges of contending with cancer-related expectancies and stereotypes provide conceptual frameworks for understanding some of the potential causes and consequences of cancer-related cognitive deficits. Methods Literatures on cancer-related cognitive deficits, self-regulatory ego depletion, expectancy-stereotypes and their points of convergence are briefly reviewed. Results A review and conceptual integration of relevant literatures suggests that coping with cancer can impair self-regulatory capacity, there is overlap between cognitive deficits associated with self-regulatory challenge and with cancer and its treatment, and restoring self-regulatory resources can attenuate cancer-related cognitive deficits. Examination of specific regulatory challenges of contending with expectancies and stereotypes related to treatment suggest insights that can inform when and among whom cognitive deficits may most likely emerge. Conclusions Integrating social psychological ideas with a substantial knowledge base can illustrate novel research trajectories that can deepen our understanding of cancer-related cognitive deficits and their impact on psychosocial well-being. PMID:23839818

Animal model of dementia induced by entorhinal synaptic damage and partial restoration of cognitive deficits by BDNF and carnitine.

PubMed

Ando, Susumu; Kobayashi, Satoru; Waki, Hatsue; Kon, Kazuo; Fukui, Fumiko; Tadenuma, Tomoko; Iwamoto, Machiko; Takeda, Yasuo; Izumiyama, Naotaka; Watanabe, Kazutada; Nakamura, Hiroaki

2002-11-01

A rat dementia model with cognitive deficits was generated by synapse-specific lesions using botulinum neurotoxin (BoNTx) type B in the entorhinal cortex. To detect cognitive deficits, different tasks were needed depending upon the age of the model animals. Impaired learning and memory with lesions were observed in adult rats using the Hebb-Williams maze, AKON-1 maze and a continuous alternation task in T-maze. Cognitive deficits in lesioned aged rats were detected by a continuous alternation and delayed non-matching-to-sample tasks in T-maze. Adenovirus-mediated BDNF gene expression enhanced neuronal plasticity, as revealed by behavioral tests and LTP formation. Chronic administration of carnitine over time pre- and post-lesions seemed to partially ameliorate the cognitive deficits caused by the synaptic lesion. The carnitine-accelerated recovery from synaptic damage was observed by electron microscopy. These results demonstrate that the BoNTx-lesioned rat can be used as a model for dementia and that cognitive deficits can be alleviated in part by BDNF gene transfer or carnitine administration. Copyright 2002 Wiley-Liss, Inc.

Comparison of the recovery patterns of language and cognitive functions in patients with post-traumatic language processing deficits and in patients with aphasia following a stroke.

PubMed

Vukovic, Mile; Vuksanovic, Jasmina; Vukovic, Irena

2008-01-01

In this study we investigated the recovery patterns of language and cognitive functions in patients with post-traumatic language processing deficits and in patients with aphasia following a stroke. The correlation of specific language functions and cognitive functions was analyzed in the acute phase and 6 months later. Significant recovery of the tested functions was observed in both groups. However, in patients with post-traumatic language processing deficits the degree of recovery of most language functions and some cognitive functions was higher. A significantly greater correlation was revealed within language and cognitive functions, as well as between language functions and other aspects of cognition in patients with post-traumatic language processing deficits than in patients with aphasia following a stroke. Our results show that patients with post-traumatic language processing deficits have a different recovery pattern and a different pattern of correlation between language and cognitive functions compared to patients with aphasia following a stroke. (1) Better understanding of the differences in recovery of language and cognitive functions in patients who have suffered strokes and those who have experienced traumatic brain injury. (2) Better understanding of the relationship between language and cognitive functions in patients with post-traumatic language processing deficits and in patients with aphasia following a stroke. (3) Better understanding of the factors influencing recovery.

Social Cognition Deficits: Current Position and Future Directions for Neuropsychological Interventions in Cerebrovascular Disease.

PubMed

Njomboro, Progress

2017-01-01

Neuropsychological assessments of cognitive dysfunction in cerebrovascular illness commonly target basic cognitive functions involving aspects of memory, attention, language, praxis, and number processing. Here, I highlight the clinical importance of often-neglected social cognition functions. These functions recruit a widely distributed neural network, making them vulnerable in most cerebrovascular diseases. Sociocognitive deficits underlie most of the problematic social conduct observed in patients and are associated with more negative clinical outcomes (compared to nonsocial cognitive deficits). In clinical settings, social cognition deficits are normally gleaned from collateral information from caregivers or from indirect inferences made from patients' performance on standard nonsocial cognitive tests. Information from these sources is however inadequate. I discuss key social cognition functions, focusing initially on deficits in emotion perception and theory of mind, two areas that have gained sizeable attention in neuroscientific research, and then extend the discussion into relatively new, less covered but crucial functions involving empathic behaviour, social awareness, social judgements, and social decision making. These functions are frequently impaired following neurological change. At present, a wide range of psychometrically robust social cognition tests is available, and this review also makes the case for their inclusion in neuropsychological assessments.

Social Cognition Deficits: Current Position and Future Directions for Neuropsychological Interventions in Cerebrovascular Disease

PubMed Central

2017-01-01

Neuropsychological assessments of cognitive dysfunction in cerebrovascular illness commonly target basic cognitive functions involving aspects of memory, attention, language, praxis, and number processing. Here, I highlight the clinical importance of often-neglected social cognition functions. These functions recruit a widely distributed neural network, making them vulnerable in most cerebrovascular diseases. Sociocognitive deficits underlie most of the problematic social conduct observed in patients and are associated with more negative clinical outcomes (compared to nonsocial cognitive deficits). In clinical settings, social cognition deficits are normally gleaned from collateral information from caregivers or from indirect inferences made from patients' performance on standard nonsocial cognitive tests. Information from these sources is however inadequate. I discuss key social cognition functions, focusing initially on deficits in emotion perception and theory of mind, two areas that have gained sizeable attention in neuroscientific research, and then extend the discussion into relatively new, less covered but crucial functions involving empathic behaviour, social awareness, social judgements, and social decision making. These functions are frequently impaired following neurological change. At present, a wide range of psychometrically robust social cognition tests is available, and this review also makes the case for their inclusion in neuropsychological assessments. PMID:28729755

Cognitive impairment in COPD: should cognitive evaluation be part of respiratory assessment?

PubMed Central

Gloeckl, Rainer; Vogiatzis, Ioannis; Kenn, Klaus

2017-01-01

Cognitive impairment is highly prevalent in patients with COPD and demonstrates multiple detrimental effects on many aspects of patient state and therapeutic outcomes. It is attributed to several overlapping pathophysiological factors, with the most common being the low level of oxygen saturation due to respiratory insufficiency. Despite the impact of cognitive impairment on clinical outcomes, the screening for coexisting cognitive deficits which may interfere with the successful progress of respiratory treatment is yet neglected. There is a special consideration that cognitive deficits should be taken into account when developing respiratory therapy plans. Cognitively impaired patients are likely to require more support and have need of an individualised respiratory care plan which can also be beneficial for their cognitive deficits. Pulmonary rehabilitation as a multidisciplinary approach could be prioritised for COPD patients with cognitive impairment. Educational aims To illustrate the common signs of cognitive impairment and define potential associations between lung and cognitive dysfunction. To illustrate the potential influence of cognitive deficits on the optimal progress of respiratory therapy. To illustrate the importance of cognitive evaluation as part of a comprehensive clinical assessment for patients suspected of suffering cognitive impairment. PMID:29184593

Attention and Other Cognitive Deficits in Aphasia: Presence and Relation to Language and Communication Measures

ERIC Educational Resources Information Center

Murray, Laura L.

2012-01-01

Purpose: This study was designed to further elucidate the relationship between cognition and aphasia, with a focus on attention. It was hypothesized that individuals with aphasia would display variable deficit patterns on tests of attention and other cognitive functions and that their attention deficits, particularly those of complex attention…

The Comprehension of Syntactic and Affective Prosody by Adults with Autism Spectrum Disorder without Accompanying Cognitive Deficits

ERIC Educational Resources Information Center

Martzoukou, Maria; Papadopoulou, Despina; Kosmidis, Mary-Helen

2017-01-01

The present study investigates the comprehension of syntactic and affective prosody in adults with autism spectrum disorder without accompanying cognitive deficits (ASD w/o cognitive deficits) as well as age-, education- and gender-matched unimpaired adults, while processing orally presented sentences. Two experiments were conducted: (a) an…

Oculomotor Performance Identifies Underlying Cognitive Deficits in Attention-Deficit/Hyperactivity Disorder

ERIC Educational Resources Information Center

Loe, Irene M.; Feldman, Heidi M.; Yasui, Enami; Luna, Beatriz

2009-01-01

The evaluation of the cognitive control in children with attention-deficit hyperactivity disorder through the use of oculomotor tests reveal that this group showed susceptibility to peripheral distractors and deficits in response inhibition. All subjects were found to have intact sensorimotor function and working memory.

Cognitive Control in Autism Spectrum Disorders

PubMed Central

Solomon, Marjorie; Ozonoff, Sally; Cummings, Neil; Carter, Cameron

2009-01-01

Cognitive control refers to the ability to flexibly allocate mental resources to guide thoughts and actions in light of internal goals. Given the behavioral inflexibility exhibited by individuals with autism spectrum disorders (ASDs), it would appear they experience cognitive control deficits. Cognitive correlates of this behavioral inflexibility have been elusive in previous investigations. Study goals were to investigate deficits in cognitive control in ASDs; to explore its developmental trajectory; and to test whether control deficits are related to symptoms of inflexible thoughts and/or behaviors, and attention symptoms. Thirty-one children and adolescents aged 8 to17 with ASDs and 32 age, IQ, and gender matched control subjects completed cognitive, diagnostic, and behavorial assessments, as well as a measure of cognitive control involving overcoming a prepotent response tendency. Compared with typically developing control subjects, individuals with ASDs exhibited deficits in cognitive control. Younger children with ASDs did not demonstrate age related improvements in cognitive control. Modest relationships between cognitive control, IQ, and attention problems were found for the sample. Only the relationship between cognitive control and Full Scale IQ survived correction for multiple comparisons. PMID:18093787

Cognitive Control Deficits Associated with Antisocial Personality Disorder and Psychopathy

PubMed Central

Zeier, Joshua D.; Baskin-Sommers, Arielle R.; Newman, Joseph P.; Racer, Kristina Hiatt

2011-01-01

Antisociality has been linked to a variety of executive functioning deficits, including poor cognitive control. Surprisingly, cognitive control deficits are rarely found in psychopathic individuals, despite their notoriously severe and persistent antisocial behavior. In fact, primary (low-anxious) psychopathic individuals display superior performance on cognitive control-type tasks under certain circumstances. To clarify these seemingly contradictory findings, we administered a response competition (i.e. flanker) task to incarcerated offenders, who were assessed for Antisocial Personality Disorder (APD) symptoms and psychopathy. As hypothesized, APD related to poorer accuracy, especially on incongruent trials. Contrary to expectation, however, the same pattern of results was found in psychopathy. Additional analyses indicated that these effects of APD and psychopathy were associated with overlapping variance. The findings suggest that psychopathy and APD symptoms are both associated with deficits in cognitive control, and that this deficit relates to general antisociality as opposed to a specific antisocial syndrome. PMID:22452754

Poor school and cognitive functioning with silent cerebral infarcts and sickle cell disease.

PubMed

Schatz, J; Brown, R T; Pascual, J M; Hsu, L; DeBaun, M R

2001-04-24

The authors evaluated education attainment and neuropsychological deficits in children with sickle cell disease (SCD) and silent cerebral infarcts. Children with silent infarcts had twice the rate of school difficulties as children without infarcts. Eighty percent of silent infarct cases had clinically significant cognitive deficits, whereas 35% had deficits in academic skills. Children with silent cerebral infarcts show high rates of poor educational attainment, cognitive deficits, and frontal lobe injury. Poor school performance in SCD is one indicator of silent infarcts.

Variability in Depressive Symptoms of Cognitive Deficit and Cognitive Bias During the First 2 Years After Diagnosis in Australian Men With Prostate Cancer.

PubMed

Sharpley, Christopher F; Bitsika, Vicki; Christie, David R H

2016-01-01

The incidence and contribution to total depression of the depressive symptoms of cognitive deficit and cognitive bias in prostate cancer (PCa) patients were compared from cohorts sampled during the first 2 years after diagnosis. Survey data were collected from 394 patients with PCa, including background information, treatments, and disease status, plus total scores of depression and scores for subscales of the depressive symptoms of cognitive bias and cognitive deficit via the Zung Self-Rating Depression Scale. The sample was divided into eight 3-monthly time-since-diagnosis cohorts and according to depression severity. Mean scores for the depressive symptoms of cognitive deficit were significantly higher than those for cognitive bias for the whole sample, but the contribution of cognitive bias to total depression was stronger than that for cognitive deficit. When divided according to overall depression severity, patients with clinically significant depression showed reversed patterns of association between the two subsets of cognitive symptoms of depression and total depression compared with those patients who reported less severe depression. Differences in the incidence and contribution of these two different aspects of the cognitive symptoms of depression for patients with more severe depression argue for consideration of them when assessing and diagnosing depression in patients with PCa. Treatment requirements are also different between the two types of cognitive symptoms of depression, and several suggestions for matching treatment to illness via a personalized medicine approach are discussed. © The Author(s) 2014.

Cognitive Behavioral Therapies in older adults with depression and cognitive deficits: a systematic review.

PubMed

Simon, Sharon Sanz; Cordás, Táki Athanássios; Bottino, Cássio M C

2015-03-01

The objective of this study is to investigate the effectiveness of cognitive behavioral therapies (CBTs) in improving depressive symptoms, disability, and cognition in older adults with depression and cognitive deficits. It was performed a systematic search for articles published between 1994 and February 2014 in the MEDLINE/Pubmed, PsycINFO, and SCIELO. The studies should have provided information about benefits after CBTs to older adults with depression and cognitive deficits. Cognitive behavioral therapy focused on problem solving is the main approach studied, having better effectiveness than supportive therapy in randomized clinical trials. Significant improvements in mood and disability were consistent, although evidence of changes in cognitive measures is controversial, less studied, and limited. Nevertheless, improvements in executive functions, processing speed, and changes in patients' perspectives of problem solving skills, such as generating alternatives and decision-making, were described. Also, it would be necessary that future studies more often evaluate cognitive status of depressed elders, as well as cognitive changes after psychotherapy. It should be emphasized that there is a lack of studies in this field, and more approaches in CBTs need to be investigated to this population. Older adults with depression and cognitive deficits can benefit from CBTs. Improvements in mood and disability are more consistent than changes in cognition, which are little studied after CBTs. It is necessary more studies in the field, as well as, to investigate more approaches in CBTs to older adults with depression and cognitive deficits. Copyright © 2014 John Wiley & Sons, Ltd.

Attention and memory deficits in breast cancer survivors: implications for nursing practice and research.

PubMed

Frank, Jennifer Sandson; Vance, David E; Jukkala, Angela; Meneses, Karen M

2014-10-01

Breast cancer survivors (BCSs) commonly report deficits in attention and memory, cognitive functions crucial for daily optimal functioning. Perceived deficits are reported before, during, and after adjuvant therapy and affect quality of life throughout survivorship. Deficits of attention and memory are particularly disruptive for BCSs working or attending school who report that subtle impairment diminishes their confidence and their performance at all levels of occupation. Chemotherapy and endocrine therapy contribute to attention and memory deficits, but research findings have not fully established the extent or timing of that influence. Fortunately, potential interventions for attention and memory deficits in BCSs are promising. These include cognitive remediation therapies aimed at training for specific areas of deficit, cognitive behavioral therapies aimed at developing compensatory strategies for areas of deficit, complementary therapies, and pharmacologic therapies.

The social-cognitive basis of personality disorders.

PubMed

Herpertz, Sabine C; Bertsch, Katja

2014-01-01

The review summarizes recent results on abnormalities in social cognition in patients with personality disorders that predispose them to develop dysfunctional interaction with others. The review starts with more basic social cognition processes, such as emotion recognition and reactions to social exclusion that are followed by more complex processes such as cognitive and affective empathy. The deficits in social cognition depend on the particular function that is investigated and is strongly associated with characteristic symptoms of particular personality disorders. Thus, patients with borderline personality disorder are hypersensitive for social threat, they show deficits in cognitive empathy and high emotion contagion, that is, they share emotions of others without properly discriminating between one's own feelings and those of others. Psychopaths are characterized by deficiency in facial fear recognition and emotional empathy similar to patients with narcissistic personality disorder. Studies on social cognition in cluster A and C personality disorders are sparse. Research indicates deficits in social cognition in patients with personality disorders, but more research is needed to investigate social cognition in cluster A and C personality disorders and to compare deficits in social cognitive functions across personality disorders.

Cognitive and Behavioral Impairments Evoked by Low-Level Exposure to Tobacco Smoke Components: Comparison with Nicotine Alone.

PubMed

Hall, Brandon J; Cauley, Marty; Burke, Dennis A; Kiany, Abtin; Slotkin, Theodore A; Levin, Edward D

2016-06-01

Active maternal smoking has adverse effects on neurobehavioral development of the offspring, with nicotine (Nic) providing much of the underlying causative mechanism. To determine whether the lower exposures caused by second-hand smoke are deleterious, we administered tobacco smoke extract (TSE) to pregnant rats starting preconception and continued through the second postnatal week, corresponding to all 3 trimesters of fetal brain development. Dosing was adjusted to produce maternal plasma Nic concentrations encountered with second-hand smoke, an order of magnitude below those seen in active smokers. We then compared TSE effects to those of an equivalent dose of Nic alone, and to a 10-fold higher Nic dose. Gestational exposure to TSE and Nic significantly disrupted cognitive and behavioral function in behavioral tests given during adolescence and adulthood (postnatal weeks 4-40), producing hyperactivity, working memory deficits, and impairments in emotional processing, even at the low exposure levels corresponding to second-hand smoke. Although TSE effects were highly correlated with those of Nic, the effects of TSE were much larger than could be attributed to just the Nic in the mixture. Indeed, TSE effects more closely resembled those of the 10-fold higher Nic levels, but still exceeded their magnitude. In combination with our earlier findings, this study thus completes the chain of causation to prove that second-hand smoke exposure causes neurodevelopmental deficits, originating in disruption of neurodifferentiation, leading to miswiring of neuronal circuits, and as shown here, culminating in behavioral dysfunction. As low level exposure to Nic alone produced neurobehavioral teratology, 'harm reduction' Nic products do not abolish the potential for neurodevelopmental damage. © The Author 2016. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

The effect of left frontal transcranial direct-current stimulation on propranolol-induced fear memory acquisition and consolidation deficits.

PubMed

Nasehi, Mohammad; Khani-Abyaneh, Mozhgan; Ebrahimi-Ghiri, Mohaddeseh; Zarrindast, Mohammad-Reza

2017-07-28

Accumulating evidence supports the efficacy of transcranial direct current stimulation (tDCS) in modulating numerous cognitive functions. Despite the fact that tDCS has been used for the enhancement of memory and cognition, very few animal studies have addressed its impact on the modulation of fear memory. This study was designed to determine whether pre/post-training frontal tDCS application would alter fear memory acquisition and/or consolidation deficits induced by propranolol in NMRI mice. Results indicated that administration of β1-adrenoceptor blocker propranolol (0.1mg/kg) impaired fear memory retrieval. Pre/post-training application of anodal tDCS when propranolol was administered prior to training reversed contextual memory retrieval whereas only the anodal application prior to training could induce the same result in the auditory test. Meanwhile, anodal stimulation had no effect on fear memories by itself. Moreover, regardless of when cathode was applied and propranolol administered, their combination restored contextual memory retrieval, while only cathodal stimulation prior to training facilitated the contextual memory retrieval. Also, auditory memory retrieval was restored when cathodal stimulation and propranolol occurred prior to training but it was abolished when stimulation occurred after training and propranolol was administered prior to training. Collectively, our findings show that tDCS applied on the left frontal cortex of mice affects fear memory performance. This alteration seems to be task-dependent and varies depending on the nature and timing of the stimulation. In certain conditions, tDCS reverses the effect of propranolol. These results provide initial evidence to support the timely use of tDCS for the modulation of fear-related memories. Copyright © 2017 Elsevier B.V. All rights reserved.

CREB Overexpression Ameliorates Age-related Behavioral and Biophysical Deficits

NASA Astrophysics Data System (ADS)

Yu, Xiao-Wen

Age-related cognitive deficits are observed in both humans and animals. Yet, the molecular mechanisms underlying these deficits are not yet fully elucidated. In aged animals, a decrease in intrinsic excitability of pyramidal neurons from the CA1 sub-region of hippocampus is believed to contribute to age-related cognitive impairments, but the molecular mechanism(s) that modulate both these factors has yet to be identified. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents has been shown to facilitate cognition, and increase intrinsic excitability of their neurons. However, how CREB changes with age, and how that impacts cognition in aged animals, is not clear. Therefore, we first systematically characterized age- and training-related changes in CREB levels in dorsal hippocampus. At a remote time point after undergoing behavioral training, levels of total CREB and activated CREB (phosphorylated at S133, pCREB) were measured in both young and aged rats. We found that pCREB, but not total CREB was significantly reduced in dorsal CA1 of aged rats. Importantly, levels of pCREB were found to be positively correlated with short-term spatial memory in both young and aged rats i.e. higher pCREB in dorsal CA1 was associated with better spatial memory. These findings indicate that an age-related deficit in CREB activity may contribute to the development of age-related cognitive deficits. However, it was still unclear if increasing CREB activity would be sufficient to ameliorate age-related cognitive, and biophysical deficits. To address this question, we virally overexpressed CREB in CA1, where we found the age-related deficit. Young and aged rats received control or CREB virus, and underwent water maze training. While control aged animals exhibited deficits in long-term spatial memory, aged animals with CREB overexpression performed at levels comparable to young animals. Concurrently, aged neurons overexpressing CREB had increased excitability. This indicates that overexpression of CREB was sufficient to rescue both the cognitive deficits, and the biophysical dysfunction normally seen in aged animals. Together, the results from this thesis identify CREB as a new mechanism underlying age-related cognitive deficits. This not only furthers our understanding of how cognitive processes change with age, but also suggests that increasing activity of CREB or its downstream transcription targets may be a novel therapeutic for the treatment of age-related cognitive decline.

Dyslexia and dyscalculia: two learning disorders with different cognitive profiles.

PubMed

Landerl, Karin; Fussenegger, Barbara; Moll, Kristina; Willburger, Edith

2009-07-01

This study tests the hypothesis that dyslexia and dyscalculia are associated with two largely independent cognitive deficits, namely a phonological deficit in the case of dyslexia and a deficit in the number module in the case of dyscalculia. In four groups of 8- to 10-year-olds (42 control, 21 dyslexic, 20 dyscalculic, and 26 dyslexic/dyscalculic), phonological awareness, phonological and visual-spatial short-term and working memory, naming speed, and basic number processing skills were assessed. A phonological deficit was found for both dyslexic groups, irrespective of additional arithmetic deficits, but not for the dyscalculia-only group. In contrast, deficits in processing of symbolic and nonsymbolic magnitudes were observed in both groups of dyscalculic children, irrespective of additional reading difficulties, but not in the dyslexia-only group. Cognitive deficits in the comorbid dyslexia/dyscalculia group were additive; that is, they resulted from the combination of two learning disorders. These findings suggest that dyslexia and dyscalculia have separable cognitive profiles, namely a phonological deficit in the case of dyslexia and a deficient number module in the case of dyscalculia.

Impaired affective and cognitive theory of mind and behavioural change in amyotrophic lateral sclerosis.

PubMed

van der Hulst, Egberdina-Józefa; Bak, Thomas H; Abrahams, Sharon

2015-11-01

Executive and behavioural changes are well-recognised in classical amyotrophic lateral sclerosis (ALS), indicating a subclinical behavioural-variant frontotemporal dementia (bvFTD) in some patients. Social cognitive deficits in ALS have been recently described and an impairment was identified on a simple Theory of Mind (ToM) test, which assesses the judgement of the preference of another through direction of eye gaze. The present study further delineated this deficit, by distinguishing between Affective and Cognitive subcomponents, and determining the relationship to behavioural change, levels of empathy and self-awareness. The Cognitive-Affective Judgement of Preference Test was administered to 33 patients with ALS and 26 controls. Furthermore, a comprehensive neuropsychological battery and detailed behavioural assessment, with measures of empathy and awareness, were included. Patients with ALS showed a significant impairment in Affective ToM only when compared with healthy controls, with a deficit in 36% of patients; 12% showed an isolated Affective ToM deficit while 24% showed more generic ToM dysfunction. A Cognitive ToM deficit was found in 27% of patients, with 3% showing an isolated Cognitive ToM deficit. The patients with ALS showed reduced empathy (Fantasy scale) and increased behavioural dysfunction with high levels of apathy. In addition, patients with either an Affective and/or Cognitive ToM deficit exhibited poor self-awareness of their performance and abnormalities on verbal fluency, while those with an Affective ToM deficit also displayed higher levels of apathy and a naming deficit. Dysfunctional ToM is a prominent feature of the cognitive profile of ALS. This specific difficulty in identifying and distinguishing the feelings and thoughts of another from a self-perspective may underpin the social behavioural abnormalities present in some patients with ALS, manifest as apathy and loss of awareness. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Disrupted reward circuits is associated with cognitive deficits and depression severity in major depressive disorder.

PubMed

Gong, Liang; Yin, Yingying; He, Cancan; Ye, Qing; Bai, Feng; Yuan, Yonggui; Zhang, Haisan; Lv, Luxian; Zhang, Hongxing; Xie, Chunming; Zhang, Zhijun

2017-01-01

Neuroimaging studies have demonstrated that major depressive disorder (MDD) patients show blunted activity responses to reward-related tasks. However, whether abnormal reward circuits affect cognition and depression in MDD patients remains unclear. Seventy-five drug-naive MDD patients and 42 cognitively normal (CN) subjects underwent a resting-state functional magnetic resonance imaging scan. The bilateral nucleus accumbens (NAc) were selected as seeds to construct reward circuits across all subjects. A multivariate linear regression analysis was employed to investigate the neural substrates of cognitive function and depression severity on the reward circuits in MDD patients. The common pathway underlying cognitive deficits and depression was identified with conjunction analysis. Compared with CN subjects, MDD patients showed decreased reward network connectivity that was primarily located in the prefrontal-striatal regions. Importantly, distinct and common neural pathways underlying cognition and depression were identified, implying the independent and synergistic effects of cognitive deficits and depression severity on reward circuits. This study demonstrated that disrupted topological organization within reward circuits was significantly associated with cognitive deficits and depression severity in MDD patients. These findings suggest that in addition to antidepressant treatment, normalized reward circuits should be a focus and a target for improving depression and cognitive deficits in MDD patients. Copyright © 2016 Elsevier Ltd. All rights reserved.

[Self-consciousness in elderly persons with cognitive impairment and vascular dementia].

PubMed

Dubinina, E A; Novikova, Yu G; Kalitskaya, A V; Finagentova, N V

2016-01-01

Self-consciousness was compared in 17 elderly (aged 65-89 years old) persons with cognitive impairment without dementia and 17 patients with vascular dementia. Neurocognitive functions and mental health complaints were evaluated. Neuropsychological assessment included evaluation of higher psychological functions, such as attention, memory, conceptualization, gnosis (optic, acoustic), manual skill, speech. Older persons with cognitive impairment assessed their neurocognitive functions adequately. Patients with vascular dementia usually denied cognitive deficit or explained it as a result of aging. Regardless of physical health, older persons with cognitive impairment have active attitude to aging. They could find ways of compensation of cognitive deficits without assistance. Patients with vascular dementia could not compensate their cognitive deficit even with support.

Cognitive enhancement effects of Bacopa monnieri (Brahmi) on novel object recognition and neuronal density in the prefrontal cortex, striatum and hippocampus in sub-chronic phencyclidine administration rat model of schizophrenia.

PubMed

Wetchateng, Thanitsara; Piyabhan, Pritsana

2015-03-01

Cognitive deficit is a significant problem, which finally occurs in all schizophrenic patients. It can not be attenuated by any antipsychotic drugs. It is well known that changes of neuronal density are correlated with learning and memory deficits. Bacopa monnieri (Brahmi), popularly known as a cognitive enhancer; might be a novel therapeutic agentfor cognitive deficit in schizophrenia by changing cerebral neuronal density. The objective of this study was to determine the effects of Brahmi on attenuation at cognitive deficit and on the neuronal density in the prefrontal cortex, striatum and cornu ammonis subfield 1 (CA1) and 2/3 (CA2/3) of hippocampus in sub-chronic phencyclidine (PCP) rat model of schizophrenia. Rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: PCP + Brahmi. Rats were testedfor cognitive ability by using the novel object recognition test. Neuronal density from a serial Nissl stain sections ofthe prefrontal cortex, striatum and hippocampus ofrat model ofschizophrenia were measured by using Image ProPlus software and manual counting. Sub-chronic administration of PCP results in cognitive deficits in novel object recognition task. This occurred alongside significantly increased neuronal density in CA1. The cognitive deficit was recovery to normal in PCP + Brahmi group and it occurred alongside significantly decreased neuronal density in CA1. On the other hand, significantly increased neuronal density was observed in CA2/3 of PCP + Brahmi group compared with PCP alone. Brahmi is a potential cognitive enhancer against schizophrenia. It reduces neuronal density, most likely glutamatergic neuron, which results in neuronal toxicity and cognitive deficit. Therefore, Brahmi has cognitive enhancement effect by reducing glutamatergic neuron in CAI. Moreover, it also has neurogenesis effect in CA2/3, which is needed to be investigated in the further study.

Cognitive impairment, clinical severity and MRI changes in MELAS syndrome.

PubMed

Kraya, Torsten; Neumann, Lena; Paelecke-Habermann, Yvonne; Deschauer, Marcus; Stoevesandt, Dietrich; Zierz, Stephan; Watzke, Stefan

2017-12-29

To examine clinical severity, cognitive impairment, and MRI changes in patients with MELAS syndrome. Cognitive-mnestic functions, brain MRI (lesion load, cella media index) and clinical severity of ten patients with MELAS syndrome were examined. All patients carried the m.3243A>G mutation. The detailed neuropsychological assessment revealed cognitive deficits in attention, executive function, visuoperception, and -construction. There were significant correlations between these cognitive changes, lesion load in MRI, disturbances in everyday life (clinical scale), and high scores in NMDAS. Patients with MELAS syndrome showed no global neuropsychological deficit, but rather distinct cognitive deficits. Copyright © 2018 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

Executive Functions, Memory, and Social Cognitive Deficits and Recovery in Chronic Alcoholism: A Critical Review to Inform Future Research.

PubMed

Le Berre, Anne-Pascale; Fama, Rosemary; Sullivan, Edith V

2017-08-01

Alcoholism is a complex and dynamic disease, punctuated by periods of abstinence and relapse, and influenced by a multitude of vulnerability factors. Chronic excessive alcohol consumption is associated with cognitive deficits, ranging from mild to severe, in executive functions, memory, and metacognitive abilities, with associated impairment in emotional processes and social cognition. These deficits can compromise efforts in initiating and sustaining abstinence by hampering efficacy of clinical treatment and can obstruct efforts in enabling good decision making success in interpersonal/social interactions, and awareness of cognitive and behavioral dysfunctions. Despite evidence for differences in recovery levels of selective cognitive processes, certain deficits can persist even with prolonged sobriety. Herein is presented a review of alcohol-related cognitive impairments affecting component processes of executive functioning, memory, and the recently investigated cognitive domains of metamemory, social cognition, and emotional processing; also considered are trajectories of cognitive recovery with abstinence. Finally, in the spirit of critical review, limitations of current knowledge are noted and avenues for new research efforts are proposed that focus on (i) the interaction among emotion-cognition processes and identification of vulnerability factors contributing to the development of emotional and social processing deficits and (ii) the time line of cognitive recovery by tracking alcoholism's dynamic course of sobriety and relapse. Knowledge about the heterochronicity of cognitive recovery in alcoholism has the potential of indicating at which points during recovery intervention may be most beneficial. Copyright © 2017 by the Research Society on Alcoholism.

Cognitive Flexibility in Children with and without Speech Disorder

ERIC Educational Resources Information Center

Crosbie, Sharon; Holm, Alison; Dodd, Barbara

2009-01-01

Most children's speech difficulties are "functional" (i.e. no known sensory, motor or intellectual deficits). Speech disorder may, however, be associated with cognitive deficits considered core abilities in executive function: rule abstraction and cognitive flexibility. The study compares the rule abstraction and cognitive flexibility of…

Self-Instructional Cognitive Training to Reduce Impulsive Cognitive Style in Children with Attention Deficit with Hyperactivity Disorder

ERIC Educational Resources Information Center

Rivera-Flores, Gladys Wilma

2015-01-01

Introduction: Children with attention deficit with hyperactivity disorder (ADHD) have an impulsive, rigid and field-dependent cognitive style. This study examines whether self-instructional cognitive training reduces impulsive cognitive style in children diagnosed with this disorder. Method: The subjects were 10 children between the ages of 6 and…

Neurological and Psychiatric Diseases and Their Unique Cognitive Profiles: Implications for Nursing Practice and Research

PubMed Central

Vance, David E.; Dodson, Joan E.; Watkins, Jason; Kennedy, Bridgett H.; Keltner, Norman L.

2013-01-01

To successfully negotiate and interact with one’s environment, optimal cognitive functioning is needed. Unfortunately, many neurological and psychiatric diseases impede certain cognitive abilities such as executive functioning or speed of processing; this can produce a poor fit between the patient and the cognitive demands of his or her environment. Such non-dementia diseases include bipolar disorder, schizophrenia, post-traumatic stress syndrome, depression, and anxiety disorders, just to name a few. Each of these diseases negatively affects particular areas of the brain, resulting in distinct cognitive profiles (e.g., deficits in executive functioning but normal speed of processing as seen in schizophrenia). In fact, it is from these cognitive deficits in which such behavioral and emotional symptoms may manifest (e.g., delusions, paranoia). This article highlights the distinct cognitive profiles of such common neurological and psychiatric diseases. An understanding of such disease-specific cognitive profiles can assist nurses in providing care to patients by knowing what cognitive deficits are associated with each disease and how these cognitive deficits impact everyday functioning and social interactions. Implications for nursing practice and research are posited within the framework of cognitive reserve and neuroplasticity. PMID:23422693

Prefrontal Cortical GABA Transmission Modulates Discrimination and Latent Inhibition of Conditioned Fear: Relevance for Schizophrenia

PubMed Central

Piantadosi, Patrick T; Floresco, Stan B

2014-01-01

Inhibitory gamma-aminobutyric acid (GABA) transmission within the prefrontal cortex (PFC) regulates numerous functions, and perturbations in GABAergic transmission within this region have been proposed to contribute to some of the cognitive and behavioral abnormalities associated with disorders such as schizophrenia. These abnormalities include deficits in emotional regulation and aberrant attributions of affective salience. Yet, how PFC GABA regulates these types of emotional processes are unclear. To address this issue, we investigated the contribution of PFC GABA transmission to different aspects of Pavlovian emotional learning in rats using translational discriminative fear conditioning and latent inhibition (LI) assays. Reducing prelimbic PFC GABAA transmission via infusions of the antagonist bicuculline before the acquisition or expression of fear conditioning eliminated the ability to discriminate between an aversive conditioned stimulus (CS+) paired with footshock vs a neutral CS–, resembling similar deficits observed in schizophrenic patients. In a separate experiment, blockade of PFC GABAA receptors before CS preexposure (PE) and conditioning did not affect subsequent expression of LI, but did enhance fear in rats that were not preexposed to the CS. In contrast, PFC GABA-blockade before a fear expression test disrupted the recall of learned irrelevance and abolished LI. These data suggest that normal PFC GABA transmission is critical for regulating and mitigating multiple aspects of aversive learning, including discrimination between fear vs safety signals and recall of information about the irrelevance of stimuli. Furthermore, they suggest that similar deficits in emotional regulation observed in schizophrenia may be driven in part by deficient PFC GABA activity. PMID:24784549

Prefrontal cortical GABA transmission modulates discrimination and latent inhibition of conditioned fear: relevance for schizophrenia.

PubMed

Piantadosi, Patrick T; Floresco, Stan B

2014-09-01

Inhibitory gamma-aminobutyric acid (GABA) transmission within the prefrontal cortex (PFC) regulates numerous functions, and perturbations in GABAergic transmission within this region have been proposed to contribute to some of the cognitive and behavioral abnormalities associated with disorders such as schizophrenia. These abnormalities include deficits in emotional regulation and aberrant attributions of affective salience. Yet, how PFC GABA regulates these types of emotional processes are unclear. To address this issue, we investigated the contribution of PFC GABA transmission to different aspects of Pavlovian emotional learning in rats using translational discriminative fear conditioning and latent inhibition (LI) assays. Reducing prelimbic PFC GABAA transmission via infusions of the antagonist bicuculline before the acquisition or expression of fear conditioning eliminated the ability to discriminate between an aversive conditioned stimulus (CS+) paired with footshock vs a neutral CS-, resembling similar deficits observed in schizophrenic patients. In a separate experiment, blockade of PFC GABAA receptors before CS preexposure (PE) and conditioning did not affect subsequent expression of LI, but did enhance fear in rats that were not preexposed to the CS. In contrast, PFC GABA-blockade before a fear expression test disrupted the recall of learned irrelevance and abolished LI. These data suggest that normal PFC GABA transmission is critical for regulating and mitigating multiple aspects of aversive learning, including discrimination between fear vs safety signals and recall of information about the irrelevance of stimuli. Furthermore, they suggest that similar deficits in emotional regulation observed in schizophrenia may be driven in part by deficient PFC GABA activity.

BDNF (brain-derived neurotrophic factor) serum levels in schizophrenic patients with cognitive deficits

NASA Astrophysics Data System (ADS)

Utami, N.; Effendy, E.; Amin, M. M.

2018-03-01

Schizophrenia is a complex neurodevelopmental disorder with cognitive impairment as the main part. BDNF regulates aspects of developmental plasticity in the brain and is involved in cognitive function. Cognitive functions include capabilities such as attention, executive functioning, assessing, monitoring and evaluating. The aim of the study was to know the BDNF levels in schizophrenic patients with cognitive deficits. The study was held in October 2016 - March 2017, and was the first in Indonesia, especially in North Sumatra. The study was approved by the medical ethics committee of the University of North Sumatera. The study is descriptive based on a retrospective method with cross-sectional approach. The subject is 40 male schizophrenia. Cognitive deficits were assessed by MoCA-Ina. BDNF serum levels were analyzed using the quantitative sandwich enzyme immunoassay. The average MoCA-Ina score is 21.03±5.21. This suggests that there is a cognitive function deficit in schizophrenic patients. The mean serum BDNF level was 26629±6762. MoCA-Ina scores in schizophrenic patients <26 who experienced a deficit of 77.5% and serum BDNF levels with normal values ranging from 6.186 to 42.580pg/ml.

Mangiferin regulates cognitive deficits and heme oxygenase-1 induced by lipopolysaccharide in mice.

PubMed

Fu, Yanyan; Liu, Hongzhi; Song, Chengjie; Zhang, Fang; Liu, Yi; Wu, Jian; Wen, Xiangru; Liang, Chen; Ma, Kai; Li, Lei; Zhang, Xunbao; Shao, Xiaoping; Sun, Yafeng; Du, Yang; Song, Yuanjian

2015-12-01

Accumulating evidence reveals that lipopolysaccharide (LPS) can induce neuroinflammation, ultimately leading to cognitive deficits. Mangiferin, a natural glucoxilxanthone, is known to possess various biological activities. The present study aimed to investigate the effects of mangiferin on LPS-induced cognitive deficits and explore the underlying mechanisms. Brain injury was induced in mice via intraperitoneal LPS injection (1mg/kg) for five consecutive days. Mangiferin was orally pretreatmented (50mg/kg) for seven days and then treatmented (50mg/kg) for five days after LPS injection. The Morris water maze was used to detect changes in cognitive function. Immunohistochemical and immunoblotting were respectively performed to measure the expression of interleukin-6 (IL-6) and heme oxygenase-1 (HO-1) in the hippocampus. The results showed that mangiferin can ameliorate cognitive deficits. Moreover, mangiferin decreased LPS-induced IL-6 production and increase HO-1 in the hippocampus. Taken together, these results suggest that mangiferin attenuates LPS-induced cognitive deficits, which may be potentially linked to modulating HO-1 in the hippocampus. Copyright © 2015. Published by Elsevier B.V.

Effects of social isolation and re-socialization on cognition and ADAR1 (p110) expression in mice.

PubMed

Chen, Wei; An, Dong; Xu, Hong; Cheng, Xiaoxin; Wang, Shiwei; Yu, Weizhi; Yu, Deqin; Zhao, Dan; Sun, Yiping; Deng, Wuguo; Tang, Yiyuan; Yin, Shengming

2016-01-01

It has been reported that social isolation stress could be a key factor that leads to cognitive deficit for both humans and rodent models. However, detailed mechanisms are not yet clear. ADAR1 (Adenosine deaminase acting on RNA) is an enzyme involved in RNA editing that has a close relation to cognitive function. We have hypothesized that social isolation stress may impact the expression of ADAR1 in the brain of mice with cognitive deficit. To test our hypothesis, we evaluated the cognition ability of mice isolated for different durations (2, 4, and 8 weeks) using object recognition and object location tests; we also measured ADAR1 expression in hippocampus and cortex using immunohistochemistry and western blot. Our study showed that social isolation stress induced spatial and non-spatial cognition deficits of the tested mice. In addition, social isolation significantly increased both the immunoreactivity and protein expression of ADAR1 (p110) in the hippocampus and frontal cortex. Furthermore, re-socialization could not only recover the cognition deficits, but also bring ADAR1 (p110) immunoreactivity of hippocampus and frontal cortex, as well as ADAR1 (p110) protein expression of hippocampus back to the normal level for the isolated mice in adolescence. In conclusion, social isolation stress significantly increases ADAR1 (p110) expression in the hippocampus and frontal cortex of the mice with cognitive deficit. This finding may open a window to better understand the reasons (e.g., epigenetic change) that are responsible for social isolation-induced cognitive deficit and help the development of novel therapies for the resulted diseases.

Cognition, dopamine and bioactive lipids in schizophrenia

PubMed Central

Condray, Ruth; Yao, Jeffrey K.

2011-01-01

Schizophrenia is a remarkably complex disorder with a multitude of behavioral and biological perturbations. Cognitive deficits are a core feature of this disorder, and involve abnormalities across multiple domains, including memory, attention, and perception. The complexity of this debilitating illness has led to a view that the key to unraveling its pathophysiology lies in deconstructing the clinically-defined syndrome into pathophysiologically distinct intermediate phenotypes. Accumulating evidence suggests that one of these intermediate phenotypes may involve phospholipid signaling abnormalities, particularly in relation to arachidonic acid (AA). Our data show relationships between levels of AA and performance on tests of cognition for schizophrenia patients, with defects in AA signaling associated with deficits in cognition. Moreover, dopamine may moderate these relationships between AA and cognition. Taken together, cognitive deficits, dopaminergic neurotransmission, and bioactive lipids have emerged as related features of schizophrenia. Existing treatment options for cognitive deficits in schizophrenia do not specifically target lipid-derived signaling pathways; understanding these processes could inform efforts to identify novel targets for treatment innovation. PMID:21196378

The paradox of cognitive flexibility in autism

PubMed Central

Geurts, Hilde M.; Corbett, Blythe; Solomon, Marjorie

2017-01-01

We present an overview of current literature addressing cognitive flexibility in autism spectrum disorders. Based on recent studies at multiple sites, using diverse methods and participants of different autism subtypes, ages and cognitive levels, no consistent evidence for cognitive flexibility deficits was found. Researchers and clinicians assume that inflexible everyday behaviors in autism are directly related to cognitive flexibility deficits as assessed by clinical and experimental measures. However, there is a large gap between the day-to-day behavioral flexibility and that measured with these cognitive flexibility tasks. To advance the field, experimental measures must evolve to reflect mechanistic models of flexibility deficits. Moreover, ecologically valid measures are required to be able to resolve the paradox between cognitive and behavioral inflexibility. PMID:19138551

Cognitive control deficits associated with antisocial personality disorder and psychopathy.

PubMed

Zeier, Joshua D; Baskin-Sommers, Arielle R; Hiatt Racer, Kristina D; Newman, Joseph P

2012-07-01

Antisociality has been linked to a variety of executive functioning deficits, including poor cognitive control. Surprisingly, cognitive control deficits are rarely found in psychopathic individuals, despite their notoriously severe and persistent antisocial behavior. In fact, primary (low-anxious) psychopathic individuals display superior performance on cognitive control-type tasks under certain circumstances. To clarify these seemingly contradictory findings, we administered a response competition (i.e., flanker) task to incarcerated offenders, who were assessed for Antisocial Personality Disorder (APD) symptoms and psychopathy. As hypothesized, APD related to poorer accuracy, especially on incongruent trials. Contrary to expectation, however, the same pattern of results was found in psychopathy. Additional analyses indicated that these effects of APD and psychopathy were associated with overlapping variance. The findings suggest that psychopathy and APD symptoms are both associated with deficits in cognitive control, and that this deficit relates to general antisociality as opposed to a specific antisocial syndrome. PsycINFO Database Record (c) 2012 APA, all rights reserved.

[PASS neurocognitive dysfunction in attention deficit].

PubMed

Pérez-Alvarez, F; Timoneda-Gallart, C

Attention deficit disorder shows both cognitive and behavioral patterns. To determine a particular PASS (planning, attention, successive and simultaneous) pattern in order to early diagnosis and remediation according to PASS theory. 80 patients were selected from the neuropediatric attendance, aged 6 to 12 years old, 55 boys and 25 girls. Inclusion criteria were inattention (80 cases) and inattention with hyperactive symptoms (40 cases) according to the Diagnostic and Statistical Manual (DSM-IV). Exclusion criteria were the criteria of phonologic awareness previously reported, considered useful to diagnose dyslexia. A control group of 300 individuals, aged 5 to 12 years old, was used, criteria above mentioned being controlled. DN:CAS (Das-Naglieri Cognitive Assessment System) battery, translated to native language, was given to assess PASS cognitive processes. Results were analyzed with cluster analysis and t-Student test. Statistical factor analysis of the control group had previously identified the four PASS processes: planning, attention, successive and simultaneous. The dendrogram of the cluster analysis discriminated three categories of attention deficit disorder: 1. The most frequent, with planning deficit; 2. Without planning deficit but with deficit in other processes, and 3. Just only a few cases, without cognitive processing deficit. Cognitive deficiency in terms of means of scores was statistically significant when compared to control group (p = 0.001). According to PASS pattern, planning deficiency is a relevant factor. Neurological planning is not exactly the same than neurological executive function. The behavioral pattern is mainly linked to planning deficiency, but also to other PASS processing deficits and even to no processing deficit.

The association between cognitive deficits and prefrontal hemodynamic responses during performance of working memory task in patients with schizophrenia.

PubMed

Pu, Shenghong; Nakagome, Kazuyuki; Itakura, Masashi; Iwata, Masaaki; Nagata, Izumi; Kaneko, Koichi

2016-04-01

Schizophrenia-associated cognitive deficits are resistant to treatment and thus pose a lifelong burden. The Brief Assessment of Cognition in Schizophrenia (BACS) provides reliable and valid assessments across cognitive domains. However, because the prefrontal functional abnormalities specifically associated with the level of cognitive deficits in schizophrenia have not been examined, we explored this relationship. Patients with schizophrenia (N=87) and matched healthy controls (N=50) participated in the study. Using near-infrared spectroscopy (NIRS), we measured the hemodynamic responses in the prefrontal and superior temporal cortical surface areas during a working memory task. Correlation analyses revealed a relationship between the hemodynamics and the BACS composite and domain scores. Hemodynamic responses of the left dorsolateral prefrontal cortex (DLPFC) and left frontopolar cortex (FPC) in the higher-level-of-cognitive-function schizophrenia group were weaker than the responses of the controls but similar to those of the lower-level-of-cognitive-function schizophrenia group. However, hemodynamic responses in the right DLPFC, bilateral ventrolateral PFC (VLPFC), and right temporal regions decreased with increasing cognitive deficits. In addition, the hemodynamic response correlated positively with the level of cognitive function (BACS composite scores) in the right DLPFC, bilateral VLPFC, right FPC, and bilateral temporal regions in schizophrenia. The correlation was driven by all BACS domains. Our results suggest that the linked functional deficits in the right DLPFC, bilateral VLPFC, right FPC, and bilateral temporal regions may be related to BACS-measured cognitive impairments in schizophrenia and show that linking the neurocognitive deficits and brain abnormalities can increase our understanding of schizophrenia pathophysiology. Copyright © 2015 Elsevier B.V. All rights reserved.

Mutation of the 3-Phosphoinositide-Dependent Protein Kinase 1 (PDK1) Substrate-Docking Site in the Developing Brain Causes Microcephaly with Abnormal Brain Morphogenesis Independently of Akt, Leading to Impaired Cognition and Disruptive Behaviors

PubMed Central

Cordón-Barris, Lluís; Pascual-Guiral, Sònia; Yang, Shaobin; Giménez-Llort, Lydia; Lope-Piedrafita, Silvia; Niemeyer, Carlota; Claro, Enrique; Lizcano, Jose M.

2016-01-01

The phosphoinositide (PI) 3-kinase/Akt signaling pathway plays essential roles during neuronal development. 3-Phosphoinositide-dependent protein kinase 1 (PDK1) coordinates the PI 3-kinase signals by activating 23 kinases of the AGC family, including Akt. Phosphorylation of a conserved docking site in the substrate is a requisite for PDK1 to recognize, phosphorylate, and activate most of these kinases, with the exception of Akt. We exploited this differential mechanism of regulation by generating neuron-specific conditional knock-in mice expressing a mutant form of PDK1, L155E, in which the substrate-docking site binding motif, termed the PIF pocket, was disrupted. As a consequence, activation of all the PDK1 substrates tested except Akt was abolished. The mice exhibited microcephaly, altered cortical layering, and reduced circuitry, leading to cognitive deficits and exacerbated disruptive behavior combined with diminished motivation. The abnormal patterning of the adult brain arises from the reduced ability of the embryonic neurons to polarize and extend their axons, highlighting the essential roles that the PDK1 signaling beyond Akt plays in mediating the neuronal responses that regulate brain development. PMID:27644329

Neurocognitive Impairments in Deficit and Non-Deficit Schizophrenia and Their Relationships with Symptom Dimensions and Other Clinical Variables

PubMed Central

Zhang, XiangRong; Zhang, XiaoBin; Sha, WeiWei; Yao, ShuQiao; Shu, Ni; Zhang, XiangYang; Zhang, ZhiJun

2015-01-01

Background Deficit schizophrenia (DS) has been proposed as a pathophysiologically distinct subgroup within schizophrenia. Earlier studies focusing on neurocognitive function of DS patients have yielded inconsistent findings ranging from substantial deficits to no significant difference relative to non-deficit schizophrenia patients (NDS). The present study investigated the severity and characteristic patterns of neurocognitive impairments in DS and NDS patients and their relationships with clinical variables. Methods Attention, ideation fluency, cognitive flexibility and visuospatial memory function were assessed in 40 DS patients, 57 NDS patients, and 52 healthy controls by a comprehensive neuropsychological battery. Results Both schizophrenia subgroups had overall more severe cognitive impairments than controls while DS performed worse on every neuropsychological measure except the Stroop interference than the NDS patients with age and education as the covariates. Profile analysis found significantly different patterns of cognitive profiles between two patients group mainly due to their differences in attention and cognitive flexibility functions. Age, education, illness duration and negative symptoms were found to have the correlations with cognitive impairments in the NDS group, while only age and the negative symptoms were correlated with the cognitive impairments in the DS group. Multiple regression analyses revealed that sustained attention and cognitive flexibility were the core impaired cognitive domains mediating other cognitive functions in DS and NDS patients respectively. Conclusions DS patients exemplified worse in almost all cognitive domains than NDS patients. Sustained attention and cognitive flexibility might be the key impaired cognitive domains for DS and NDS patients respectively. The present study suggested the DS as a specific subgroup of schizophrenia. PMID:26381645

Neurocognitive Impairments in Deficit and Non-Deficit Schizophrenia and Their Relationships with Symptom Dimensions and Other Clinical Variables.

PubMed

Yu, Miao; Tang, XiaoWei; Wang, Xiang; Zhang, XiangRong; Zhang, XiaoBin; Sha, WeiWei; Yao, ShuQiao; Shu, Ni; Zhang, XiangYang; Zhang, ZhiJun

2015-01-01

Deficit schizophrenia (DS) has been proposed as a pathophysiologically distinct subgroup within schizophrenia. Earlier studies focusing on neurocognitive function of DS patients have yielded inconsistent findings ranging from substantial deficits to no significant difference relative to non-deficit schizophrenia patients (NDS). The present study investigated the severity and characteristic patterns of neurocognitive impairments in DS and NDS patients and their relationships with clinical variables. Attention, ideation fluency, cognitive flexibility and visuospatial memory function were assessed in 40 DS patients, 57 NDS patients, and 52 healthy controls by a comprehensive neuropsychological battery. Both schizophrenia subgroups had overall more severe cognitive impairments than controls while DS performed worse on every neuropsychological measure except the Stroop interference than the NDS patients with age and education as the covariates. Profile analysis found significantly different patterns of cognitive profiles between two patients group mainly due to their differences in attention and cognitive flexibility functions. Age, education, illness duration and negative symptoms were found to have the correlations with cognitive impairments in the NDS group, while only age and the negative symptoms were correlated with the cognitive impairments in the DS group. Multiple regression analyses revealed that sustained attention and cognitive flexibility were the core impaired cognitive domains mediating other cognitive functions in DS and NDS patients respectively. DS patients exemplified worse in almost all cognitive domains than NDS patients. Sustained attention and cognitive flexibility might be the key impaired cognitive domains for DS and NDS patients respectively. The present study suggested the DS as a specific subgroup of schizophrenia.

Comparison of the extent and pattern of cognitive impairment among predialysis, dialysis and transplant patients: A cross-sectional study from Australia.

PubMed

Lambert, Kelly; Mullan, Judy; Mansfield, Kylie; Lonergan, Maureen

2017-11-01

The aim of this study was to compare the extent of cogntive impairment and the types of cognitive deficits in an Australian cohort of four patient groups with end stage kidney disease. Characteristics predicting the presence of cognitive impairment were also evaluated. Observational cross-sectional study of 155 patients with end stage kidney disease are recruited from a regional Australian renal unit. Eligible participants included those whose estimated Glomerular Filtration Rate was < 30 ml/min per 1.73 m 2 , were undertaking peritoneal or haemodialysis, or had received a kidney transplant. The Montreal Cognitive Assessment tool was used to screen the study participants for cognitive impairment and evaluate cognitive deficits. Cognitive impairment was defined as a total Montreal Cognitive Assessment tool score ≤24/30. The extent of cognitive impairment varied between the four groups with end stage kidney disease. Factors predicting the presence of cognitive impairment included undertaking dialysis, age ≥65, male gender and the presence of diabetes or cerebrovascular disease. Deficits in executive function, attention, language, visuospatial skills, memory and orientation were common among the study participants, and the extent of these deficits varied between groups. Limitations to the study included the cross-sectional design, and that the presence of confounders like depression were not recorded. The impact of disparities in the cognitive capabilities identified in this study are likely to be far reaching. Tailoring of education and self-management programmes to the cognitive deficits of individuals is required. © 2016 Asian Pacific Society of Nephrology.

A multiple deficit model of reading disability and attention-deficit/hyperactivity disorder: searching for shared cognitive deficits.

PubMed

McGrath, Lauren M; Pennington, Bruce F; Shanahan, Michelle A; Santerre-Lemmon, Laura E; Barnard, Holly D; Willcutt, Erik G; Defries, John C; Olson, Richard K

2011-05-01

This study tests a multiple cognitive deficit model of reading disability (RD), attention-deficit/hyperactivity disorder (ADHD), and their comorbidity. A structural equation model (SEM) of multiple cognitive risk factors and symptom outcome variables was constructed. The model included phonological awareness as a unique predictor of RD and response inhibition as a unique predictor of ADHD. Processing speed, naming speed, and verbal working memory were modeled as potential shared cognitive deficits. Model fit indices from the SEM indicated satisfactory fit. Closer inspection of the path weights revealed that processing speed was the only cognitive variable with significant unique relationships to RD and ADHD dimensions, particularly inattention. Moreover, the significant correlation between reading and inattention was reduced to non-significance when processing speed was included in the model, suggesting that processing speed primarily accounted for the phenotypic correlation (or comorbidity) between reading and inattention. This study illustrates the power of a multiple deficit approach to complex developmental disorders and psychopathologies, particularly for exploring comorbidities. The theoretical role of processing speed in the developmental pathways of RD and ADHD and directions for future research are discussed. © 2010 The Authors. Journal of Child Psychology and Psychiatry © 2010 Association for Child and Adolescent Mental Health.

(-)-P7C3-S243 Protects a Rat Model of Alzheimer's Disease From Neuropsychiatric Deficits and Neurodegeneration Without Altering Amyloid Deposition or Reactive Glia.

PubMed

Voorhees, Jaymie R; Remy, Matthew T; Cintrón-Pérez, Coral J; El Rassi, Eli; Khan, Michael Z; Dutca, Laura M; Yin, Terry C; McDaniel, Latisha N; Williams, Noelle S; Brat, Daniel J; Pieper, Andrew A

2017-11-06

In addition to cognitive deficits, Alzheimer's disease (AD) is associated with other neuropsychiatric symptoms, including severe depression. Indeed, depression often precedes cognitive deficits in patients with AD. Unfortunately, the field has seen only minimal therapeutic advances, underscoring the critical need for new treatments. P7C3 aminopropyl carbazoles promote neuronal survival by enhancing nicotinamide adenine dinucleotide flux in injured neurons. Neuroprotection with P7C3 compounds has been demonstrated in preclinical models of neurodegeneration by virtue of promoting neuronal survival independently of early disease-specific pathology, resulting in protection from cognitive deficits and depressive-like behavior. We hypothesize that P7C3 compounds might be uniquely applicable to patients with AD, given the comorbid presentation of depression and cognitive deficits. Aging male and female wild-type and TgF344-AD rats, a well-characterized preclinical AD model, were administered (-)-P7C3-S243 daily for 9 and 18 months, beginning at 6 months of age. Behavioral phenotypes related to cognition and depression were assessed at 15 and 24 months, and brain pathology and biochemistry were assessed at 24 months. (-)-P7C3-S243 safely protected aging male and female wild-type and TgF344-AD rats from cognitive deficits and depressive-like behavior. Depressive-like behavior occurred earlier than cognitive deficits in TgF344-AD rats, consistent with AD in many patients. Treatment with (-)-P7C3-S243 blocked neurodegeneration in TgF344-AD rats, without altering amyloid deposition or indicators of neuroinflammation. Neuronal cell death-specific treatment approaches, such as P7C3 compounds, may represent a new treatment approach for patients experiencing the combination of cognitive deficits and depression associated with AD. Published by Elsevier Inc.

Effect of Treating Anxiety Disorders on Cognitive Deficits and Behaviors Associated with Attention Deficit Hyperactivity Disorder: A Preliminary Study.

PubMed

Denis, Isabelle; Guay, Marie-Claude; Foldes-Busque, Guillaume; BenAmor, Leila

2016-06-01

Twenty-five percent of children with ADHD also have an anxiety disorder (AD). As per Quay and in light of Barkley's model, anxiety may have a protective effect on cognitive deficits and behaviors associated with ADHD. This study aimed to evaluate the effect of treating AD on cognitive deficits and behaviors associated with ADHD in children with both disorders. Twenty-four children with ADHD and AD were divided into two groups: treatment for AD, and wait list. Participants were assessed at pre-treatment, post-treatment, and 6-month follow-up with the ADIS-C, the CBCL, and neuropsychological measures. The results revealed a significant improvement in automatic response inhibition and flexibility, and a decrease in inattention/hyperactivity behaviors following the treatment for AD. No significant differences were observed in motor response inhibition, working memory, or attention deficits. The results do not seem to support Quay's hypothesis: treating AD did not exacerbate cognitive deficits and behaviors associated with ADHD in our sample.

Self-awareness of cognitive functioning in schizophrenia: patients and their relatives.

PubMed

Poletti, Sara; Anselmetti, Simona; Riccaboni, Roberta; Bosia, Marta; Buonocore, Mariachiara; Smeraldi, Enrico; Cavallaro, Roberto

2012-07-30

Cognitive impairment has been recognized since the earliest descriptions of schizophrenia as a core feature of the illness and different programmes have been developed to remediate these deficits. In all likelihood it is important for compliance and adherence to treatment that not only the patients but also their relatives be aware of the patients; cognitive deficits. Sixty-two patients with a diagnosis of schizophrenia and, for each one of them, one family member and an informant from the medical staff, were recruited and administered the Schizophrenia Cognition Rating Scale (SCoRS) ratings. Patients were tested for cognitive deficits with a neuropsychological battery and their performance was compared to the ratings of cognitive functioning provided by the patient himself, his family member and the informant. Results show no significant association between cognitive performance and SCoRS ratings in patients; only for executive functions the patient's performance was found to be predictive of the respective judgment on the SCoRS that was given by the relative. This is the first study to investigate awareness of the patients' cognitive deficits, both in the patients themselves and in their first degree relatives, through a direct comparison between subjective clinical ratings and objective measures of cognitive performances. When both patients and relatives are unaware of the patients' cognitive deficits, this could affect adherence to remediation treatment and need to be specifically addressed in future rehabilitation strategies. Copyright © 2012 Elsevier Ltd. All rights reserved.

Memory deficits with intact cognitive control in the methylazoxymethanol acetate (MAM) exposure model of neurodevelopmental insult.

PubMed

O'Reilly, Kally C; Perica, Maria I; Fenton, André A

2016-10-01

Cognitive impairments are amongst the most debilitating deficits of schizophrenia and the best predictor of functional outcome. Schizophrenia is hypothesized to have a neurodevelopmental origin, making animal models of neurodevelopmental insult important for testing predictions that early insults will impair cognitive function. Rats exposed to methylazoxymethanol acetate (MAM) at gestational day 17 display morphological, physiological and behavioral abnormalities relevant to schizophrenia. Here we investigate the cognitive abilities of adult MAM rats. We examined brain activity in MAM rats by histochemically assessing cytochrome oxidase enzyme activity, a metabolic marker of neuronal activity. To assess cognition, we used a hippocampus-dependent two-frame active place avoidance paradigm to examine learning and spatial memory, as well as cognitive control and flexibility using the same environment and evaluating the same set of behaviors. We confirmed that adult MAM rats have altered hippocampal morphology and brain function, and that they are hyperactive in an open field. The latter likely indicates MAM rats have a sensorimotor gating deficit that is common to many animal models used for schizophrenia research. On first inspection, cognitive control seems impaired in MAM rats, indicated by more errors during the two-frame active place avoidance task. Because MAM rats are hyperactive throughout place avoidance training, we considered the possibility that the hyperlocomotion may account for the apparent cognitive deficits. These deficits were reduced on the basis of measures of cognitive performance that account for motor activity differences. However, though other aspects of memory are intact, the ability of MAM rats to express trial-to-trial memory is delayed compared to control rats. These findings suggest that spatial learning and cognitive abilities are largely intact, that the most prominent cognitive deficit is specific to acquiring memory in the MAM neurodevelopmental model, and that hyperactivity can confound assessments of cognition in animal models of mental dysfunction. Copyright © 2016 Elsevier Inc. All rights reserved.

Multimodal Intervention Trial for Cognitive Deficits in Neurofibromatosis Type 1: Efficacy of Computerized Cognitive Training and Stimulant Medication

DTIC Science & Technology

2017-10-01

AWARD NUMBER: W81XWH-15-1-0508 TITLE: Multimodal Intervention Trial for Cognitive Deficits in Neurofibromatosis Type 1: Efficacy of...Computerized Cognitive Training and Stimulant Medication PRINCIPAL INVESTIGATOR: Maria T. Acosta, M.D. CONTRACTING ORGANIZATION: Children’s National Health...database. 15. SUBJECT TERMS Neurofibromatosis, cognition , pediatric, computerized training programs, working memory 16. SECURITY CLASSIFICATION OF: 17

Mice heterozygous for an inactivated allele of the schizophrenia associated Brd1 gene display selective cognitive deficits with translational relevance to schizophrenia.

PubMed

Qvist, Per; Rajkumar, Anto P; Redrobe, John P; Nyegaard, Mette; Christensen, Jane H; Mors, Ole; Wegener, Gregers; Didriksen, Michael; Børglum, Anders D

2017-05-01

Schizophrenia is a debilitating brain disorder characterized by disturbances of emotion, perception and cognition. Cognitive impairments predict functional outcome in schizophrenia and are detectable even in the prodromal stage of the disorder. However, our understanding of the underlying neurobiology is limited and procognitive treatments remain elusive. We recently demonstrated that mice heterozygous for an inactivated allele of the schizophrenia-associated Brd1 gene (Brd1 +/ - mice) display behaviors reminiscent of schizophrenia, including impaired social cognition and long-term memory. Here, we further characterize performance of these mice by following the preclinical guidelines recommended by the 'Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS)' and 'Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS)' initiatives to maximize translational value. Brd1 +/- mice exhibit relational encoding deficits, compromised working and long term memory, as well as impaired executive cognitive functioning with cognitive behaviors relying on medial prefrontal cortex being particularly affected. Akin to patients with schizophrenia, the cognitive deficits displayed by Brd1 +/ - mice are not global, but selective. Our results underline the value of Brd1 +/ - mice as a promising tool for studying the neurobiology of cognitive deficits in schizophrenia. Copyright © 2017 Elsevier Inc. All rights reserved.

Speech Deficits in Serious mental Illness: A Cognitive Resource Issue?

PubMed Central

Cohen, Alex S.; McGovern, Jessica E.; Dinzeo, Thomas J.; Covington, Michael A.

2014-01-01

Speech deficits, notably those involved in psychomotor retardation, blunted affect, alogia and poverty of content of speech, are pronounced in a wide range of serious mental illnesses (e.g., schizophrenia, unipolar depression, bipolar disorders). The present project evaluated the degree to which these deficits manifest as a function of cognitive resource limitations. We examined natural speech from 52 patients meeting criteria for serious mental illnesses (i.e., severe functional deficits with a concomitant diagnosis of schizophrenia, unipolar and/or bipolar affective disorders) and 30 non-psychiatric controls using a range of objective, computer-based measures tapping speech production (“alogia”), variability (“blunted vocal affect”) and content (“poverty of content of speech”). Subjects produced natural speech during a baseline condition and while engaging in an experimentally-manipulated cognitively-effortful task. For correlational analysis, cognitive ability was measured using a standardized battery. Generally speaking, speech deficits did not differ as a function of SMI diagnosis. However, every speech production and content measure was significantly abnormal in SMI versus control groups. Speech variability measures generally did not differ between groups. For both patients and controls as a group, speech during the cognitively-effortful task was sparser and less rich in content. Relative to controls, patients were abnormal under cognitive load with respect only to average pause length. Correlations between the speech variables and cognitive ability were only significant for this same variable: average pause length. Results suggest that certain speech deficits, notably involving pause length, may manifest as a function of cognitive resource limitations. Implications for treatment, research and assessment are discussed. PMID:25464920

Speech deficits in serious mental illness: a cognitive resource issue?

PubMed

Cohen, Alex S; McGovern, Jessica E; Dinzeo, Thomas J; Covington, Michael A

2014-12-01

Speech deficits, notably those involved in psychomotor retardation, blunted affect, alogia and poverty of content of speech, are pronounced in a wide range of serious mental illnesses (e.g., schizophrenia, unipolar depression, bipolar disorders). The present project evaluated the degree to which these deficits manifest as a function of cognitive resource limitations. We examined natural speech from 52 patients meeting criteria for serious mental illnesses (i.e., severe functional deficits with a concomitant diagnosis of schizophrenia, unipolar and/or bipolar affective disorders) and 30 non-psychiatric controls using a range of objective, computer-based measures tapping speech production ("alogia"), variability ("blunted vocal affect") and content ("poverty of content of speech"). Subjects produced natural speech during a baseline condition and while engaging in an experimentally-manipulated cognitively-effortful task. For correlational analysis, cognitive ability was measured using a standardized battery. Generally speaking, speech deficits did not differ as a function of SMI diagnosis. However, every speech production and content measure was significantly abnormal in SMI versus control groups. Speech variability measures generally did not differ between groups. For both patients and controls as a group, speech during the cognitively-effortful task was sparser and less rich in content. Relative to controls, patients were abnormal under cognitive load with respect only to average pause length. Correlations between the speech variables and cognitive ability were only significant for this same variable: average pause length. Results suggest that certain speech deficits, notably involving pause length, may manifest as a function of cognitive resource limitations. Implications for treatment, research and assessment are discussed. Copyright © 2014 Elsevier B.V. All rights reserved.

Late-Life Depressive Symptoms and Lifetime History of Major Depression: Cognitive Deficits are Largely Due to Incipient Dementia rather than Depression.

PubMed

Heser, Kathrin; Bleckwenn, Markus; Wiese, Birgitt; Mamone, Silke; Riedel-Heller, Steffi G; Stein, Janine; Lühmann, Dagmar; Posselt, Tina; Fuchs, Angela; Pentzek, Michael; Weyerer, Siegfried; Werle, Jochen; Weeg, Dagmar; Bickel, Horst; Brettschneider, Christian; König, Hans-Helmut; Maier, Wolfgang; Scherer, Martin; Wagner, Michael

2016-08-01

Late-life depression is frequently accompanied by cognitive impairments. Whether these impairments indicate a prodromal state of dementia, or are a symptomatic expression of depression per se is not well-studied. In a cohort of very old initially non-demented primary care patients (n = 2,709, mean age = 81.1 y), cognitive performance was compared between groups of participants with or without elevated depressive symptoms and with or without subsequent dementia using ANCOVA (adjusted for age, sex, and education). Logistic regression analyses were computed to predict subsequent dementia over up to six years of follow-up. The same analytical approach was performed for lifetime major depression. Participants with elevated depressive symptoms without subsequent dementia showed only small to medium cognitive deficits. In contrast, participants with depressive symptoms with subsequent dementia showed medium to very large cognitive deficits. In adjusted logistic regression models, learning and memory deficits predicted the risk for subsequent dementia in participants with depressive symptoms. Participants with a lifetime history of major depression without subsequent dementia showed no cognitive deficits. However, in adjusted logistic regression models, learning and orientation deficits predicted the risk for subsequent dementia also in participants with lifetime major depression. Marked cognitive impairments in old age depression should not be dismissed as "depressive pseudodementia", but require clinical attention as a possible sign of incipient dementia. Non-depressed elderly with a lifetime history of major depression, who remained free of dementia during follow-up, had largely normal cognitive performance.

Color discrimination deficits in Parkinson's disease are related to cognitive impairment and white-matter alterations.

PubMed

Bertrand, Josie-Anne; Bedetti, Christophe; Postuma, Ronald B; Monchi, Oury; Génier Marchand, Daphné; Jubault, Thomas; Gagnon, Jean-François

2012-12-01

Color discrimination deficit is a common nonmotor manifestation of Parkinson's disease (PD). However, the pathophysiology of this dysfunction remains poorly understood. Although retinal structure changes found in PD have been suggested to cause color discrimination deficits, the impact of cognitive impairment and cortical alterations remains to be determined. We investigated the contribution of cognitive impairment to color discrimination deficits in PD and correlated them with cortical anomalies. Sixty-six PD patients without dementia and 20 healthy controls performed the Farnsworth-Munsell 100 hue test and underwent a comprehensive neuropsychological assessment for mild cognitive impairment diagnosis. In a subgroup of 26 PD patients, we also used high-definition neuroanatomical magnetic resonance imaging for cortical thickness and diffusion tensor analysis. PD patients with mild cognitive impairment performed poorly on the Farnsworth-Munsell 100 hue test compared with PD patients without mild cognitive impairment and controls. In PD patients, performance on the Farnsworth-Munsell 100 hue test was correlated with measures of visuospatial abilities and executive functions. Neuroimaging analysis revealed higher mean and radial diffusivity values in right posterior white-matter structures that correlated with poor performance on the Farnsworth-Munsell 100 hue test. No cortical thickness correlation reached significance. This study showed that cognitive impairment makes a major contribution to the color discrimination deficits reported in PD. Thus, performance on the Farnsworth-Munsell 100 hue test may reflect cognitive impairment more than color discrimination deficits in PD. Poor performance on the Farnsworth-Munsell 100 hue test was also associated with white-matter alterations in right posterior brain regions. Copyright © 2012 Movement Disorder Society.

Motivated to do well: an examination of the relationships between motivation, effort, and cognitive performance in schizophrenia.

PubMed

Foussias, G; Siddiqui, I; Fervaha, G; Mann, S; McDonald, K; Agid, O; Zakzanis, K K; Remington, G

2015-08-01

The uncertain relationship between negative symptoms, and specifically motivational deficits, with cognitive dysfunction in schizophrenia is in need of further elucidation as it pertains to the interpretation of cognitive test results. Findings to date have suggested a possible mediating role of motivational deficits on cognitive test measures, although findings from formal examinations of effort using performance validity measures have been inconsistent. The aim of this study was to examine the relationships between motivation, effort exerted during cognitive testing, and cognitive performance in schizophrenia. Sixty-nine outpatients with schizophrenia or schizoaffective disorder were evaluated for psychopathology, severity of motivational deficits, effort exerted during cognitive testing, and cognitive performance. Motivation and degree of effort exerted during cognitive testing were significantly related to cognitive performance, specifically verbal fluency, verbal and working memory, attention and processing speed, and reasoning and problem solving. Further, effort accounted for 15% of the variance in cognitive performance, and partially mediated the relationship between motivation and cognitive performance. Examining cognitive performance profiles for individuals exerting normal or reduced effort revealed significant differences in global cognition, as well as attention/processing speed and reasoning and problem solving. These findings suggest that cognitive domains may be differentially affected by impairments in motivation and effort, and highlight the importance of understanding the interplay between motivation and cognitive performance deficits, which may guide the appropriate selection of symptom targets for promoting recovery in patients. Copyright © 2015 Elsevier B.V. All rights reserved.

Effect of Neuroscience-Based Cognitive Skill Training on Growth of Cognitive Deficits Associated with Learning Disabilities in Children Grades 2-4

ERIC Educational Resources Information Center

Avtzon, Sarah Abitbol

2012-01-01

Working memory, executive functions, and cognitive processes associated with specific academic areas, are empirically identified as being the core underlying cognitive deficits in students with specific learning disabilities. Using Hebb's theory of neuroplasticity and the principle of automaticity as theoretical bases, this experimental study…

Heading in Soccer: Integral Skill or Grounds for Cognitive Dysfunction?

ERIC Educational Resources Information Center

Kirkendall, Donald T.; Garrett, William E., Jr.

2001-01-01

Discusses how purposeful heading of soccer balls and head injuries affect soccer players' cognitive dysfunction. Cognitive deficits may occur for many reasons. Heading cannot be blamed when details of the actual event and impact are unknown. Concussions are the most common head injury in soccer and a factor in cognitive deficits and are probably…

The Outcome of a Social Cognitive Training for Mainstream Adolescents with Social Communication Deficits in a Chinese Community

ERIC Educational Resources Information Center

Lee, Kathy Y. S.; Crooke, Pamela J.; Lui, Aster L. Y.; Kan, Peggy P. K.; Mark, Yuen-mai; van Hasselt, Charles Andrew; Tong, Michael C. F.

2016-01-01

The use of cognitive-based strategies for improving social communication behaviours for individuals who have solid language and cognition is an important question. This study investigated the outcome of teaching Social Thinking®, a framework based in social-cognition, to Chinese adolescents with social communication deficits. Thirty-nine students…

Transient decrements in mood during energy deficit are independent of dietary protein-to-carbohydrate ratio

USDA-ARS?s Scientific Manuscript database

Energy deficit and dietary macronutrient intake are thought to independently modulate cognition, mood and sleep. To what extent manipulating the dietary ratio of protein-to-carbohydrate affects mood, cognition and sleep during short-term energy deficit is undetermined. Using a randomized, block desi...

[Facial emotion recognition, theory of mind and empathy in multiple sclerosis].

PubMed

Ayache, Samar S; Chalah, Moussa A; Kuempfel, Tania; Padberg, Frank; Lefaucheur, Jean-Pascal; Palm, Ulrich

2017-11-01

Multiple sclerosis (MS), a chronic progressive inflammatory disease of the central nervous system, causes frequent disability, mood disorders, fatigue, and cognitive dysfunction. As a part of the last, social cognition is frequently disturbed in MS patients. It comprises empathy and social perception of emotions from facial, bodily and vocal cues. Social cognitive deficits worsen affect decoding, interpersonal relationship, and quality of life. Despite the impact of these deficits on global functioning, only a small number of studies have investigated its correlations and overlaps with MS symptoms. This review focuses on the definition and anatomy of social cognition and draws attention to findings of neuropsychological and neuroimaging studies on social cognitive performance in MS.Results of the available studies show that social cognitive deficits are already measurable in early stages of MS. Over time course of the disease, neuropsychological and neuroimaging studies show an increase of disease burden and social and non-social cognitive impairment following the hypothesis of a disconnection syndrome resulting from gray and white matters lesions. These structural changes might exceed a threshold of compensatory restorative and neuroplasticity mechanisms and finally lead to deficits in social cognition. Considering this burden in social functioning, a further assessment of sociocognitive deficits in MS is urgently needed to provide specific therapeutic approaches and to improve quality of life. Georg Thieme Verlag KG Stuttgart · New York.

Clinical correlates of working memory deficits in youth with and without ADHD: A controlled study.

PubMed

Fried, Ronna; Chan, James; Feinberg, Leah; Pope, Amanda; Woodworth, K Yvonne; Faraone, Stephen V; Biederman, Joseph

2016-01-01

Both working memory (WM; a brain system that provides temporary storage and manipulation of the information) and attention-deficit/hyperactivity disorder (ADHD) have been associated with educational deficits. Since WM deficits are prevalent in children with ADHD, the main aim of the present study was to examine whether educational deficits are driven by working memory deficits or driven by the effect of ADHD itself. Participants were referred youth with (N = 276) and without (N = 241) ADHD ascertained from pediatric and psychiatric sources. Assessment included measures of psychiatric, psychosocial, educational, and cognitive functioning. Education deficits were defined as grade retention or placement in special classes and were assessed using interviews and written rating scales. Working memory was assessed using the Wechsler Intelligence Scale for Children-Revised (WISC-R) Freedom from Distractibility (FFD) factor based on Digit Span, Arithmetic, and Coding. Significantly more youth with ADHD had WM deficits than controls (31.9% vs. 13.7%, p < .05). In ADHD children, WM deficits were significantly (p < .01) associated with an increased risk for grade retention and placement in special classes as well as lower scores on reading and math achievement tests than for ADHD children without WM deficits. In contrast, no other differences were noted in other areas of functioning. Although WM deficits also had some adverse impact on educational and cognitive correlates in non-ADHD controls, these differences failed to attain statistical significance. WM deficits significantly and selectively increase the risk for academic deficits and cognitive dysfunction in children with ADHD beyond those conferred by ADHD. Screening for WM deficits may help identify children with ADHD at high risk for academic and cognitive dysfunction.

Clinical Correlates of Working Memory Deficits in Youth With and Without ADHD: A Controlled Study

PubMed Central

Fried, Ronna; Chan, James; Feinberg, Leah; Pope, Amanda; Woodworth, K. Yvonne; Faraone, Stephen V.; Biederman, Joseph

2016-01-01

Objective Both working memory (WM) (a brain system that provides temporary storage and manipulation of the information) and attention-deficit/hyperactivity disorder (ADHD) have been associated with educational deficits. Since WM deficits are prevalent in children with ADHD, the main aim of the present study was to examine whether educational deficits are driven by working memory deficits or driven by the effect of ADHD itself. Method Participants were referred youth with (N=276) and without (N=241) ADHD ascertained from pediatric and psychiatric sources. Assessment included measures of psychiatric, psychosocial, educational, and cognitive functioning. Education deficits were defined as grade retention or placement in special classes, and were assessed using interviews and written rating scales. Working memory was assessed using the WISC-R Freedom from Distractibility (FFD) factor based on digit span, arithmetic and coding. Results Significantly more youth with ADHD had WM deficits than controls (31.9% vs. 13.7%, p< 0.05). In ADHD children, WM deficits were significantly (p<0.01) associated with an increased risk for grade retention and placement in special classes as well as lower scores on reading and math achievement tests, relative to ADHD children without WM deficits. In contrast, no other differences were noted in other areas of functioning. Although WM deficits also had some adverse impact on educational and cognitive correlates in non ADHD controls, these differences failed to attain statistical significance. Conclusion WM deficits significantly and selectively increase the risk for academic deficits and cognitive dysfunction in children with ADHD beyond those conferred by ADHD. Screening for WM deficits may help identify children with ADHD at high risk for academic and cognitive dysfunction. PMID:26902180

Impact of Education on Memory Deficits in Subclinical Depression

PubMed Central

McLaren, Molly E.; Szymkowicz, Sarah M.; Kirton, Joshua W.; Dotson, Vonetta M.

2015-01-01

Elevated depressive symptoms are associated with cognitive deficits, while higher education protects against cognitive decline. This study was conducted to test if education level moderates the relationship between depressive symptoms and cognitive function. Seventy-three healthy, dementia-free adults aged 18–81 completed neuropsychological tests, as well as depression and anxiety questionnaires. Controlling for age, sex, and state anxiety, we found a significant interaction of depressive symptoms and education for immediate and delayed verbal memory, such that those with a higher education level performed well regardless of depressive symptomatology, whereas those with lower education and high depressive symptoms had worse performance. No effects were found for executive functioning or processing speed. Results suggest that education protects against verbal memory deficits in individuals with elevated depressive symptoms. Further research on cognitive reserve in depression-related cognitive deficits and decline is needed to understand the mechanisms behind this phenomenon. PMID:26109434

GABA neuron alterations, cortical circuit dysfunction and cognitive deficits in schizophrenia.

PubMed

Gonzalez-Burgos, Guillermo; Fish, Kenneth N; Lewis, David A

2011-01-01

Schizophrenia is a brain disorder associated with cognitive deficits that severely affect the patients' capacity for daily functioning. Whereas our understanding of its pathophysiology is limited, postmortem studies suggest that schizophrenia is associated with deficits of GABA-mediated synaptic transmission. A major role of GABA-mediated transmission may be producing synchronized network oscillations which are currently hypothesized to be essential for normal cognitive function. Therefore, cognitive deficits in schizophrenia may result from a GABA synapse dysfunction that disturbs neural synchrony. Here, we highlight recent studies further suggesting alterations of GABA transmission and network oscillations in schizophrenia. We also review current models for the mechanisms of GABA-mediated synchronization of neural activity, focusing on parvalbumin-positive GABA neurons, which are altered in schizophrenia and whose function has been strongly linked to the production of neural synchrony. Alterations of GABA signaling that impair gamma oscillations and, as a result, cognitive function suggest paths for novel therapeutic interventions.

Deficit of entropy modulation of the EEG in schizophrenia associated to cognitive performance and symptoms. A replication study.

PubMed

Molina, Vicente; Bachiller, Alejandro; Gomez-Pilar, Javier; Lubeiro, Alba; Hornero, Roberto; Cea-Cañas, Benjamín; Valcárcel, César; Haidar, Mahmoun-Karim; Poza, Jesús

2018-05-01

Spectral entropy (SE) is a measurement from information theory field that provides an estimation of EEG regularity and may be useful as a summary of its spectral properties. Previous studies using small samples reported a deficit of EEG entropy modulation in schizophrenia during cognitive activity. The present study is aimed at replicating this finding in a larger sample, to explore its cognitive and clinical correlates and to discard antipsychotic treatment as the main source of that deficit. We included 64 schizophrenia patients (21 first episodes, FE) and 65 healthy controls. We computed SE during performance of an odd-ball paradigm, at the windows prior (-300 to 0ms) and following (150 to 450ms) stimulus presentation. Modulation of SE was defined as the difference between post- and pre-stimulus windows. In comparison to controls, patients showed a deficit of SE modulation over frontal and central regions, also shown by FE patients. Baseline SE did not differ between patients and controls. Modulation deficit was directly associated with cognitive deficits and negative symptoms, and inversely with positive symptoms. SE modulation was not related to antipsychotic doses. Patients also showed a smaller change of median frequency (i.e., smaller slowing of oscillatory activity) of the EEG from pre- to post-stimulus windows. These results support that a deficit of fast modulation contributes to cognitive deficits and symptoms in schizophrenia patients. Copyright © 2017 Elsevier B.V. All rights reserved.

Primate Phencyclidine Model of Schizophrenia: Sex-Specific Effects on Cognition, Brain Derived Neurotrophic Factor, Spine Synapses, and Dopamine Turnover in Prefrontal Cortex

PubMed Central

Groman, Stephanie M.; Jentsch, James D.; Leranth, Csaba; Redmond, D. Eugene; Kim, Jung D.; Diano, Sabrina; Roth, Robert H.

2015-01-01

Background: Cognitive deficits are a core symptom of schizophrenia, yet they remain particularly resistant to treatment. The model provided by repeatedly exposing adult nonhuman primates to phencyclidine has generated important insights into the neurobiology of these deficits, but it remains possible that administration of this psychotomimetic agent during the pre-adult period, when the dorsolateral prefrontal cortex in human and nonhuman primates is still undergoing significant maturation, may provide a greater understanding of schizophrenia-related cognitive deficits. Methods: The effects of repeated phencyclidine treatment on spine synapse number, dopamine turnover and BDNF expression in dorsolateral prefrontal cortex, and working memory accuracy were examined in pre-adult monkeys. Results: One week following phencyclidine treatment, juvenile and adolescent male monkeys demonstrated a greater loss of spine synapses in dorsolateral prefrontal cortex than adult male monkeys. Further studies indicated that in juvenile males, a cognitive deficit existed at 4 weeks following phencyclidine treatment, and this impairment was associated with decreased dopamine turnover, decreased brain derived neurotrophic factor messenger RNA, and a loss of dendritic spine synapses in dorsolateral prefrontal cortex. In contrast, female juvenile monkeys displayed no cognitive deficit at 4 weeks after phencyclidine treatment and no alteration in dopamine turnover or brain derived neurotrophic factor messenger RNA or spine synapse number in dorsolateral prefrontal cortex. In the combined group of male and female juvenile monkeys, significant linear correlations were detected between dopamine turnover, spine synapse number, and cognitive performance. Conclusions: As the incidence of schizophrenia is greater in males than females, these findings support the validity of the juvenile primate phencyclidine model and highlight its potential usefulness in understanding the deficits in dorsolateral prefrontal cortex in schizophrenia and developing novel treatments for the cognitive deficits associated with schizophrenia. PMID:25522392

[Cognitive deficits in first episode psychosis patients and people at risk for psychosis: from diagnosis to treatment].

PubMed

Lecardeur, L; Meunier-Cussac, S; Dollfus, S

2013-05-01

Up to now, studies have not demonstrated significant efficacy of antipsychotics on cognitive impairments in patients with psychotic disorders. These cognitive deficits are of particular interest since they traditionally start early before the diagnosis of psychosis. They are observed during premorbid and prodromal stages, and during the first episode of psychosis. Moreover, cognitive impairments may be detected without any psychotic symptoms (such as positive symptoms) suggesting their development independently of the psychotic symptoms. Cognitive disturbances consist of impairments of episodic and working memories, intellectual functioning, executive functions (planning, inhibition, and cognitive flexibility), selective and sustained attentions and social cognition (emotion, recognition, theory of mind). The altered cognitive functions observed in schizophrenia are the same as in earlier stages but at a lower level of severity. Data suggest that cognitive deficits can be considered as vulnerability markers of psychosis since they have been described in healthy relatives of psychotic patients with high genetic risk. Cognitive deficits might also be considered as predictive of the occurrence of the disease after the first episode of psychosis. Indeed, retrospective studies suggest cognitive impairments in patients with schizophrenia during premorbid and prodromal phases but not in bipolar patients. Cognitive assessment might be of particular interest in people at risk for psychosis, in order to differentiate diagnostic outcomes. Cognitive functioning impairs until the diagnosis of first episode psychosis, even though cognitive profiles are quite heterogeneous in these patients. Once the diagnosis of schizophrenia is considered, cognitive deficits may be stable, although the literature is still controversial. Several factors such as symptoms and gender can contribute in diversifying the cognitive profiles. Moreover, age of onset might worsen the prognosis because of a disruption of the cognitive development and the disturbance of scholarship in young individuals. Considering these results, the treatment of cognitive deficits should be initiated as soon as possible, e.g. in people at risk for psychosis in order to reinforce the normal cognitive development, prevent cognitive decline and to preserve the educational, professional and social status. Since antipsychotic medications do not impact on cognitive functioning, alternative therapeutics should be developed such as cognitive remediation. Several studies and meta-analyses have shown that cognitive remediation programs are particularly efficient in patients with schizophrenia or bipolar disorders. Contrary to antipsychotics, these techniques should be used in patients with a first psychotic episode, but also in individuals with subpsychotic symptoms, subthreshold to the diagnosis of schizophrenia. Copyright © 2013. Published by Elsevier Masson SAS.

Diagnosing Contributions of Sensory and Cognitive Deficits to Hearing Dysfunction in Blast Exposed/TBI Service Members

DTIC Science & Technology

2016-10-01

1 AWARD NUMBER: W81XWH-15-1-0490 TITLE: Diagnosing Contributions of Sensory and Cognitive Deficits to Hearing Dysfunction in Blast-Exposed/ TBI...3. DATES COVERED 15 Sep 2015 - 14 Sep 2016 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER Diagnosing Contributions of Sensory and Cognitive Deficits to...installed at WRNMMC, and is running finalized versions of both the auditory and visual selective attention tasks. Subject recruitment has started, and

Impaired math achievement in patients with acute vestibular neuritis.

PubMed

Moser, Ivan; Vibert, Dominique; Caversaccio, Marco D; Mast, Fred W

2017-12-01

Broad cognitive difficulties have been reported in patients with peripheral vestibular deficit, especially in the domain of spatial cognition. Processing and manipulating numbers relies on the ability to use the inherent spatial features of numbers. It is thus conceivable that patients with acute peripheral vestibular deficit show impaired numerical cognition. Using the number Stroop task and a short math achievement test, we tested 20 patients with acute vestibular neuritis and 20 healthy, age-matched controls. On the one hand, patients showed normal congruency and distance effects in the number Stroop task, which is indicative of normal number magnitude processing. On the other hand, patients scored lower than healthy controls in the math achievement test. We provide evidence that the lower performance cannot be explained by either differences in prior math knowledge (i.e., education) or slower processing speed. Our results suggest that peripheral vestibular deficit negatively affects numerical cognition in terms of the efficient manipulation of numbers. We discuss the role of executive functions in math performance and argue that previously reported executive deficits in patients with peripheral vestibular deficit provide a plausible explanation for the lower math achievement scores. In light of the handicapping effects of impaired numerical cognition in daily living, it is crucial to further investigate the mechanisms that cause mathematical deficits in acute PVD and eventually develop adequate means for cognitive interventions. Copyright © 2017 Elsevier Ltd. All rights reserved.

Battery for ECT Related Cognitive Deficits (B4ECT-ReCoDe): development and validation.

PubMed

Viswanath, Biju; Harihara, Shashidhara N; Nahar, Abhinav; Phutane, Vivek Haridas; Taksal, Aarati; Thirthalli, Jagadisha; Gangadhar, Bangalore N

2013-06-01

The use of electroconvulsive therapy (ECT) in treatment of psychiatric disorders is associated with adverse cognitive effects. There is a need to develop a short assessment tool of cognitive functions during the course of ECT. This study aimed at developing and validating a short, sensitive battery to assess cognitive deficits associated with ECT in India. Battery for ECT Related Cognitive Deficits (B4ECT-ReCoDe), a brief cognitive battery (20-30 min) to assess verbal, visual, working and autobiographic memory, sustained attention, psychomotor speed and subjective memory impairment, was administered to 30 in-patients receiving bilateral ECT, one day after the 1st, 3rd and 6th ECT. Data was analysed using repeated measures analysis of variance and Pearson's correlation. Significant deficits were found in verbal, visual and autobiographic memory, psychomotor speed. Subjective experience of memory loss correlated positively with verbal memory impairment. B4ECT-ReCoDe, a brief, sensitive measure of cognitive impairments associated with ECT can be used in routine clinical practice. Copyright © 2013 Elsevier B.V. All rights reserved.

[Epigenetic research of cognitive deficit in schizophrenia: some methodological considerations].

PubMed

Lezheiko, T V; Alfimova, M V

To highlights the problems of assessing cognitive deficits in schizophrenia, relevant to the epigenetic, as well as a wide range of other approaches to the search for biological bases of cognition. The literature on the weaknesses in the evaluation of cognitive functions in patients with schizophrenia are summarized and discussed. The analysis is illustrated by our experience in developing a cognitive battery and a sample to examine relationships between DNA methylation in blood cells and cognitive deficits in schizophrenia. It has been shown that to assess cognitive deficits in patients and to reduce the influence of confounders in epigenetic analysis it is necessary (1) to use a battery with the existing co-normative data in the target population, which allows to evaluate representativeness of control and patients included in the study sample, (2) to verify the theoretically driven battery structure using normative population and a cohort of patients, (3) to balance groups of cases and controls on the number, age and sex, for which an individual matching of cases and controls is best suited, (4) to conduct an additional statistical analysis controlling for education and smoking.

Cognitive Dysfunction, Affective States, and Vulnerability to Nicotine Addiction: A Multifactorial Perspective

PubMed Central

Besson, Morgane; Forget, Benoît

2016-01-01

Although smoking prevalence has declined in recent years, certain subpopulations continue to smoke at disproportionately high rates and show resistance to cessation treatments. Individuals showing cognitive and affective impairments, including emotional distress and deficits in attention, memory, and inhibitory control, particularly in the context of psychiatric conditions, such as attention-deficit hyperactivity disorder, schizophrenia, and mood disorders, are at higher risk for tobacco addiction. Nicotine has been shown to improve cognitive and emotional processing in some conditions, including during tobacco abstinence. Self-medication of cognitive deficits or negative affect has been proposed to underlie high rates of tobacco smoking among people with psychiatric disorders. However, pre-existing cognitive and mood disorders may also influence the development and maintenance of nicotine dependence, by biasing nicotine-induced alterations in information processing and associative learning, decision-making, and inhibitory control. Here, we discuss the potential forms of contribution of cognitive and affective deficits to nicotine addiction-related processes, by reviewing major clinical and preclinical studies investigating either the procognitive and therapeutic action of nicotine or the putative primary role of cognitive and emotional impairments in addiction-like features. PMID:27708591

The effects of cognitive rehabilitation on social knowledge in patients with schizophrenia.

PubMed

Matsui, Mié; Arai, Hirofumi; Yonezawa, Mineo; Sumiyoshi, Tomiki; Suzuki, Michio; Kurachi, Masayoshi

2009-07-01

This study examined the extent to which cognitive rehabilitation alleviates cognitive deficits in schizophrenia compared to treatment as usual, and explored the mediating and moderating effects on cognitive improvement. Two groups who received cognitive rehabilitation and treatment as usual were assessed at baseline, three months (immediately post-intervention) and at follow-up (three months post-intervention). Cognitive rehabilitation focused on deficits in social knowledge and was conducted once a week for three months. The principles of errorless leaning and scaffolding informed the intervention. Outcomes were assessed using Script Test measures of social cognition. Other cognitive functions (executive functions and memory) and clinical symptoms were also assessed. Script Test for social knowledge and Rule Shift Test for cognitive flexibility scores were significantly better post-intervention in the cognitive rehabilitation group, while in the control group only free recall Script Test scores improved. Cognitive rehabilitation focused on social knowledge deficits can contribute to improvements in the social cognitive abilities of schizophrenic patients. Improvements in social cognitive functioning were durable at three-month follow-up. Cognitive rehabilitation can clearly benefit schizophrenic patients, at least when combined with atypical antipsychotic medication.

High fat diet-induced diabetes in mice exacerbates cognitive deficit due to chronic hypoperfusion

PubMed Central

Zuloaga, Kristen L; Johnson, Lance A; Roese, Natalie E; Marzulla, Tessa; Zhang, Wenri; Nie, Xiao; Alkayed, Farah N; Hong, Christine; Grafe, Marjorie R; Pike, Martin M; Raber, Jacob

2015-01-01

Diabetes causes endothelial dysfunction and increases the risk of vascular cognitive impairment. However, it is unknown whether diabetes causes cognitive impairment due to reductions in cerebral blood flow or through independent effects on neuronal function and cognition. We addressed this using right unilateral common carotid artery occlusion to model vascular cognitive impairment and long-term high-fat diet to model type 2 diabetes in mice. Cognition was assessed using novel object recognition task, Morris water maze, and contextual and cued fear conditioning. Cerebral blood flow was assessed using arterial spin labeling magnetic resonance imaging. Vascular cognitive impairment mice showed cognitive deficit in the novel object recognition task, decreased cerebral blood flow in the right hemisphere, and increased glial activation in white matter and hippocampus. Mice fed a high-fat diet displayed deficits in the novel object recognition task, Morris water maze and fear conditioning tasks and neuronal loss, but no impairments in cerebral blood flow. Compared to vascular cognitive impairment mice fed a low fat diet, vascular cognitive impairment mice fed a high-fat diet exhibited reduced cued fear memory, increased deficit in the Morris water maze, neuronal loss, glial activation, and global decrease in cerebral blood flow. We conclude that high-fat diet and chronic hypoperfusion impair cognitive function by different mechanisms, although they share commons features, and that high-fat diet exacerbates vascular cognitive impairment pathology. PMID:26661233

Cognitive-Linguistic Deficit and Speech Intelligibility in Chronic Progressive Multiple Sclerosis

ERIC Educational Resources Information Center

Mackenzie, Catherine; Green, Jan

2009-01-01

Background: Multiple sclerosis is a disabling neurological disease with varied symptoms, including dysarthria and cognitive and linguistic impairments. Association between dysarthria and cognitive-linguistic deficit has not been explored in clinical multiple sclerosis studies. Aims: In patients with chronic progressive multiple sclerosis, the…

Cognitive deficits in heart failure: Re-cognition of vulnerability as a strange new world.

PubMed

Sloan, Rebecca S; Pressler, Susan J

2009-01-01

Patients with chronic heart failure (HF) have impairment in memory, psychomotor speed, and executive function. The aim of this study was to describe how individuals with HF and cognitive deficits manage self-care in their daily lives. Using an interpretive phenomenology method, HF patients completed unstructured face-to-face interviews about their ability to manage complex health regimens and maintain their health-related quality of life. Analysis of data was aided by use of Atlas.ti computer software. The sample consisted of 12 patients (10 men; aged 43-81 years) who had previously undergone neuropsychological testing and were found to have deficits in 3 or more cognitive domains. Patients confirmed that they followed the advice of healthcare providers by adherence to medication regimens, dietary sodium restrictions, and HF self-care. One overarching theme was identified: "Re-cognition of Vulnerability: A Strange New World." This theme was further differentiated into 3 components: (1) not recognizing cognitive deficits; (2) recognizing cognitive deficits, described as (a) never could remember anything, (b) just old age, (c) HF-related change, and (d) making normal accommodations; and (3) recognizing vulnerability, explained by perception of (a) cognitive, (b) physical, and (c) social vulnerabilities, as well as perception of (d) the nearness of death. Although the study was designed to focus on the cognitive changes in HF patients, it was difficult to separate cognitive, physical, and social challenges. These changes are most useful when taken as a constellation. Healthcare professionals can use the knowledge to identify problems and interventions for HF patients.

Cognitive deficits in recent-onset and chronic schizophrenia☆

PubMed Central

Sponheim, S.R.; Jung, R.E.; Seidman, L.J.; Mesholam-Gately, R.I.; Manoach, D.S.; O'Leary, D.S.; Ho, B.C.; Andreasen, N.C.; Lauriello, J.; Schulz, S.C.

2014-01-01

Although cognitive dysfunction is a primary characteristic of schizophrenia, only recently have investigations begun to pinpoint when the dysfunction develops in the individual afflicted by the disorder. Research to date provides evidence for significant cognitive impairments prior to disorder onset. Less is known about the course of cognitive dysfunction from onset to the chronic phase of schizophrenia. Although longitudinal studies are optimal for assessing stability of cognitive deficits, practice effects often confound assessments, and large and representative subject samples have not been followed over long periods of time. We report results of a cross-sectional study of cognitive deficits early and late in the course of schizophrenia carried out at four different geographic locations to increase sample size and generalizability of findings. We examined a broad set of cognitive functions in 41 recent-onset schizophrenia patients and 106 chronic schizophrenia patients. The study included separate groups of 43 matched controls for the recent-onset sample and 105 matched controls for the chronic schizophrenia sample in order to evaluate the effects of cohort (i.e., age) and diagnosis (i.e., schizophrenia) on cognitive functions. All measures of cognitive function showed effects of diagnosis; however, select time-based measures of problem solving and fine motor dexterity exhibited interactions of diagnosis and cohort indicating that these deficits may progress beyond what is expected with normal aging. Also, worse recall of material in episodic memory was associated with greater length of illness. Nevertheless, findings indicate that nearly all cognitive deficits are comparably impaired across recent-onset and chronic schizophrenia. PMID:19878956

Cognitive deficits in recent-onset and chronic schizophrenia.

PubMed

Sponheim, S R; Jung, R E; Seidman, L J; Mesholam-Gately, R I; Manoach, D S; O'Leary, D S; Ho, B C; Andreasen, N C; Lauriello, J; Schulz, S C

2010-05-01

Although cognitive dysfunction is a primary characteristic of schizophrenia, only recently have investigations begun to pinpoint when the dysfunction develops in the individual afflicted by the disorder. Research to date provides evidence for significant cognitive impairments prior to disorder onset. Less is known about the course of cognitive dysfunction from onset to the chronic phase of schizophrenia. Although longitudinal studies are optimal for assessing stability of cognitive deficits, practice effects often confound assessments, and large and representative subject samples have not been followed over long periods of time. We report results of a cross-sectional study of cognitive deficits early and late in the course of schizophrenia carried out at four different geographic locations to increase sample size and generalizability of findings. We examined a broad set of cognitive functions in 41 recent-onset schizophrenia patients and 106 chronic schizophrenia patients. The study included separate groups of 43 matched controls for the recent-onset sample and 105 matched controls for the chronic schizophrenia sample in order to evaluate the effects of cohort (i.e., age) and diagnosis (i.e., schizophrenia) on cognitive functions. All measures of cognitive function showed effects of diagnosis; however, select time-based measures of problem solving and fine motor dexterity exhibited interactions of diagnosis and cohort indicating that these deficits may progress beyond what is expected with normal aging. Also, worse recall of material in episodic memory was associated with greater length of illness. Nevertheless, findings indicate that nearly all cognitive deficits are comparably impaired across recent-onset and chronic schizophrenia. Published by Elsevier Ltd.

Deficits of long-term memory in ecstasy users are related to cognitive complexity of the task.

PubMed

Brown, John; McKone, Elinor; Ward, Jeff

2010-03-01

Despite animal evidence that methylenedioxymethamphetamine (ecstasy) causes lasting damage in brain regions related to long-term memory, results regarding human memory performance have been variable. This variability may reflect the cognitive complexity of the memory tasks. However, previous studies have tested only a limited range of cognitive complexity. Furthermore, comparisons across different studies are made difficult by regional variations in ecstasy composition and patterns of use. The objective of this study is to evaluate ecstasy-related deficits in human verbal memory over a wide range of cognitive complexity using subjects drawn from a single geographical population. Ecstasy users were compared to non-drug using controls on verbal tasks with low cognitive complexity (stem completion), moderate cognitive complexity (stem-cued recall and word list learning) and high cognitive complexity (California Verbal Learning Test, Verbal Paired Associates and a novel Verbal Triplet Associates test). Where significant differences were found, both groups were also compared to cannabis users. More cognitively complex memory tasks were associated with clearer ecstasy-related deficits than low complexity tasks. In the most cognitively demanding task, ecstasy-related deficits remained even after multiple learning opportunities, whereas the performance of cannabis users approached that of non-drug using controls. Ecstasy users also had weaker deliberate strategy use than both non-drug and cannabis controls. Results were consistent with the proposal that ecstasy-related memory deficits are more reliable on tasks with greater cognitive complexity. This could arise either because such tasks require a greater contribution from the frontal lobe or because they require greater interaction between multiple brain regions.

Cognitive impairments associated with CFS and POTS.

PubMed

Shanks, Lindzi; Jason, Leonard A; Evans, Meredyth; Brown, Abigail

2013-01-01

Chronic fatigue syndrome (CFS) is characterized by fatigue, sleep dysfunction, and cognitive deficits (Fukuda et al., 1994). Research surrounding cognitive functioning among patients with CFS has found difficulty with memory, attention, and information processing. A similar disorder, postural tachycardia syndrome (POTS), is characterized by increased heart rate, fatigue, and mental cloudiness (Raj et al., 2009). Potential implications of cognitive deficits for patients with CFS and/or POTS are discussed, including difficulties with school and/or employment. A few biological theories (i.e., kindling, impairments in the central nervous system, and difficulty with blood flow) have emerged as potential explanations for the cognitive deficits reported in both CFS and POTS Future research should continue to examine possible explanations for cognitive impairments in CFS and POTS, and ultimately use this information to try and reduce cognitive impairments for these patients.

Is a picture worth a thousand (forgotten) words?: neuroimaging evidence for the cognitive deficits in 'chemo-fog'/'chemo-brain'.

PubMed

Raffa, R B

2010-02-01

The diminution in cognitive function reported to occur in patients treated with adjuvant cancer chemotherapy (a phenomenon known as 'chemo-fog, 'chemo-brain' or similar designation) is supported with varying degrees of evidence by prospective and retrospective clinical studies. However, the cognitive deficits are often subtle and the methodologies used to measure them not consistent. Additionally, patients might be able to compensate for the deficits, thereby leading to underestimates of the problem by this type of assessment. For these reasons, direct neuroimaging techniques might provide additional insight. The relatively few such studies, and fewer electrophysiological studies, offer an alternative way to evaluate changes that might be related to cognitive deficits in patients treated with cancer chemotherapeutic regimens.

Cognition in multiple sclerosis

PubMed Central

Benedict, Ralph; Enzinger, Christian; Filippi, Massimo; Geurts, Jeroen J.; Hamalainen, Paivi; Hulst, Hanneke; Inglese, Matilde; Leavitt, Victoria M.; Rocca, Maria A.; Rosti-Otajarvi, Eija M.; Rao, Stephen

2018-01-01

Cognitive decline is recognized as a prevalent and debilitating symptom of multiple sclerosis (MS), especially deficits in episodic memory and processing speed. The field aims to (1) incorporate cognitive assessment into standard clinical care and clinical trials, (2) utilize state-of-the-art neuroimaging to more thoroughly understand neural bases of cognitive deficits, and (3) develop effective, evidence-based, clinically feasible interventions to prevent or treat cognitive dysfunction, which are lacking. There are obstacles to these goals. Our group of MS researchers and clinicians with varied expertise took stock of the current state of the field, and we identify several important practical and theoretical challenges, including key knowledge gaps and methodologic limitations related to (1) understanding and measurement of cognitive deficits, (2) neuroimaging of neural bases and correlates of deficits, and (3) development of effective treatments. This is not a comprehensive review of the extensive literature, but instead a statement of guidelines and priorities for the field. For instance, we provide recommendations for improving the scientific basis and methodologic rigor for cognitive rehabilitation research. Toward this end, we call for multidisciplinary collaborations toward development of biologically based theoretical models of cognition capable of empirical validation and evidence-based refinement, providing the scientific context for effective treatment discovery. PMID:29343470

Review of recent studies on interventions for cognitive deficits in patients with cancer.

PubMed

Gehring, Karin; Roukema, Jan Anne; Sitskoorn, Margriet M

2012-02-01

Research has demonstrated that patients with cancer experience cognitive deficits, often due to aggressive anticancer treatments. In this article, we critically review the interventional studies that have been conducted to investigate beneficial effects on cognitive function in cancer patients. Pharmacological agents that have been studied include psychostimulants, such as methylphenidate and modafinil, erythropoietin, and hormonal (supplement) treatments for patients who receive hormonal suppression therapy. In addition, several cognitive rehabilitation programs have been evaluated in cancer patients. Recently, the approach of physical exercise to treat cognitive deficits has received great interest, and findings from novel studies are keenly anticipated. Although, in general, the studies reviewed were well designed, future studies may wish to include larger sample sizes and pay more attention to the accurate assessment of cognitive function.

Everyday Cognitive Failures and Memory Problems in Parkinson's Patients without Dementia

ERIC Educational Resources Information Center

Poliakoff, Ellen; Smith-Spark, James H.

2008-01-01

There is growing evidence that Parkinson's disease patients without dementia exhibit cognitive deficits in some executive, memory and selective attention tasks. However, the impact of these deficits on their everyday cognitive functioning remains largely unknown. This issue was explored using self-report questionnaires. Twenty-four Parkinson's…

Cognitive Inflexibility and Frontal-Cortical Activation in Pediatric Obsessive-Compulsive Disorder

ERIC Educational Resources Information Center

Britton, Jennifer C.; Rauch, Scott L.; Rosso, Isabelle M.; Killgore, William D. S.; Price, Lauren M.; Ragan, Jennifer; Chosak, Anne; Hezel, Dianne M.; Pine, Daniel S.; Leibenluft, Ellen; Pauls, David L.; Jenike, Michael A.; Stewart, S. Evelyn

2010-01-01

Objective: Deficits in cognitive flexibility and response inhibition have been linked to perturbations in cortico-striatal-thalamic circuitry in adult obsessive-compulsive disorder (OCD). Although similar cognitive deficits have been identified in pediatric OCD, few neuroimaging studies have been conducted to examine its neural correlates in the…

[Cognition - the core of major depressive disorder].

PubMed

Polosan, M; Lemogne, C; Jardri, R; Fossati, P

2016-02-01

Cognitive deficits have been only recently recognized as a major phenotype determinant of major depressive disorder, although they are an integral part of the definition of the depressive state. Congruent evidence suggest that these cognitive deficits persist beyond the acute phase and may be identified at all ages. The aim of the current study was to review the main meta-analyses on cognition and depression, which encompasses a large range of cognitive domains. Therefore, we discuss the "cold" (attention, memory, executive functions) and "hot" (emotional bias) cognitive impairments in MDD, as well as those of social cognition domains (empathy, theory of mind). Several factors interfere with cognition in MDD such as clinical (melancholic, psychotic...) features, age, age of onset, illness severity, medication and comorbid condition. As still debated in the literature, the type of relationship between the severity of cognitive symptoms and functioning in depression is detailed, thus highlighting their predictive value of functional outcome, independently of the affective symptoms. A better identification of the cognitive deficits in MDD and a monitoring of the effects of different treatments require appropriate instruments, which may be developed by taking advantage of the increasing success of computing tools. Overall, current data suggest a core role for different cognitive deficits in MDD, therefore opening new perspectives for optimizing the treatment of depression. Copyright © 2016 Elsevier Ltd. All rights reserved.

Pharmacologic Treatment with GABAB Receptor Agonist of Methamphetamine-Induced Cognitive Impairment in Mice

PubMed Central

Mizoguchi, Hiroyuki; Yamada, Kiyofumi

2011-01-01

Methamphetamine (METH) is a highly addictive drug, and addiction to METH has increased to epidemic proportions worldwide. Chronic use of METH causes psychiatric symptoms, such as hallucinations and delusions, and long-term cognitive deficits, which are indistinguishable from paranoid schizophrenia. The GABA receptor system is known to play a significant role in modulating the dopaminergic neuronal system, which is related to behavioral changes induced by drug abuse. However, few studies have investigated the effects of GABA receptor agonists on cognitive deficits induced by METH. In the present review, we show that baclofen, a GABA receptor agonist, is effective in treating METH-induced impairment of object recognition memory and prepulse inhibition (PPI) of the startle reflex, a measure of sensorimotor gating in mice. Acute and repeated treatment with METH induced a significant impairment of PPI. Furthermore, repeated but not acute treatment of METH resulted in a long-lasting deficit of object recognition memory. Baclofen, a GABAB receptor agonist, dose-dependently ameliorated the METH-induced PPI deficits and object recognition memory impairment in mice. On the other hand, THIP, a GABAA receptor agonist, had no effect on METH-induced cognitive deficits. These results suggest that GABAB receptors may constitute a putative new target in treating cognitive deficits in chronic METH users. PMID:21886573

[Cognitive impairments in alcohol dependence: From screening to treatment improvements].

PubMed

Cabé, N; Laniepce, A; Ritz, L; Lannuzel, C; Boudehent, C; Vabret, F; Eustache, F; Beaunieux, H; Pitel, A-L

2016-02-01

Alcohol-related cognitive impairments are largely underestimated in clinical practice, even though they could limit the benefit of alcohol treatment and hamper the patient's ability to remain abstinent or to respect his/her therapeutic contract. These neuropsychological deficits can impact the management of patients well before the development of the well-known Korsakoff's syndrome. Indeed, even in the absence of ostensible neurological complications, excessive and chronic alcohol consumption results in damage of brain structure and function. The frontocerebellar circuit and the circuit of Papez, respectively involved in motor and executive abilities and episodic memory, are mainly affected. Those brain dysfunctions are associated with neuropsychological deficits, including deficits of executive functions, episodic memory, social cognition, as well as visuospatial and motor abilities. Such cognitive disorders can interfere with the motivation process to abandon maladjusted drinking behavior in favor of a healthier lifestyle (such as abstinence or controlled alcohol consumption). They can also limit the patient's capacity to fully benefit from treatment (notably psychoeducation and cognitive-behavioural treatments) currently widely proposed in French Addiction departments. In addition, they may contribute to relapse which is multi-determinated. A neuropsychological assessment appears therefore crucial to take relevant clinical decisions. However, very few addiction departments have the human and financial resources to conduct an extensive neuropsychological examination of all patients with alcohol dependence. Some brief screening tools can be used, notably the MOntreal Cognitive Assessment and the Brief Evaluation of Alcohol-Related Neuropsychological Impairments, which has been especially designed to assess cognitive and motor deficits in alcoholism. These tools can be used by non-psychologist clinicians to detect alcohol-related cognitive deficits, which require an extensive cognitive examination conducted by a neuropsychologist. The presence of cognitive dysfunctions in patients early in abstinence should encourage clinicians to adjust the modalities of the treatment. The fact to favor recovery of cognitive functions and brain volumes with abstinence or drastic reduction of alcohol consumption could be a first way to make it possible for patients to be cognitively able to benefit from treatment. Further studies are required to determine whether specifically designed cognitive remediation could boost (accelerate or increase) the recovery of brain functioning. Additionally, a potential effect of thiamine to limit alcohol-related cognitive deficits before the development of neurological complications remains to be determined. In this review, we presented the pattern of structural brain damage and the associated cognitive and motor impairments in alcohol-dependent patients. We then emphasized the harmful effects of neuropsychological deficits in the management of these patients. We also pointed how relevant it is to screen patients with neuropsychological impairments and we focused on the presentation of two brief screening tools for cognitive impairments, especially designed for alcohol-related deficits or not. Finally, we reported how these neuropsychological impairments could be taken into consideration the treatment of alcohol addiction by adjusting its timing and modalities. Copyright © 2015 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.

Persistent cognitive and dopamine transporter deficits in abstinent methamphetamine users.

PubMed

McCann, Una D; Kuwabara, Hiroto; Kumar, Anil; Palermo, Michael; Abbey, Rubyna; Brasic, James; Ye, Weiguo; Alexander, Mohab; Dannals, Robert F; Wong, Dean F; Ricaurte, George A

2008-02-01

Studies in abstinent methamphetamine (METH) users have demonstrated reductions in brain dopamine transporter (DAT) binding potential (BP), as well as cognitive and motor deficits, but it is not yet clear whether cognitive deficits and brain DAT reductions fully reverse with sustained abstinence, or whether behavioral deficits in METH users are related to dopamine (DA) deficits. This study was conducted to further investigate potential persistent psychomotor deficits secondary to METH abuse, and their relationship to brain DAT availability, as measured using quantitative PET methods with [(11)C]WIN 35428. Twenty-two abstinent METH users and 17 healthy non-METH using controls underwent psychometric testing to test the hypothesis that METH users would demonstrate selective deficits in neuropsychiatric domains known to involve DA neurons (e.g., working memory, executive function, motor function). A subset of subjects also underwent PET scanning with [(11)C]WIN 35428. METH users were found to have modest deficits in short-term memory, executive function, and manual dexterity. Exploratory correlational analyses revealed that deficits in memory, but not those in executive or motor function, were associated with decreases in striatal DAT BP. These results suggest a possible relationship between DAT BP and memory deficits in abstinent METH users, and lend support to the notion that METH produces lasting effects on central DA neurons in humans. As METH can also produce toxic effects on serotonin (5-HT) neurons, further study is needed to address the potential role of brain 5-HT depletion in cognitive deficits in abstinent METH users. (c) 2007 Wiley-Liss, Inc.

The long-term effects of cocaine use on cognitive functioning: A systematic critical review.

PubMed

Frazer, Kirsten M; Richards, Qwynten; Keith, Diana R

2018-08-01

The predominant view of chronic cocaine use maintains that it causes a broad range of cognitive deficits. However, concerns about the possibly deleterious impact of cocaine on cognitive functioning have yet to be thoroughly vetted. This review addresses the impact of cocaine use on such cognitive domains as executive function, memory, language, and psychomotor speed. Additionally, relevant neuroimaging data is considered to understand the neural basis underlying cocaine-related effects on cognitive functioning. We searched PubMed, Google Scholar, and Embase using the search terms "cocaine and cognition," "cocaine and cognitive functioning," and "cocaine and cognitive deficits or impairment." To meet inclusion criteria we evaluated only cognitive and neuroimaging studies describing the long-term effects of cocaine on cognitive functioning published from 1999 to 2016. The majority of studies reported statistically significant differences between cocaine users and non-drug-using controls in brain structures, blood-oxygen-level dependent signals, and brain metabolism. However, differences in cognitive performance were observed on a minority of measures. Additionally, the majority of studies were not compared against normative data. The current evidence does not support the view that chronic cocaine use is associated with broad cognitive deficits. The view that cocaine users have broad cognitive deficits is inaccurate based upon current evidence, and the perpetuation of this view may have negative implications for treatment programs and development of public policies. Copyright © 2018 Elsevier B.V. All rights reserved.

A cog in cognition: how the alpha 7 nicotinic acetylcholine receptor is geared towards improving cognitive deficits.

PubMed

Leiser, Steven C; Bowlby, Mark R; Comery, Thomas A; Dunlop, John

2009-06-01

Cognition, memory, and attention and arousal have been linked to nicotinic acetylcholine receptors (nAChRs). Thus it is not surprising that nAChRs have been strongly implicated as therapeutic targets for treating cognitive deficits in disorders such as schizophrenia and Alzheimer's disease (AD). In particular the alpha7 (alpha7) nAChR has been closely linked with normalization of P50 auditory evoked potential (AEP) gating deficits, and to a lesser extent improvements in pre-pulse inhibition (PPI) of the acoustic startle response. These two brain phenomena can be considered as pre-attentive, occurring while sensory information is being processed, and are important endophenotypes in schizophrenia with deficits likely contributing to the cognitive fragmentation associated with the disease. In addition alpha7 nAChRs have been implicated in attention, in particular under high attentional demand, and in more demanding working memory tasks such as long delays in delayed matching tasks. Efficacy of alpha7 nAChR agonists across a range of cognitive processes ranging from pre-attentive to attentive states and working and recognition memory provides a solid basis for their pro-cognitive effects. This review will focus on the recent work highlighting the role of alpha7 in cognition and cognitive processes.

Predictive value of cognition for different domains of outcome in recent-onset schizophrenia.

PubMed

Holthausen, Esther A E; Wiersma, Durk; Cahn, Wiepke; Kahn, René S; Dingemans, Peter M; Schene, Aart H; van den Bosch, Robert J

2007-01-15

The aim of this study was to see whether and how cognition predicts outcome in recent-onset schizophrenia in a large range of domains such as course of illness, self-care, interpersonal functioning, vocational functioning and need for care. At inclusion, 115 recent-onset patients were tested on a cognitive battery and 103 patients participated in the follow-up 2 years after inclusion. Differences in outcome between cognitively normal and cognitively impaired patients were also analysed. Cognitive measures at inclusion did not predict number of relapses, activities of daily living and interpersonal functioning. Time in psychosis or in full remission, as well as need for care, were partly predicted by specific cognitive measures. Although statistically significant, the predictive value of cognition with regard to clinical outcome was limited. There was a significant difference between patients with and without cognitive deficits in competitive employment status and vocational functioning. The predictive value of cognition for different social outcome domains varies. It seems that cognition most strongly predicts work performance, where having a cognitive deficit, regardless of the nature of the deficit, acts as a rate-limiting factor.

Dopamine dysregulation in the prefrontal cortex relates to cognitive deficits in the sub-chronic PCP-model for schizophrenia: A preliminary investigation.

PubMed

McLean, Samantha L; Harte, Michael K; Neill, Joanna C; Young, Andrew Mj

2017-06-01

Dopamine dysregulation in the prefrontal cortex (PFC) plays an important role in cognitive dysfunction in schizophrenia. Sub-chronic phencyclidine (scPCP) treatment produces cognitive impairments in rodents and is a thoroughly validated animal model for cognitive deficits in schizophrenia. The aim of our study was to investigate the role of PFC dopamine in scPCP-induced deficits in a cognitive task of relevance to the disorder, novel object recognition (NOR). Twelve adult female Lister Hooded rats received scPCP (2 mg/kg) or vehicle via the intraperitoneal route twice daily for 7 days, followed by 7 days washout. In vivo microdialysis was carried out prior to, during and following the NOR task. Vehicle rats successfully discriminated between novel and familiar objects and this was accompanied by a significant increase in dopamine in the PFC during the retention trial ( p < 0.01). scPCP produced a significant deficit in NOR ( p < 0.05 vs. control) and no PFC dopamine increase was observed. These data demonstrate an increase in dopamine during the retention trial in vehicle rats that was not observed in scPCP-treated rats accompanied by cognitive disruption in the scPCP group. This novel finding suggests a mechanism by which cognitive deficits are produced in this animal model and support its use for investigating disorders in which PFC dopamine is central to the pathophysiology.

Olanzapine Reverses MK-801-Induced Cognitive Deficits and Region-Specific Alterations of NMDA Receptor Subunits

PubMed Central

Liu, Xiao; Li, Jitao; Guo, Chunmei; Wang, Hongli; Sun, Yaxin; Wang, Han; Su, Yun-Ai; Li, Keqing; Si, Tianmei

2018-01-01

Cognitive dysfunction constitutes an essential component in schizophrenia for its early presence in the pathophysiology of the disease and close relatedness to life quality of patients. To develop effective treatment of cognitive deficits, it is important to understand their neurobiological causes and to identify potential therapeutic targets. In this study, adopting repeated MK-801 treatment as an animal model of schizophrenia, we investigated whether antipsychotic drugs, olanzapine and haloperidol, can reverse MK-801-induced cognitive deficits and how the reversal processes recruited proteins involved in glutamate neurotransmission in rat medial prefrontal cortex (mPFC) and hippocampus. We found that low-dose chronic MK-801 treatment impaired object-in-context recognition memory and reversal learning in the Morris water maze, leaving reference memory relatively unaffected, and that these cognitive deficits can be partially reversed by olanzapine, not haloperidol, treatment. At the molecular level, chronic MK-801 treatment resulted in the reduction of multiple N-methyl-D-aspartate (NMDA) receptor subunits in rat mPFC and olanzapine, not haloperidol, treatment restored the levels of GluN1 and phosphorylated GluN2B in this region. Taken together, MK-801-induced cognitive deficits may be associated with region-specific changes in NMDA receptor subunits and the reversal of specific NMDA receptor subunits may underlie the cognition-enhancing effects of olanzapine. PMID:29375333

Exploring the Cognitive Features in Children with Autism Spectrum Disorder, Their Co-Twins, and Typically Developing Children within a Population-Based Sample

ERIC Educational Resources Information Center

Brunsdon, Victoria E. A.; Colvert, Emma; Ames, Catherine; Garnett, Tracy; Gillan, Nicola; Hallett, Victoria; Lietz, Stephanie; Woodhouse, Emma; Bolton, Patrick; Happé, Francesca

2015-01-01

Background: The behavioural symptoms of autism spectrum disorder (ASD) are thought to reflect underlying cognitive deficits/differences. The findings in the literature are somewhat mixed regarding the cognitive features of ASD. This study attempted to address this issue by investigating a range of cognitive deficits and the prevalence of multiple…

Structural correlates of cognitive deficit and elevated gamma noise power in schizophrenia.

PubMed

Suazo, Vanessa; Díez, Álvaro; Montes, Carlos; Molina, Vicente

2014-03-01

The aim of this study was to assess the relation between cognition, gray matter (GM) volumes and gamma noise power (amount of background oscillatory activity in the gamma band) in schizophrenia. We explored the relation between cognitive performance and regional GM volumes using voxel-based morphometry (VBM), in order to discover if the association between gamma noise power (an electroencephalography measurement of background activity in the gamma band) and cognition is observed through structural deficits related to the disease. Noise power, magnetic resonance imaging and cognitive assessments were obtained in 17 drug-free paranoid patients with schizophrenia and 13 healthy controls. In comparison with controls, patients showed GM deficits at posterior cingulate (bilateral),left inferior parietal (supramarginal gyrus) and left inferior dorsolateral prefrontal regions. Patients exhibited a direct association between performance in working memory and right temporal (superior and inferior gyri) GM densities. They also displayed a negative association between right anterior cerebellum volume and gamma noise power at the frontal midline (Fz) site. A structural deficit in the cerebellum may be involved in gamma activity disorganization in schizophrenia. Temporal structural deficits may relate to cognitive dysfunction in this illness. © 2013 The Authors. Psychiatry and Clinical Neurosciences © 2013 Japanese Society of Psychiatry and Neurology.

16p11.2 Deletion mice display cognitive deficits in touchscreen learning and novelty recognition tasks.

PubMed

Yang, Mu; Lewis, Freeman C; Sarvi, Michael S; Foley, Gillian M; Crawley, Jacqueline N

2015-12-01

Chromosomal 16p11.2 deletion syndrome frequently presents with intellectual disabilities, speech delays, and autism. Here we investigated the Dolmetsch line of 16p11.2 heterozygous (+/-) mice on a range of cognitive tasks with different neuroanatomical substrates. Robust novel object recognition deficits were replicated in two cohorts of 16p11.2+/- mice, confirming previous findings. A similarly robust deficit in object location memory was discovered in +/-, indicating impaired spatial novelty recognition. Generalizability of novelty recognition deficits in +/- mice extended to preference for social novelty. Robust learning deficits and cognitive inflexibility were detected using Bussey-Saksida touchscreen operant chambers. During acquisition of pairwise visual discrimination, +/- mice required significantly more training trials to reach criterion than wild-type littermates (+/+), and made more errors and correction errors than +/+. In the reversal phase, all +/+ reached criterion, whereas most +/- failed to reach criterion by the 30-d cutoff. Contextual and cued fear conditioning were normal in +/-. These cognitive phenotypes may be relevant to some aspects of cognitive impairments in humans with 16p11.2 deletion, and support the use of 16p11.2+/- mice as a model system for discovering treatments for cognitive impairments in 16p11.2 deletion syndrome. © 2015 Yang et al.; Published by Cold Spring Harbor Laboratory Press.

The development and initial validation of a sensitive bedside cognitive screening test.

PubMed

Faust, D; Fogel, B S

1989-01-01

Brief bedside cognitive examinations such as the Mini-Mental State Examination are designed to detect delirium and dementia but not more subtle or delineated cognitive deficits. Formal neuropsychological evaluation provides greater sensitivity and detects a wider range of cognitive deficits but is too lengthy for efficient use at the bedside or in epidemiological studies. The authors developed the High Sensitivity Cognitive Screen (HSCS), a 20-minute interview-based test, to identify patients who show disorder on formal neuropsychological evaluation. An initial study demonstrated satisfactory test-retest and interrater reliability. The HSCS was then administered to 60 psychiatric and neurological patients with suspected cognitive deficits but without gross impairment, who also completed formal neuropsychological testing. Results of both tests were independently classified as either normal, borderline, or abnormal. The HSCS correctly classified 93% of patients across the normal-abnormal dichotomy and showed promise for characterizing the extent and severity of cognitive dysfunction.

Cognitive Patterns and Learning Disabilities in Cleft Palate Children with Verbal Deficits.

ERIC Educational Resources Information Center

Richman, Lynn C.

1980-01-01

The study examined patterns of cognitive ability in 57 cleft lip and palate children (ages 7 to 9) with verbal deficit, but without general intellectual retardation to evaluate whether the verbal disability displayed by these children was related primarily to a specific verbal expression deficit or a more general symbolic mediation problem.…

Dyslexia and Dyscalculia: Two Learning Disorders with Different Cognitive Profiles

ERIC Educational Resources Information Center

Landerl, Karin; Fussenegger, Barbara; Moll, Kristina; Willburger, Edith

2009-01-01

This study tests the hypothesis that dyslexia and dyscalculia are associated with two largely independent cognitive deficits, namely a phonological deficit in the case of dyslexia and a deficit in the number module in the case of dyscalculia. In four groups of 8- to 10-year-olds (42 control, 21 dyslexic, 20 dyscalculic, and 26…

Number Processing and Heterogeneity of Developmental Dyscalculia: Subtypes with Different Cognitive Profiles and Deficits

ERIC Educational Resources Information Center

Skagerlund, Kenny; Träff, Ulf

2016-01-01

This study investigated if developmental dyscalculia (DD) in children with different profiles of mathematical deficits has the same or different cognitive origins. The defective approximate number system hypothesis and the access deficit hypothesis were tested using two different groups of children with DD (11-13 years old): a group with…

ECT and Pronounced Impairment in Spatial Cognition: The Fallacy of Drawing Conclusions From a Single Case.

PubMed

Andrade, Chittaranjan; Prasad, Yameni; Devaraj, Aathira; Pinto, Ekta Franscina; Shukla, Lekhansh

2018-06-01

Electroconvulsive therapy (ECT) is associated with memory deficits on neuropsychological assessment. The association of ECT with nonmemory cognitive deficits has been poorly studied. We present a 40-year-old woman who showed a bizarre form of spatial cognition impairment on a subtest of the Tactual Performance Test (TPT) after recovering from depression with 6 alternate day, thrice-weekly, inpatient ECT treatments. This woman was part of a naturalistic, nonblind study that examined nonmemory cognitive deficits in antidepressant-treated depressed patients who did and did not receive ECT. The impairment was in the form of bizarrely drawn reproductions of differently shaped wooden blocks that had been presented to the patient when she was blindfolded. The impairment was still evident when she was retested (3 hours later) under substantially simplified conditions but was much attenuated approximately 2.5 weeks later. On the surface, it seems that ECT had induced severe impairment in spatial cognition and that the impairment showed the familiar pattern of attenuation with the passage of time. However, another recovered patient in the study, who did not receive ECT, also showed substantial spatial deficits on the same subtest of the TPT, and the attenuation of the deficits across time in the ECT-treated patient was probably a result of repeated exposure to the task. We suggest that not all patients who seem to experience spectacular cognitive impairment after ECT have deficits that are attributable to ECT.

Does Sport-Drink Use During Exercise Promote an Acute Positive Energy Balance?

PubMed

Dragusin, Iulian B; Horswill, Craig A

2016-10-01

Sports drinks have been implicated in contributing to obesity and chronic diseases by providing surplus calories and excess sugars. Using existing literature we compared energy intake from sports drinks consumed during exercise with the exercise-induced calorie expenditure to determine whether sports drink use might eliminate the energy deficit and jeopardize conditions for improved metabolic fitness. We identified 11 published studies that compared sport drink consumption to placebo during exercise with a primary focused on the effect of sport drinks or total carbohydrate content on enhancing physical performance. Energy expenditure (EE) was calculated using VO 2 , RER, and exercise duration for the exercise protocol. Energy ingestion (EI) was determined using the carbohydrate dosing regimen administered before and during the exercise protocol. A two-tailed t test was used to test whether the energy balance (EI-EE) was different from zero (alpha level = 0.05). Sport drink consumption during aerobic exercise of sufficient duration (≥ 60 min) did not abolish the energy deficit (p < .001). Mean ± SD were EE, 1600 ± 639 Cal; EI, 394 ± 289 Cal; and EI-EE,-1206+594 Cal; VO 2 , 3.05 ± 0.55 L/min; RER, 0.91 ± 0.04; exercise duration 110 ± 42 min. Ingesting sports drinks to enhance performance did not abolish the caloric deficit of aerobic exercise. Sports drinks can be used in accordance with research protocols that typically provide 30-60 g of carbohydrate per hour when exercising at adequate durations for moderate to high intensity and still maintain a substantive caloric deficit.

[Subjective cognition in schizophrenia].

PubMed

Potvin, S; Aubin, G; Stip, E

2017-02-01

Given the extent, magnitude and functional significance of the neurocognitive deficits of schizophrenia, growing attention has been paid recently to patients' self-awareness of their own deficits. Thus far, the literature has shown either that patients fail to recognize their cognitive deficits or that the association between subjective and objective cognition is weak in schizophrenia. The reasons for this lack of consistency remain unexplained but may have to do, among others, with the influence of potential confounding clinical variables and the choice of the scale used to measure self-awareness of cognitive deficits. In the current study, we sought to examine the relationships between subjective and objective cognitive performance in schizophrenia, while controlling for the influence of sociodemographic and psychiatric variables. Eighty-two patients with a schizophrenia-spectrum disorder (DSM-IV criteria) were recruited. Patients' subjective cognitive complaints were evaluated with the Subjective Scale to Investigate Cognition in Schizophrenia (SSTICS), the most frequently used scale to measure self-awareness of cognitive deficits in schizophrenia. Neurocognition was evaluated with working memory, planning and visual learning tasks taken from Cambridge Neuropsychological Tests Automated Battery. The Stroop Color-Word test was also administered. Psychiatric symptoms were evaluated with the Positive and Negative Syndrome Scale and the Calgary Depression Scale for Schizophrenia. The relationships between subjective and objective cognition were evaluated with multivariate hierarchic linear regression analyses, taking into consideration potential confounders such as sociodemographic and psychiatric variables. Finally, a factor analysis of the SSTICS was performed. For the SSTICS total score, the regression analysis produced a model including two predictors, namely visual learning and Stoop interference performance, explaining a moderate portion of the variance. Visual learning performance was the most consistent predictor of most SSTICS subscores (e.g. episodic memory, attention, executive functioning, language and praxis). Modest associations were found between the PANSS cognitive factor and objective cognition (e.g. Stroop interference, visual learning, and working memory). Finally, the factor analysis revealed a 6-factor solution that echoes the classification of the items of the SSTICS based on the neuropsychological literature. Using a scale having good internal validity, as shown by the factor analysis, the current study highlighted modest associations between subjective and objective cognitive performance, which suggests that schizophrenia patients are only partially aware of their own cognitive deficits. The results also showed a lack of correspondence between the impaired cognitive domain and the domain of cognitive awareness. It should be noted that clinicians were not better than patients at evaluating their cognitive deficits. Future research will need to determine if the observations reported here are schizophrenia-specific or not. Copyright © 2016 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.

The Relationship between Specific Cognitive Impairment and Behaviour in Prader-Willi Syndrome

ERIC Educational Resources Information Center

Woodcock, K. A.; Oliver, C.; Humphreys, G. W.

2011-01-01

Background: Individuals with Prader-Willi syndrome (PWS) have been shown to demonstrate a particular cognitive deficit in attention switching and high levels of preference for routine and temper outbursts. This study assesses whether a specific pathway between a cognitive deficit and behaviour via environmental interaction can exist in individuals…

Measuring Discrimination- and Reversal Learning in Mouse Models within 4 Days and without Prior Food Deprivation

ERIC Educational Resources Information Center

Remmelink, Esther; Smit, August B.; Verhage, Matthijs; Loos, Maarten

2016-01-01

Many neurological and psychiatric disorders are characterized by deficits in cognitive flexibility. Modeling cognitive flexibility in mice enables the investigation of mechanisms underlying these deficits. The majority of currently available behavioral tests targeting this cognitive domain are reversal learning tasks that require scheduled food…

Overlapping prefrontal systems involved in cognitive and emotional processing in euthymic bipolar disorder and following sleep deprivation: A review of functional neuroimaging studies

PubMed Central

McKenna, Benjamin S; Eyler, Lisa T

2013-01-01

Prefrontal cortex (PFC) mediated cognitive and emotional processing deficits in bipolar disorder lead to functional limitations even during periods of mood stability. Alterations of sleep and circadian functioning are well-documented in bipolar disorder, but there is little research directly examining the mechanistic role of sleep and/or circadian rhythms in the observed cognitive and emotional processing deficits. We systematically review the cognitive and emotional processing deficits reliant upon PFC functioning of euthymic patients with bipolar disorder and in healthy individuals deprived of sleep. The evidence from two parallel lines of investigation suggests that sleep and circadian rhythms may be involved in the cognitive and emotional processing deficits seen in bipolar disorder through overlapping neurobiological systems. We discuss current models of bipolar highlighting the PFC-limbic connections and discuss inclusion of sleep-related mechanisms. Sleep and circadian dysfunction is a core feature of bipolar disorder and models of neurobiological abnormalities should incorporate chronobiological measures. Further research into the role of sleep and circadian rhythms in cognition and emotional processing in bipolar disorder is warranted. PMID:22926687

Memory deficit in patients with schizophrenia and posttraumatic stress disorder: relational vs item-specific memory

PubMed Central

Jung, Wookyoung; Lee, Seung-Hwan

2016-01-01

It has been well established that patients with schizophrenia have impairments in cognitive functioning and also that patients who experienced traumatic events suffer from cognitive deficits. Of the cognitive deficits revealed in schizophrenia or posttraumatic stress disorder (PTSD) patients, the current article provides a brief review of deficit in episodic memory, which is highly predictive of patients’ quality of life and global functioning. In particular, we have focused on studies that compared relational and item-specific memory performance in schizophrenia and PTSD, because measures of relational and item-specific memory are considered the most promising constructs for immediate tangible development of clinical trial paradigm. The behavioral findings of schizophrenia are based on the tasks developed by the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS) initiative and the Cognitive Neuroscience Test Reliability and Clinical Applications for Schizophrenia (CNTRACS) Consortium. The findings we reviewed consistently showed that schizophrenia and PTSD are closely associated with more severe impairments in relational memory compared to item-specific memory. Candidate brain regions involved in relational memory impairment in schizophrenia and PTSD are also discussed. PMID:27274250

Using Textual Prompts to Teach Mands for Information Using "Who?"

ERIC Educational Resources Information Center

Shillingsburg, M. Alice; Gayman, Cassondra M.; Walton, William

2016-01-01

Recent research on teaching mands for information to children with language deficits has focused on manipulating establishing operations (EOs). However, only a few of those studies have programmed both EO conditions (in which information is needed) and abolishing operation (AO) conditions (in which information has already been provided) to ensure…

Working memory impairment in probands with schizoaffective disorder and first degree relatives of schizophrenia probands extend beyond deficits predicted by generalized neuropsychological impairment.

PubMed

Kristian Hill, S; Buchholz, Alison; Amsbaugh, Hayley; Reilly, James L; Rubin, Leah H; Gold, James M; Keefe, Richard S E; Pearlson, Godfrey D; Keshavan, Matcheri S; Tamminga, Carol A; Sweeney, John A

2015-08-01

Working memory impairment is well established in psychotic disorders. However, the relative magnitude, diagnostic specificity, familiality pattern, and degree of independence from generalized cognitive deficits across psychotic disorders remain unclear. Participants from the Bipolar and Schizophrenia Network on Intermediate Phenotypes (B-SNIP) study included probands with schizophrenia (N=289), psychotic bipolar disorder (N=227), schizoaffective disorder (N=165), their first-degree relatives (N=315, N=259, N=193, respectively), and healthy controls (N=289). All were administered the WMS-III Spatial Span working memory test and the Brief Assessment of Cognition in Schizophrenia (BACS) battery. All proband groups displayed significant deficits for both forward and backward span compared to controls. However, after covarying for generalized cognitive impairments (BACS composite), all proband groups showed a 74% or greater effect size reduction with only schizoaffective probands showing residual backward span deficits compared to controls. Significant familiality was seen in schizophrenia and bipolar pedigrees. In relatives, both forward and backward span deficits were again attenuated after covarying BACS scores and residual backward span deficits were seen in relatives of schizophrenia patients. Overall, both probands and relatives showed a similar pattern of robust working memory deficits that were largely attenuated when controlling for generalized cognitive deficits. Copyright © 2015 Elsevier B.V. All rights reserved.

Diet-Induced Cognitive Deficits: The Role of Fat and Sugar, Potential Mechanisms and Nutritional Interventions

PubMed Central

Beilharz, Jessica E.; Maniam, Jayanthi; Morris, Margaret J.

2015-01-01

It is of vital importance to understand how the foods which are making us fat also act to impair cognition. In this review, we compare the effects of acute and chronic exposure to high-energy diets on cognition and examine the relative contributions of fat (saturated and polyunsaturated) and sugar to these deficits. Hippocampal-dependent memory appears to be particularly vulnerable to the effects of high-energy diets and these deficits can occur rapidly and prior to weight gain. More chronic diet exposure seems necessary however to impair other sorts of memory. Many potential mechanisms have been proposed to underlie diet-induced cognitive decline and we will focus on inflammation and the neurotrophic factor, brain-derived neurotrophic factor (BDNF). Finally, given supplementation of diets with omega-3 and curcumin has been shown to have positive effects on cognitive function in healthy ageing humans and in disease states, we will discuss how these nutritional interventions may attenuate diet-induced cognitive decline. We hope this approach will provide important insights into the causes of diet-induced cognitive deficits, and inform the development of novel therapeutics to prevent or ameliorate such memory impairments. PMID:26274972

Diet-Induced Cognitive Deficits: The Role of Fat and Sugar, Potential Mechanisms and Nutritional Interventions.

PubMed

Beilharz, Jessica E; Maniam, Jayanthi; Morris, Margaret J

2015-08-12

It is of vital importance to understand how the foods which are making us fat also act to impair cognition. In this review, we compare the effects of acute and chronic exposure to high-energy diets on cognition and examine the relative contributions of fat (saturated and polyunsaturated) and sugar to these deficits. Hippocampal-dependent memory appears to be particularly vulnerable to the effects of high-energy diets and these deficits can occur rapidly and prior to weight gain. More chronic diet exposure seems necessary however to impair other sorts of memory. Many potential mechanisms have been proposed to underlie diet-induced cognitive decline and we will focus on inflammation and the neurotrophic factor, brain-derived neurotrophic factor (BDNF). Finally, given supplementation of diets with omega-3 and curcumin has been shown to have positive effects on cognitive function in healthy ageing humans and in disease states, we will discuss how these nutritional interventions may attenuate diet-induced cognitive decline. We hope this approach will provide important insights into the causes of diet-induced cognitive deficits, and inform the development of novel therapeutics to prevent or ameliorate such memory impairments.

Using upper limb kinematics to assess cognitive deficits in people living with both HIV and stroke.

PubMed

Bui, Kevin D; Rai, Roshan; Johnson, Michelle J

2017-07-01

In this study, we aim to explore ways to objectively assess cognitive deficits in the stroke and HIV/stroke populations, where cognitive and motor impairments can be hard to separate. Using an upper limb rehabilitation robot called the Haptic TheraDrive, we collect performance error scores and motor learning data on the impaired and unimpaired limb during a trajectory tracking task. We compare these data to clinical cognitive scores. The preliminary results suggest a possible relationship between unimpaired upper limb performance error and visuospatial/executive function cognitive domains, but more work needs to be done to further investigate this. The potential of using robot-assisted technologies to measure unimpaired limb kinematics as a tool to assess cognitive deficits would be useful to inform more effective rehabilitation strategies for HIV, stroke, and HIV/stroke populations.

GABA Neuron Alterations, Cortical Circuit Dysfunction and Cognitive Deficits in Schizophrenia

PubMed Central

Gonzalez-Burgos, Guillermo; Fish, Kenneth N.; Lewis, David A.

2011-01-01

Schizophrenia is a brain disorder associated with cognitive deficits that severely affect the patients' capacity for daily functioning. Whereas our understanding of its pathophysiology is limited, postmortem studies suggest that schizophrenia is associated with deficits of GABA-mediated synaptic transmission. A major role of GABA-mediated transmission may be producing synchronized network oscillations which are currently hypothesized to be essential for normal cognitive function. Therefore, cognitive deficits in schizophrenia may result from a GABA synapse dysfunction that disturbs neural synchrony. Here, we highlight recent studies further suggesting alterations of GABA transmission and network oscillations in schizophrenia. We also review current models for the mechanisms of GABA-mediated synchronization of neural activity, focusing on parvalbumin-positive GABA neurons, which are altered in schizophrenia and whose function has been strongly linked to the production of neural synchrony. Alterations of GABA signaling that impair gamma oscillations and, as a result, cognitive function suggest paths for novel therapeutic interventions. PMID:21904685

Impact of Education on Memory Deficits in Subclinical Depression.

PubMed

McLaren, Molly E; Szymkowicz, Sarah M; Kirton, Joshua W; Dotson, Vonetta M

2015-08-01

Elevated depressive symptoms are associated with cognitive deficits, while higher education protects against cognitive decline. This study was conducted to test if education level moderates the relationship between depressive symptoms and cognitive function. Seventy-three healthy, dementia-free adults aged 18-81 completed neuropsychological tests, as well as depression and anxiety questionnaires. Controlling for age, sex, and state anxiety, we found a significant interaction of depressive symptoms and education for immediate and delayed verbal memory, such that those with a higher education level performed well regardless of depressive symptomatology, whereas those with lower education and high depressive symptoms had worse performance. No effects were found for executive functioning or processing speed. Results suggest that education protects against verbal memory deficits in individuals with elevated depressive symptoms. Further research on cognitive reserve in depression-related cognitive deficits and decline is needed to understand the mechanisms behind this phenomenon. © The Author 2015. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Effects of decompressive surgery on prognosis and cognitive deficits in herpes simplex encephalitis.

PubMed

Midi, Ipek; Tuncer, Nese; Midi, Ahmet; Mollahasanoglu, Aynur; Konya, Deniz; Sav, Aydin

2007-01-01

Herpes simplex encephalitis (HSE) is a serious viral infection with a high rate of mortality. The most commonly seen complications are behavioral changes, seizures and memory deficits. We report the case of a 37-year-old man with HSE in the right temporal lobe and a severe midline shift who was treated with acyclovir. The patient underwent anterior temporal lobe resection. Although HSE can cause permanent cognitive deficits, in this case, early surgical intervention minimized any deficit, as determined by detailed neuropsychological examination. Surgical decompression is indicated as early as possible in severe cases. This case report emphasizes the effect of surgical decompression for HSE on cognitive function, which has rarely been mentioned before.

Neurocognitive deficits in older patients with cancer.

PubMed

Edwards, Beatrice J; Zhang, Xiaotao; Sun, Ming; Holmes, Holly M; Ketonen, Leena; Guha, Nandita; Khalil, Peter; Song, Juhee; Kesler, Shelli; Shah, Jay B; Tripathy, Debasish; Valero, Vicente; Champlin, Richard E

2018-03-09

To assess cognitive function in older adults undergoing cancer care. This is a cross-sectional study, in the University of Texas MD Anderson Cancer Center, in older adults undergoing cancer care. Comprehensive geriatric assessments were conducted prior to surgery, chemotherapy or allogeneic stem cell transplantation, at the Program for Healthy Aging from January 1, 2013 through March 31, 2015. Cognitive assessment was conducted through personal and family interview, and the Montreal cognitive assessment (MoCA). Functional, physical, nutritional, social support, comorbidity assessment and medication review were conducted. Patients with mild cognitive impairment (MCI) or dementia were compared to patients who were cognitively intact. One hundred and ninety-two patients underwent geriatric assessment, mean (±SD) age was 78 ± 7 years, 121 (63%) had some degree of neurocognitive deficit, with 64 patients (33%) presenting with major neurocognitive deficit (dementia), and 57 cases (30%), minor neurocognitive deficit (MCI). Early stage dementia was evident in 50% of cases, moderate stage in 32%, and severe stage in 18%. The prevalence of dementia and MCI were higher than in the general population studies (70-79 years). Associated factors for neurocognitive deficits as compared to older patients with cancer with normal cognition, included a higher comorbidity index (p = 0.04), stroke (p = 0.03), metastatic disease (p = 0.04), and warfarin use (p = 0.03). Neurocognitive deficits (MCI and dementia) are more common in older adults with cancer. Factors associated with neurocognitive deficits include high comorbidity, stroke, warfarin use and metastatic cancer. Identification and management of these conditions is of great relevance in the course of cancer therapy. Copyright © 2018. Published by Elsevier Ltd.

Ursolic acid improves domoic acid-induced cognitive deficits in mice

DOE Office of Scientific and Technical Information (OSTI.GOV)

Wu, Dong-mei; Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Xuzhou Normal University, Xuzhou 221116, Jiangsu Province; Lu, Jun, E-mail: lu-jun75@163.com

Our previous findings suggest that mitochondrial dysfunction is the mechanism underlying cognitive deficits induced by domoic acid (DA). Ursolic acid (UA), a natural triterpenoid compound, possesses many important biological functions. Evidence shows that UA can activate PI3K/Akt signaling and suppress Forkhead box protein O1 (FoxO1) activity. FoxO1 is an important regulator of mitochondrial function. Here we investigate whether FoxO1 is involved in the oxidative stress-induced mitochondrial dysfunction in DA-treated mice and whether UA inhibits DA-induced mitochondrial dysfunction and cognitive deficits through regulating the PI3K/Akt and FoxO1 signaling pathways. Our results showed that FoxO1 knockdown reversed the mitochondrial abnormalities and cognitivemore » deficits induced by DA in mice through decreasing HO-1 expression. Mechanistically, FoxO1 activation was associated with oxidative stress-induced JNK activation and decrease of Akt phosphorylation. Moreover, UA attenuated the mitochondrial dysfunction and cognitive deficits through promoting Akt phosphorylation and FoxO1 nuclear exclusion in the hippocampus of DA-treated mice. LY294002, an inhibitor of PI3K/Akt signaling, significantly decreased Akt phosphorylation in the hippocampus of DA/UA mice, which weakened UA actions. These results suggest that UA could be recommended as a possible candidate for the prevention and therapy of cognitive deficits in excitotoxic brain disorders. - Highlights: • Ursolic acid (UA) is a naturally triterpenoid compound. • UA attenuated the mitochondrial dysfunction and cognitive deficits. • Mechanistically, UA activates PI3K/Akt signaling and suppresses FoxO1 activity. • UA could be recommended as a possible candidate for anti-excitotoxic brain disorders.« less

Visual cognition in amnesic H.M.: selective deficits on the What's-Wrong-Here and Hidden-Figure tasks.

PubMed

MacKay, Donald G; James, Lori E

2009-10-01

Two experiments compared the visual cognition performance of amnesic H.M. and memory-normal controls matched for age, background, intelligence, and education. In Experiment 1 H.M. exhibited deficits relative to the controls in detecting "erroneous objects" in complex visual scenes--for example, a bird flying inside a fishbowl. In Experiment 2 H.M. exhibited deficits relative to the controls in standard Hidden-Figure tasks when detecting unfamiliar targets but not when detecting familiar targets--for example, circles, squares, and right-angle triangles. H.M.'s visual cognition deficits were not due to his well-known problems in explicit learning and recall, inability to comprehend or remember the instructions, general slowness, motoric difficulties, low motivation, low IQ relative to the controls, or working-memory limitations. Parallels between H.M.'s selective deficits in visual cognition, language, and memory are discussed. These parallels contradict the standard "systems theory" account of H.M.'s condition but comport with the hypothesis that H.M. has difficulty representing unfamiliar but not familiar information in visual cognition, language, and memory. Implications of our results are discussed for binding theory and the ongoing debate over what counts as "memory" versus "not-memory."

Neuroprotective potential of sesamol and its loaded solid lipid nanoparticles in ICV-STZ-induced cognitive deficits: behavioral and biochemical evidence.

PubMed

Sachdeva, Anand Kamal; Misra, Shubham; Pal Kaur, Indu; Chopra, Kanwaljit

2015-01-15

Neuroinflammation is a prominent feature of Alzheimer disease (AD) and other chronic neurodegenerative disorders. Intracerebroventricular (ICV) streptozotocin (STZ) induced-cognitive impairment has been widely used as an experimental paradigm of Alzheimer׳s disease. Sesamol is a potent inhibitor of cytokine production as well as an antioxidant. The present study was designed to evaluate the effectiveness of sesamol in ICV-STZ-induced cognitive deficits in rats by incorporating it into solid lipid nanoparticles (SLNs). ICV-STZ administration produced significant cognitive deficits as assessed by both Morris water maze and elevated plus maze task which is accompanied by significantly enhanced nitrodative stress, altered acetylcholinesterase in rat brain along with significantly increased serum TNF-α levels. Chronic treatment with sesamol and sesamol loaded SLNs dose dependently restored cognitive deficits in ICV-STZ rats along with mitigation of nitrodative stress and cytokine release. Effectiveness of SLNs to deliver sesamol to the brain was shown by a significantly better alleviation of the oxidative stress parameters. Our findings demonstrate that loading of sesamol in SLNs is an effective strategy to mitigate ICV-STZ-induced neuronal dysfunction and memory deficits. Copyright © 2014 Elsevier B.V. All rights reserved.

Changes in Cognition and Decision Making Capacity Following Brain Tumour Resection: Illustrated with Two Cases.

PubMed

Veretennikoff, Katie; Walker, David; Biggs, Vivien; Robinson, Gail

2017-09-24

Changes in cognition, behaviour and emotion frequently occur in patients with primary and secondary brain tumours. This impacts the ability to make considered decisions, especially following surgical resection, which is often overlooked in the management of patients. Moreover, the impact of cognitive deficits on decision making ability affects activities of daily living and functional independence. The assessment process to ascertain decision making capacity remains a matter of debate. One avenue for evaluating a patient's ability to make informed decisions in the context of brain tumour resection is neuropsychological assessment. This involves the assessment of a wide range of cognitive abilities on standard measurement tools, providing a robust approach to ascertaining capacity. Evidence has shown that a comprehensive and tailored neuropsychological assessment has greater sensitivity than brief cognitive screening tools to detect subtle and/or specific cognitive deficits in brain tumours. It is the precise nature and severity of any cognitive deficits that determines any implications for decision making capacity. This paper focuses on cognitive deficits and decision making capacity following surgical resection of both benign and malignant, and primary and secondary brain tumours in adult patients, and the implications for patients' ability to consent to future medical treatment and make decisions related to everyday activities.

Changes in Cognition and Decision Making Capacity Following Brain Tumour Resection: Illustrated with Two Cases

PubMed Central

Veretennikoff, Katie; Walker, David; Biggs, Vivien; Robinson, Gail

2017-01-01

Changes in cognition, behaviour and emotion frequently occur in patients with primary and secondary brain tumours. This impacts the ability to make considered decisions, especially following surgical resection, which is often overlooked in the management of patients. Moreover, the impact of cognitive deficits on decision making ability affects activities of daily living and functional independence. The assessment process to ascertain decision making capacity remains a matter of debate. One avenue for evaluating a patient’s ability to make informed decisions in the context of brain tumour resection is neuropsychological assessment. This involves the assessment of a wide range of cognitive abilities on standard measurement tools, providing a robust approach to ascertaining capacity. Evidence has shown that a comprehensive and tailored neuropsychological assessment has greater sensitivity than brief cognitive screening tools to detect subtle and/or specific cognitive deficits in brain tumours. It is the precise nature and severity of any cognitive deficits that determines any implications for decision making capacity. This paper focuses on cognitive deficits and decision making capacity following surgical resection of both benign and malignant, and primary and secondary brain tumours in adult patients, and the implications for patients’ ability to consent to future medical treatment and make decisions related to everyday activities. PMID:28946652

Cognitive flexibility: A trait of bipolar disorder that worsens with length of illness.

PubMed

O'Donnell, Lisa A; Deldin, Patricia J; Pester, Bethany; McInnis, Melvin G; Langenecker, Scott A; Ryan, Kelly A

2017-12-01

Deficits in cognitive flexibility, a difficulty altering thoughts and behavioral responses in a changing environment, are found in individuals with bipolar disorder (BD) and are associated with poor social and work functioning. However, the current literature is inconsistent in clarifying the long-term nature of these deficits for those with BD. We administered a common task of cognitive flexibility, the Wisconsin Card Sorting Task (WCST) and accounted for demographics, clinical, and cognitive features of BD, to determine the state versus trait characteristics of these deficits. The Wisconsin Card Sorting Test (WCST) was administered to 154 adults with BD and 95 healthy controls twice, one year apart. The main findings show that cognitive inflexibility is a trait feature of BD, independent of clinical features, that may modestly worsen over time due to the presence of certain demographic, cognitive, and functional features of the disorder. In addition, improvements in WCST performance over an extended period of time in both those with and those without already existing cognitive flexibility deficits indicate potential practice effects. These findings suggest that the implementation of early interventions before the illness progresses could potentially prevent further cognitive impairment, mitigate functional outcomes, and improve the quality of life of the individual with BD.

Cognitive Abilities on Transitive Inference Using a Novel Touchscreen Technology for Mice

PubMed Central

Silverman, J.L.; Gastrell, P.T.; Karras, M.N.; Solomon, M.; Crawley, J.N.

2015-01-01

Cognitive abilities are impaired in neurodevelopmental disorders, including autism spectrum disorder (ASD) and schizophrenia. Preclinical models with strong endophenotypes relevant to cognitive dysfunctions offer a valuable resource for therapeutic development. However, improved assays to test higher order cognition are needed. We employed touchscreen technology to design a complex transitive inference (TI) assay that requires cognitive flexibility and relational learning. C57BL/6J (B6) mice with good cognitive skills and BTBR T+tf/J (BTBR), a model of ASD with cognitive deficits, were evaluated in simple and complex touchscreen assays. Both B6 and BTBR acquired visual discrimination and reversal. BTBR displayed deficits on components of TI, when 4 stimuli pairs were interspersed, which required flexible integrated knowledge. BTBR displayed impairment on the A > E inference, analogous to the A > E deficit in ASD. B6 and BTBR mice both reached criterion on the B > D comparison, unlike the B > D impairment in schizophrenia. These results demonstrate that mice are capable of complex discriminations and higher order tasks using methods and equipment paralleling those used in humans. Our discovery that a mouse model of ASD displays a TI deficit similar to humans with ASD supports the use of the touchscreen technology for complex cognitive tasks in mouse models of neurodevelopmental disorders. PMID:24293564

Understanding the effects of stimulant medications on cognition in individuals with attention-deficit hyperactivity disorder: a decade of progress.

PubMed

Swanson, James; Baler, Ruben D; Volkow, Nora D

2011-01-01

The use of stimulant drugs for the treatment of children with attention-deficit hyperactivity disorder (ADHD) is one of the most widespread pharmacological interventions in child psychiatry and behavioral pediatrics. This treatment is well grounded on controlled studies showing efficacy of low oral doses of methylphenidate and amphetamine in reducing the behavioral symptoms of the disorder as reported by parents and teachers, both for the cognitive (inattention and impulsivity) and non-cognitive (hyperactivity) domains. Our main aim is to review the objectively measured cognitive effects that accompany the subjectively assessed clinical responses to stimulant medications. Recently, methods from the cognitive neurosciences have been used to provide information about brain processes that underlie the cognitive deficits of ADHD and the cognitive effects of stimulant medications. We will review some key findings from the recent literature, and then offer interpretations of the progress that has been made over the past decade in understanding the cognitive effects of stimulant medication on individuals with ADHD.

Stable cognitive deficits in schizophrenia patients with comorbid obsessive-compulsive symptoms: a 12-month longitudinal study.

PubMed

Schirmbeck, Frederike; Rausch, Franziska; Englisch, Susanne; Eifler, Sarah; Esslinger, Christine; Meyer-Lindenberg, Andreas; Zink, Mathias

2013-11-01

Amongst schizophrenia patients, a large subgroup of up to 25% also suffers from comorbid obsessive-compulsive symptoms (OCSs). The association between comorbid OCSs in these patients and neuropsychological impairment remains unclear and somewhat contradictory. Longitudinal approaches investigating the stability of OCS-associated cognitive deficits are missing. Thirty-seven patients with schizophrenia and comorbid OCSs and 43 schizophrenia patients without OCS were assessed with a comprehensive cognitive test battery and compared at baseline and, again, 12 months later. Schizophrenia patients with comorbid OCSs showed significant pronounced deficits, with increasing effect sizes over the 12-month assessment period in specific cognitive areas such as visuospatial perception and visual memory (WAIS-R block design, Rey-Osterrieth Complex Figure Test), executive functioning (perseveration in the Wisconsin Card Sorting test), and cognitive flexibility (Trail Making test B). These cognitive domains are correlated with OCS severity and are known to be candidate cognitive domains in obsessive-compulsive disorder (OCD). OCSs in schizophrenia is associated with specific and longitudinally stable cognitive deficits, strongly arguing for at least partially overlapping neurobiological mechanisms with OCD. Prospective studies involving patients with at-risk mental states for psychosis are necessary to decipher the interaction of cognitive impairment and the clinical manifestations of schizophrenia and OCSs. This might facilitate the definition of patients at high risk for OCSs, an early detection of subclinical levels, therapeutic interventions, and clinical monitoring.

Concurrent and Prospective Effects of Psychopathic Traits on Affective and Cognitive Empathy in a Community Sample of Late Adolescents

ERIC Educational Resources Information Center

Brouns, Bart H. J.; de Wied, Minet Annette; Keijsers, Loes; Branje, Susan; van Goozen, Stephanie H. M.; Meeus, Wim H. J.

2013-01-01

Background: A deficit in affective rather than cognitive empathy is thought to be central to psychopathic traits. However, empirical evidence for empathy deficits in adolescents with psychopathic traits is limited. We investigated the concurrent and prospective effects of psychopathic traits on affective and cognitive trait empathy in late…

The Association Between Callous-Unemotional Traits, Externalizing Problems, and Gender in Predicting Cognitive and Affective Morality Judgments in Adolescence.

PubMed

Fragkaki, Iro; Cima, Maaike; Meesters, Cor

2016-09-01

Morality deficits have been linked to callous-unemotional traits and externalizing problems in response to moral dilemmas, but these associations are still obscure in response to antisocial acts in adolescence. Limited evidence on young boys suggested that callous-unemotional traits and externalizing problems were associated with affective but not cognitive morality judgments. The present study investigated these associations in a community sample of 277 adolescents (M age  = 15.35, 64 % females). Adolescents with high callous-unemotional traits showed deficits in affective but not cognitive morality, indicating that they can identify the appropriate moral emotions in others, but experience deviant moral emotions when imagining themselves committing antisocial acts. Externalizing problems and male gender were also strongly related to deficits in affective morality, but they had smaller associations with deficits in cognitive morality too. Implications for treatment and the justice system are discussed.

Temporary microglia-depletion after cosmic radiation modifies phagocytic activity and prevents cognitive deficits.

PubMed

Krukowski, Karen; Feng, Xi; Paladini, Maria Serena; Chou, Austin; Sacramento, Kristen; Grue, Katherine; Riparip, Lara-Kirstie; Jones, Tamako; Campbell-Beachler, Mary; Nelson, Gregory; Rosi, Susanna

2018-05-18

Microglia are the main immune component in the brain that can regulate neuronal health and synapse function. Exposure to cosmic radiation can cause long-term cognitive impairments in rodent models thereby presenting potential obstacles for astronauts engaged in deep space travel. The mechanism/s for how cosmic radiation induces cognitive deficits are currently unknown. We find that temporary microglia depletion, one week after cosmic radiation, prevents the development of long-term memory deficits. Gene array profiling reveals that acute microglia depletion alters the late neuroinflammatory response to cosmic radiation. The repopulated microglia present a modified functional phenotype with reduced expression of scavenger receptors, lysosome membrane protein and complement receptor, all shown to be involved in microglia-synapses interaction. The lower phagocytic activity observed in the repopulated microglia is paralleled by improved synaptic protein expression. Our data provide mechanistic evidence for the role of microglia in the development of cognitive deficits after cosmic radiation exposure.

Cognitive deficits in problematic drinkers with and without mild to borderline intellectual disability.

PubMed

van Duijvenbode, Neomi; Didden, Robert; VanDerNagel, Joanne El; Korzilius, Hubert Plm; Engels, Rutger Cme

2018-03-01

We examined cognitive deficits in problematic drinkers with and without mild to borderline intellectual disability (MBID). Problematic drinkers were expected to show a significantly lower estimated performance IQ (PIQ), but not a lower estimated verbal IQ (VIQ), compared to light drinkers. Participants ( N = 474) were divided into four groups based on IQ and severity of alcohol use-related problems. IQ was estimated using (a short form of) the Wechsler Adult Intelligence Scale third edition. Severity of alcohol use-related problems was assessed using the Alcohol Use Disorder Identification Test. Overall, there were no significant differences between light and problematic drinkers on estimated VIQ. Within the group without MBID, estimated PIQ was significantly lower. Estimated PIQ was not lower in problematic drinkers with MBID compared to light drinkers with MBID. The results are indicative of cognitive deficits in problematic drinkers without MBID. Screening for cognitive deficits with additional instruments is advised.

Prevention of Severe Hypoglycemia-Induced Brain Damage and Cognitive Impairment with Verapamil.

PubMed

Jackson, David A; Michael, Trevin; Vieira de Abreu, Adriana; Agrawal, Rahul; Bortolato, Marco; Fisher, Simon J

2018-05-03

People with insulin-treated diabetes are uniquely at risk for severe hypoglycemia-induced brain damage. Since calcium influx may mediate brain damage, we tested the hypothesis that the calcium channel blocker, verapamil, would significantly reduce brain damage and cognitive impairment caused by severe hypoglycemia. Ten-week-old Sprague-Dawley rats were randomly assigned to one of three treatments; 1) control hyperinsulinemic (200 mU.kg -1 min -1 ) euglycemic (80-100mg/dl) clamps (n=14), 2) hyperinsulinemic hypoglycemic (10-15mg/dl) clamps (n=16), or 3) hyperinsulinemic hypoglycemic clamps followed by a single treatment with verapamil (20mg/kg) (n=11). As compared to euglycemic controls, hypoglycemia markedly increased dead/dying neurons in the hippocampus and cortex, by 16-fold and 14-fold, respectively. Verapamil treatment strikingly decreased hypoglycemia-induced hippocampal and cortical damage, by 87% and 94%, respectively. Morris Water Maze probe trial results demonstrated that hypoglycemia induced a retention, but not encoding, memory deficit (noted by both abolished target quadrant preference and reduced target quadrant time). Verapamil treatment significantly rescued spatial memory as noted by restoration of target quadrant preference and target quadrant time. In summary, a one-time treatment with verapamil following severe hypoglycemia prevented neural damage and memory impairment caused by severe hypoglycemia. For people with insulin treated diabetes, verapamil may be a useful drug to prevent hypoglycemia-induced brain damage. © 2018 by the American Diabetes Association.

Agmatine for combined treatment of epilepsy, depression and cognitive impairment in chronic epileptic animals.

PubMed

Singh, Tanveer; Bagga, Neetu; Kaur, Anureet; Kaur, Navjot; Gawande, Dinesh Yugraj; Goel, Rajesh Kumar

2017-08-01

Epilepsy is fourth most common neurological disorders associated with depression and cognitive deficits. As per present scenario, none of the antiseizure drugs have been reported successful to have ameliorative effect on epilepsy associated depression and cognitive deficits. Thus, the study was envisioned to assess an ameliorative potential of agmatine on epilepsy and its efficacy and safety for management of associated depression and cognitive deficits. The animals were made epileptic employing pentylenetetrazole (35mg/kg i.p. every 48±2h) kindling model of epilepsy and subsequently were treated with vehicle, valproic acid (300mg/kg/day i.p.) and agmatine (2.5, 5, and 10mg/kg)/day/i.p. for 15days. Except naïve, all the groups were challenged with same pentylenetetrazole dose as employed during kindling on days 5, 10, and 15 to evaluate seizure severity. Two hours after seizure severity test, tail suspension test and passive shock avoidance paradigm was employed to evaluate depression and cognitive behavior respectively. Results suggested that epileptic animals were significantly associated with depression and cognitive impairment. Chronic valproate treatment significantly reduced seizure severity, but was found unable to mitigate depression and cognitive deficits. However, agmatine treatment dose dependently ameliorated seizure severity as well as associated depression and cognitive deficits. On 15th day, animals were euthanized and pertinent neurochemical estimations were carried out in cortical and hippocampal areas of the mice brain. Thus, study concluded that agmatine ameliorated seizure severity, depression and cognitive impairment in epileptic animals, possibly via restoring glutamate-GABA neurotransmission and serotonin synthesis with decreased nitrosative stress. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Cognitive and Physical Function in Relation to the Risk of Injurious Falls in Older Adults: A Population-Based Study.

PubMed

Welmer, Anna-Karin; Rizzuto, Debora; Laukka, Erika J; Johnell, Kristina; Fratiglioni, Laura

2017-05-01

We aimed to quantify the independent effect of cognitive and physical deficits on the risk of injurious falls, to verify whether this risk is modified by global cognitive impairment, and to explore whether risk varies by follow-up time. Data on 2,495 participants (≥60 years) from the population-based Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) study were analyzed using flexible parametric survival models. Two cognitive domains (processing speed and executive function) were assessed with standard tests. Physical function tests included balance (one-leg-stands), walking speed, chair stands, and grip strength. Global cognition was assessed using the Mini-Mental State Examination. A total of 167 people experienced an injurious fall over 3 years of follow-up, 310 over 5 years, and 571 over 10 years. Each standard deviation worse balance, slower walking speed, and longer chair stand time increased the risk of injurious falls over 3 years by 43%, 38%, and 23%, respectively (p < .05). Each standard deviation worse processing speed and executive function was significantly associated with 10% increased risk of injurious falls over 10 years (p < .05). In stratified analyses, deficits in physical functioning were associated with injurious falls only in people with cognitive impairment, whereas deficits in processing speed and executive function were associated with injurious falls only in people without cognitive impairment. Deficits in specific cognitive domains, such as processing speed and executive function, appear to predict injurious falls in the long term. Deficits in physical function predict falls in the short term, especially in people with global cognitive impairment. © The Author 2016. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Cognitive functioning over 2 years after intracerebral hemorrhage in school-aged children.

PubMed

Murphy, Lexa K; Compas, Bruce E; Gindville, Melissa C; Reeslund, Kristen L; Jordan, Lori C

2017-11-01

Previous research investigating outcomes after pediatric intracerebral hemorrhage (ICH) has generally been limited to global and sensorimotor outcomes. This study examined cognitive outcomes after spontaneous ICH in school-aged children with serial assessments over 2 years after stroke. Seven children (age range 6-16y, median 13; six males, one female; 57% white, 43% black) presenting with spontaneous ICH (six arteriovenous malformations) were assessed at 3 months, 12 months, and 24 months after stroke. The Pediatric Stroke Outcome Measure (PSOM) quantified neurological outcome and Wechsler Intelligence Scales measured cognitive outcomes: verbal comprehension, perceptual reasoning, working memory, and processing speed. PSOM scales showed improved neurological function over the first 12 months, with mild to no sensorimotor deficits and moderate overall deficits at 1- and 2-year follow-ups (median 2-year sensorimotor PSOM=0.5, total PSOM=1.5). Changes in cognitive function indicated a different trajectory; verbal comprehension and perceptual reasoning improved over 24 months; low performance was sustained in processing speed and working memory. Age-normed centile scores decreased between 1- and 2-year follow-ups for working memory, suggesting emerging deficits compared with peers. Early and serial cognitive testing in children with ICH is needed to assess cognitive functioning and support children in school as they age and cognitive deficits become more apparent and important for function. In children with intracerebral hemorrhage (ICH), motor function improved between 3 months and 24 months. Improvements in cognitive function were variable between 3 months and 24 months. Working memory centiles declined, suggesting emerging deficits compared with peers. Processing speed improved but remained significantly below the 50th centile. Cognitive impact of ICH may increase with age in children. © 2017 Mac Keith Press.

Adult cognitive outcomes following childhood mild traumatic brain injuries.

PubMed

Yumul, Joy Noelle; McKinlay, Audrey

2017-10-01

To investigate the adult cognitive outcomes of one versus multiple childhood mTBI and to examine the potential predictors of the outcomes. Review of neurosurgical files and hospital records, as well as community recruitment, yielded 169 participants, who were injured between ages 0-17 years and assessed between ages 18-30 years with at least five years post-injury. Each participant underwent a three-hour assessment. For data analysis, participants were grouped by type and number of injury. The mTBI group exhibited some cognitive deficits but their performance fell between the control and moderate/severe TBI groups as expected. Those with one and multiple mTBI performed comparably across all cognitive domains. Cognitive outcomes were significantly predicted by estimated IQ but not by number of mTBI and age at injury. Despite the detected cognitive deficits, those who sustained multiple mTBI did not exhibit worse or cumulative deficits compared to those with one mTBI.

Hypoglycemia induced by insulin as a triggering factor of cognitive deficit in diabetic children.

PubMed

Rodrigues Vilela, Vanessa; de Castro Ruiz Marques, Any; Schamber, Christiano Rodrigues; Bazotte, Roberto Barbosa

2014-01-01

This paper provides an overview of insulin-induced hypoglycemia as a triggering factor of cognitive deficit in children with type 1 diabetes mellitus. For this purpose, databases from 1961 to 2013 were used with the objective of detecting the primary publications that address the impact of hypoglycemia on cognitive performance of diabetic children. The results obtained from experimental animals were excluded. The majority of studies demonstrated that the cognitive deficit in diabetic children involves multiple factors including duration, intensity, severity, and frequency of hypoglycemia episodes. Additionally, age at the onset of type 1 diabetes also influences the cognitive performance, considering that early inception of the disease is a predisposing factor for severe hypoglycemia. Furthermore, the results suggest that there is a strong correlation between brain damage caused by hypoglycemia and cognitive deterioration. Therefore, a more cautious follow-up and education are needed to impede and treat hypoglycemia in children with diabetes mellitus.

Cognitive Deficits and Related Brain Lesions in Patients With Chronic Heart Failure.

PubMed

Frey, Anna; Sell, Roxane; Homola, György A; Malsch, Carolin; Kraft, Peter; Gunreben, Ignaz; Morbach, Caroline; Alkonyi, Bálint; Schmid, Eric; Colonna, Isabella; Hofer, Edith; Müllges, Wolfgang; Ertl, Georg; Heuschmann, Peter; Solymosi, László; Schmidt, Reinhold; Störk, Stefan; Stoll, Guido

2018-05-31

This study sought to determine the spectrum of brain lesions seen in heart failure (HF) patients and the extent to which lesion type contributes to cognitive impairment. Cognitive deficits have been reported in patients with HF. A total of 148 systolic and diastolic HF patients (mean age 64 ± 11 years; 16% female; mean left ventricular ejection fraction 43 ± 8%) were extensively evaluated within 2 days by cardiological, neurological, and neuropsychological testing and brain magnetic resonance imaging (MRI). A total of 288 healthy, sex- and age-matched subjects sampled from the Austrian Stroke Prevention Study served as MRI controls. Deficits in reaction times were apparent in 41% of patients and deficits in verbal memory in 46%. On brain MRI, patients showed more advanced medial temporal lobe atrophy (MTA) (Scheltens score) compared to controls (2.1 ± 0.9 vs. 1.0 ± 0.6; p < 0.001). The degree of MTA was strongly associated with the severity of cognitive impairment, whereas the extent of white matter hyperintensities was similar in patients and controls. Moreover, patients had a 2.7-fold increased risk for presence of clinically silent lacunes. HF patients exhibit cognitive deficits in the domains of attention and memory. MTA but not white matter lesion load seems to be related to cognitive impairment. Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Hot and cold cognition in unmedicated depressed subjects with bipolar disorder.

PubMed

Roiser, Jonathan P; Cannon, Dara M; Gandhi, Shilpa K; Taylor Tavares, Joana; Erickson, Kristine; Wood, Suzanne; Klaver, Jacqueline M; Clark, Luke; Zarate, Carlos A; Sahakian, Barbara J; Drevets, Wayne C

2009-03-01

Neuropsychological studies in subjects with bipolar disorder (BD) have reported deficits on a variety of cognitive measures. However, because the majority of subjects were medicated at the time of testing in previous studies, it is currently unclear whether the pattern of deficits reported is related to BD itself or to psychotropic medication. We addressed this issue by examining cognitive performance in a group of unmedicated, currently depressed subjects with BD. Forty-nine unmedicated subjects who met DSM-IV criteria for BD, depressed phase, and 55 control subjects participated in this study. Most patients were diagnosed with bipolar II disorder. Performance on emotion-dependent, or 'hot', and emotion-independent, or 'cold', cognitive tasks was assessed using tests from the Cambridge Neuropsychological Test Automated Battery. The groups were well matched with respect to general intelligence and demographic variables. Deficits in the unmedicated depressed BD group were apparent on tests tapping 'hot' cognitive processing, for example the Cambridge Gamble task and the Probabilistic Reversal Learning task. However, other than a deficit on the Spatial Span test in the depressed BD subjects, the groups performed equivalently on most measures of 'cold' cognitive processing, for example visual memory, attention, and working memory. These data suggest that deficits on tests involving reward processing, short-term spatial memory storage, and sensitivity to negative feedback in depressed BD subjects represent an effect of the illness itself and not mood-stabilizing medication.

Deficits in social cognition and response flexibility in pediatric bipolar disorder.

PubMed

McClure, Erin B; Treland, Julia E; Snow, Joseph; Schmajuk, Mariana; Dickstein, Daniel P; Towbin, Kenneth E; Charney, Dennis S; Pine, Daniel S; Leibenluft, Ellen

2005-09-01

Little is known about neuropsychological and social-cognitive function in patients with pediatric bipolar disorder. Identification of specific deficits and strengths that characterize pediatric bipolar disorder would facilitate advances in diagnosis, treatment, and research on pathophysiology. The purpose of this study was to test the hypothesis that youths with bipolar disorder would perform more poorly than matched healthy comparison subjects on measures of social cognition, motor inhibition, and response flexibility. Forty outpatients with pediatric bipolar disorder and 22 comparison subjects (no differences in age, gender, and IQ) completed measures of social cognition (the pragmatic judgment subtest of the Comprehensive Assessment of Spoken Language, facial expression recognition subtests of the Diagnostic Analysis of Nonverbal Accuracy Scale, the oral expression subtest of the Test of Language Competence), inhibition and response flexibility (stop and stop-change tasks), and motor inhibition (continuous performance tasks). Pediatric bipolar disorder patients performed more poorly than comparison subjects on social-cognitive measures (pragmatic judgment of language, facial expression recognition) and on a task requiring response flexibility. These deficits were present in euthymic patients. Differences between patients and comparison subjects could not be attributed to comorbid attention deficit hyperactivity disorder. Findings of impaired social cognition and response flexibility in youths with pediatric bipolar disorder suggest continuity between pediatric bipolar disorder and adult bipolar disorder. These findings provide a foundation for neurocognitive research designed to identify the neural mechanisms underlying these deficits.

Effects of Decompressive Surgery on Prognosis and Cognitive Deficits in Herpes Simplex Encephalitis

PubMed Central

Midi, Ipek; Tuncer, Nese; Midi, Ahmet; Mollahasanoglu, Aynur; Konya, Deniz; Sav, Aydın

2007-01-01

Herpes simplex encephalitis (HSE) is a serious viral infection with a high rate of mortality. The most commonly seen complications are behavioral changes, seizures and memory deficits. We report the case of a 37-year-old man with HSE in the right temporal lobe and a severe midline shift who was treated with acyclovir. The patient underwent anterior temporal lobe resection. Although HSE can cause permanent cognitive deficits, in this case, early surgical intervention minimized any deficit, as determined by detailed neuropsychological examination. Surgical decompression is indicated as early as possible in severe cases. This case report emphasizes the effect of surgical decompression for HSE on cognitive function, which has rarely been mentioned before. PMID:18430984

Reading Comprehension in Children with ADHD: Cognitive Underpinnings of the Centrality Deficit

PubMed Central

Miller, Amanda C.; Keenan, Janice M.; Betjemann, Rebecca S.; Willcutt, Erik; Pennington, Bruce F.; Olson, Richard K.

2012-01-01

We examined reading comprehension in children with ADHD by assessing their ability to build a coherent mental representation that allows them to recall central and peripheral information. We compared children with ADHD (mean age 9.78) to word reading-matched controls (mean age 9.89) on their ability to retell a passage. We found that even though children with ADHD recalled more central than peripheral information, they showed their greatest deficit, relative to controls, on central information – a centrality deficit (Miller & Keenan, 2009). We explored the cognitive underpinnings of this deficit using regressions to compare how well cognitive factors (working memory, inhibition, processing speed, and IQ) predicted the ability to recall central information, after controlling for word reading ability, and whether these cognitive factors interacted with ADHD symptoms. Working memory accounted for the most unique variance. Although previous evidence for reading comprehension difficulties in children with ADHD have been mixed, this study suggests that even when word reading ability is controlled, children with ADHD have difficulty building a coherent mental representation, and this difficulty is likely related to deficits in working memory. PMID:23054132

Mentalization deficit in bipolar patients during an acute depressive and manic episode: association with cognitive functions.

PubMed

Bodnar, Anna; Rybakowski, Janusz K

2017-12-06

A number of studies in bipolar patients have shown a deficit in mentalization (theory of mind), one of the main aspects of social cognition. The aim of current study was to assess both cognitive and affective mentalization in well-defined groups of depressed and manic bipolar patients, compared to healthy control subjects, using a battery of tests measuring mentalization processes. The second aim was to investigate a possible relationship between cognitive and affective mentalization and cognitive functions in bipolar patients during a depressive and manic episode. The study involved 25 bipolar disorder type I patients (10 male, 15 female) during a depressive episode (mean 24 ± 2 points in the 17-item Hamilton Depression Rating Scale) and 25 patients (10 male, 15 female) during a manic episode (mean 27 ± 4 points in the Young Mania Rating Scale). The control group consisted of 25 healthy subjects (10 male, 15 female) without psychiatric disorders. To measure mentalization, a revised version of the Reading the Mind in the Eyes (R-MET), the Strange Stories (SS), the Faux Pas Recognition (FPR), and the Moving Shapes Paradigm (MSP) tests were used. Assessment of cognitive functioning was made using the Digit Span, Trail Making, and Wisconsin Card Sorting Tests. In bipolar patients significant deficits in both cognitive and affective mentalization were demonstrated during both acute depressive and manic episodes. The impairment in FPR in manic patients was more severe than that in the depressive ones. On the other hand, in MSP, manic patients showed significantly increased intentionality for non-mentalization animations, compared with depressive patients and for "cause and effect" animations compared with control subjects. A significant relationship was found between the decrease in cognitive and affective mentalization and deficits of cognitive functions during both the depressive and manic episodes. The results obtained confirm the deficits of mentalization in bipolar I patients, during both acute depressive and manic episodes. We found that in such patients mentalization deficits significantly correlated with cognitive dysfunctions more so during depressive episodes.

[Neuropsychological changes in schizophrenia and its modification].

PubMed

Penadés, R; Boget, T; Salamero, M; Catarineu, S; Bernardo, M

2000-12-01

The main experimental works about neuropsychological impairments of schizophrenia are reviewed. The underlying mechanisms of the cognitive deficits are set in a framework of the limited capacity model. In second point, the current status of the modificability of the cognitive deficits and the clinical and psychosocial consequences of this deficits are presented. At least, neuropsychological rehabilitation programs are reviewed from a clinical point of view.

Motivational deficits in early schizophrenia: prevalent, persistent, and key determinants of functional outcome.

PubMed

Fervaha, Gagan; Foussias, George; Agid, Ofer; Remington, Gary

2015-08-01

Negative symptoms, in particular motivational deficits, are reported as impediments to functional recovery in patients with schizophrenia. This study examined the prevalence of motivational deficits in patients early in the illness, and the impact these deficits have on community functioning. Patients with schizophrenia between the ages of 18 and 35years, and within 5years of initiating antipsychotic treatment were included in the present investigation (N=166). The impact of motivation and cognition on concurrent and longitudinal functioning was evaluated. Motivational impairments were found in more than 75% of participants, and were not associated with receipt of social support. These deficits served as the most robust and reliable predictor of functional outcome, while neurocognition demonstrated significantly weaker associations with outcome. When considered together, motivational deficits demonstrated a reliable link with concurrent and longitudinal functioning, with cognition not offering any independent predictive value. Moreover, motivation was found to mediate the relationship between cognition and outcome. Changes in motivation were linked to changes in functioning; however, this was not the case for changes in cognitive performance. Motivation emerged as a significant predictor of functioning even after selected demographic and clinical characteristics (e.g., positive symptoms) were accounted for. These data indicate that motivational deficits are prevalent in patients with schizophrenia, even in the early stages of the illness, and these deficits stand as one of the most robust barriers to people with schizophrenia achieving functional recovery. Greater understanding of the mechanisms underlying these deficits is critical to effective treatment innovation. Copyright © 2015 Elsevier B.V. All rights reserved.

Activation of the canonical nuclear factor-κB pathway is involved in isoflurane-induced hippocampal interleukin-1β elevation and the resultant cognitive deficits in aged rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

Li, Zheng-Qian; Rong, Xiao-Ying; Liu, Ya-Jie

Highlights: •Isoflurane induces hippocampal IL-1β elevation and cognitive deficits in aged rats. •Isoflurane transiently activates the canonical NF-κB pathway in aged rat hippocampus. •NF-κB inhibitor mitigates isoflurane-induced IL-1β elevation and cognitive deficits. •We report a linkage between NF-κB signaling, IL-1β expression, and cognitive changes. -- Abstract: Although much recent evidence has demonstrated that neuroinflammation contributes to volatile anesthetic-induced cognitive deficits, there are few existing mechanistic explanations for this inflammatory process. This study was conducted to investigate the effects of the volatile anesthetic isoflurane on canonical nuclear factor (NF)-κB signaling, and to explore its association with hippocampal interleukin (IL)-1β levels andmore » anesthetic-related cognitive changes in aged rats. After a 4-h exposure to 1.5% isoflurane in 20-month-old rats, increases in IκB kinase and IκB phosphorylation, as well as a reduction in the NF-κB inhibitory protein (IκBα), were observed in the hippocampi of isoflurane-exposed rats compared with control rats. These events were accompanied by an increase in NF-κB p65 nuclear translocation at 6 h after isoflurane exposure and hippocampal IL-1β elevation from 1 to 6 h after isoflurane exposure. Nevertheless, no significant neuroglia activation was observed. Pharmacological inhibition of NF-κB activation by pyrrolidine dithiocarbamate markedly suppressed the IL-1β increase and NF-κB signaling, and also mitigated the severity of cognitive deficits in the Morris water maze task. Overall, our results demonstrate that isoflurane-induced cognitive deficits may stem from upregulation of hippocampal IL-1β, partially via activation of the canonical NF-κB pathway, in aged rats.« less

No lower cognitive functioning in older adults with attention-deficit/hyperactivity disorder.

PubMed

Semeijn, E J; Korten, N C M; Comijs, H C; Michielsen, M; Deeg, D J H; Beekman, A T F; Kooij, J J S

2015-09-01

Research illustrates cognitive deficits in children and younger adults with attention-deficit/hyperactivity disorder (ADHD). Few studies have focused on the cognitive functioning in older adults. This study investigates the association between ADHD and cognitive functioning in older adults. Data were collected in a cross-sectional side study of the Longitudinal Aging Study Amsterdam (LASA). A diagnostic interview to diagnose ADHD was administered among a subsample (N = 231, age 60-94). ADHD symptoms and diagnosis were assessed with the Diagnostic Interview for ADHD in Adults (DIVA) 2.0. Cognitive functioning was assessed with tests in the domains of executive functioning, information processing speed, memory, and attention/working memory. Regression analyses indicate that ADHD diagnosis and ADHD severity were only negatively associated with cognitive functioning in the attention/working memory domain. When adjusting for depression, these associations were no longer significant. The study shows that ADHD in older adults is associated with lower cognitive functioning in the attention/working memory domain. However, this was partly explained by depressive symptoms.

T cell deficiency leads to cognitive dysfunction: Implications for therapeutic vaccination for schizophrenia and other psychiatric conditions

PubMed Central

Kipnis, Jonathan; Cohen, Hagit; Cardon, Michal; Ziv, Yaniv; Schwartz, Michal

2004-01-01

The effects of the adaptive immune system on the cognitive performance and abnormal behaviors seen in mental disorders such as schizophrenia have never been documented. Here, we show that mice deprived of mature T cells manifested cognitive deficits and behavioral abnormalities, which were remediable by T cell restoration. T cell-based vaccination, using glatiramer acetate (copolymer-1, a weak agonist of numerous self-reactive T cells), can overcome the behavioral and cognitive abnormalities that accompany neurotransmitter imbalance induced by (+)dizocilpine maleate (MK-801) or amphetamine. The results, by suggesting that peripheral T cell deficit can lead to cognitive and behavioral impairment, highlight the importance of properly functioning adaptive immunity in the maintenance of mental activity and in coping with conditions leading to cognitive deficits. These findings point to critical factors likely to contribute to age- and AIDS-related dementias and might herald the development of a therapeutic vaccination for fighting off cognitive dysfunction and psychiatric conditions. PMID:15141078

Influence of empathetic pain processing on cognition in schizophrenia.

PubMed

Hu, Kesong; Lijffijt, Marijn; Beauchaine, Theodore P; Fan, Zhiwei; Shi, Hui; He, Shuchang

2015-10-01

Deficits in both empathy and cognition have been reported widely in patients with schizophrenia. However, little is known about how these deficits interact among such patients. In the present study, we used pain portraying pictures preceding a color-word Stroop task to investigate the effect of empathetic pain observation on cognition among patients with schizophrenia. Twenty patients with schizophrenia and twenty healthy controls were included. The control group showed increased Stroop facilitation and decreased interference during the empathetic pain condition compared with the non-empathetic condition. Although patients with schizophrenia exhibited deficits in cognition, they demonstrated a similar empathy effect to controls on Stroop facilitation, but a somewhat larger empathy effect on Stroop interference (a more decreased effect). In particular, the groups did not differ in either automatic or controlled processing during the non-empathetic condition, suggesting general rather than specific cognitive deficits in schizophrenia. Together, we interpret our findings in terms of two opposing effects of empathy on cognition in schizophrenia, with possible neuromodulatory mechanism. Whereas prior studies showed empathy to be impaired, our outcomes indicate that at least some components of empathetic pain processing are preserved in such patients.

Exploring social cognition in patients with apathy following acquired brain damage.

PubMed

Njomboro, Progress; Humphreys, Glyn W; Deb, Shoumitro

2014-01-23

Research on cognition in apathy has largely focused on executive functions. To the best of our knowledge, no studies have investigated the relationship between apathy symptoms and processes involved in social cognition. Apathy symptoms include attenuated emotional behaviour, low social engagement and social withdrawal, all of which may be linked to underlying socio-cognitive deficits. We compared patients with brain damage who also had apathy symptoms against similar patients with brain damage but without apathy symptoms. Both patient groups were also compared against normal controls on key socio-cognitive measures involving moral reasoning, social awareness related to making judgements between normative and non-normative behaviour, Theory of Mind processing, and the perception of facial expressions of emotion. We also controlled for the likely effects of executive deficits and depressive symptoms on these comparisons. Our results indicated that patients with apathy were distinctively impaired in making moral reasoning decisions and in judging the social appropriateness of behaviour. Deficits in Theory of Mind and perception of facial expressions of emotion did not distinguish patients with apathy from those without apathy. Our findings point to a possible socio-cognitive profile for apathy symptoms and provide initial insights into how socio-cognitive deficits in patients with apathy may affect social functioning.

Shedding light on the association between repetitive negative thinking and deficits in cognitive control - A meta-analysis.

PubMed

Zetsche, Ulrike; Bürkner, Paul-Christian; Schulze, Lars

2018-06-11

Individuals who experience recurrent negative thoughts are at elevated risk for mood and anxiety disorders. It is thus essential to understand why some individuals get stuck in recurrent negative thinking (RNT), whereas others are able to disengage eventually. Theoretical models propose that individuals high in recurrent negative thinking suffer from deficits in controlling the contents of working memory. Empirical findings, however, are inconclusive. In this meta-analysis, we synthesize findings from 94 studies to examine the proposed association between RNT and deficits in cognitive control. We included numerous effect sizes not reported in the primary publications. Moderator analyses tested the influence of variables, such as stimuli valence, cognitive control function (e.g., shifting, discarding), or type of RNT (i.e., rumination or worry). Results demonstrated an association between repetitive negative thinking and deficits in only one specific cognitive control function, namely difficulty discarding no longer relevant material from working memory (r = -0.20). This association remained significant after controlling for level of psychopathology. There was no substantial association between RNT and deficits in any other cognitive control function. All other moderators were not significant. We discuss limitations (e.g., primary sample sizes, reliability of paradigms) and highlight implications for future research and clinical interventions. Copyright © 2018 Elsevier Ltd. All rights reserved.

Adolescents born prematurely with isolated grade 2 haemorrhage in the early 1990s face increased risks of learning challenges.

PubMed

Vohr, Betty R; Allan, Walter; Katz, Karol H; Schneider, Karen; Tucker, Richard; Ment, Laura R

2014-10-01

To compare the impact of low-grade haemorrhage on neurocognitive function in 16-year-old adolescents born preterm, by grade of intraventricular haemorrhage, and term controls. We evaluated 338 preterm adolescents (birth weight 600-1250 g) for intelligence, executive function and memory tasks. Eleven had grade 3-4 haemorrhage, 44 had grade 2, 31 had grade 1, and 251 had no haemorrhage. Group comparisons were made with 102 term age-matched controls, and regression models used to identify the risk that low-grade haemorrhage posed for cognitive, executive function and memory deficits. Preterm adolescents with grade 2 haemorrhage had higher deficit rates of verbal intelligence, receptive vocabulary, phonemic fluency, cognitive flexibility and phonological fluency than preterm adolescents with grade 1 or no haemorrhage, compared with term controls. After excluding preterm adolescents with both grade 2 haemorrhage and cystic periventricular leukomalacia, those with isolated grade 2 haemorrhage remained at greater risk of cognitive and executive function deficits than term controls and of cognitive deficits than preterm adolescents with no haemorrhage. Our findings suggest that preterm adolescents born in the early 1990s with isolated grade 2 haemorrhage are at increased risk of learning challenges, including cognitive and executive function deficits. ©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

Diagnostic profile of young and middle-aged memory clinic patients.

PubMed

Vraamark Elberling, Tina; Stokholm, Jette; Høgh, Peter; Waldemar, Gunhild

2002-10-22

With the objective of characterizing the underlying conditions in younger patients with cognitive symptoms, 314 consecutive patients were studied, aged <60 years, referred to a multidisciplinary memory clinic over a period of 54 months. Fifteen percent of the patients fulfilled Diagnostic and Statistical Manual IV criteria for dementia, 17% had selective cognitive deficits, and 55% had no cognitive deficits. Cognitive symptoms in younger patients rarely reflect dementia but more often other medical and psychiatric conditions.

Early writing deficits in preschoolers with oral language difficulties.

PubMed

Puranik, Cynthia S; Lonigan, Christopher J

2012-01-01

The purpose of this study was to investigate whether preschool children with language impairments (LI), a group with documented reading difficulties, also experience writing difficulties. In addition, a purpose was to examine if the writing outcomes differed when children had concomitant cognitive deficits in addition to oral language problems. A group of 293 preschool children were administered an assessment battery that included measures to examine oral language, nonverbal cognition, emergent reading, and writing. Children were divided into four groups based on their language and cognitive performance. The findings from this study show that as early as preschool, children with weaker oral language skills lag behind their peers with stronger oral language skills in terms of their writing-related skills. Children with oral language and cognitive deficits performed more poorly than children whose deficits were confined to oral language. A child's cognitive ability also has an impact on emergent writing skills, but it appears to be moderated by oral language skills. These results are consistent with research documenting links between preschool language and emergent reading in children with a history of LI. © Hammill Institute on Disabilities 2012.

Early Writing Deficits in Preschoolers with Oral Language Difficulties

PubMed Central

Puranik, Cynthia S.; Lonigan, Christopher J.

2016-01-01

The purpose of this study was to investigate whether preschool children with language impairments (LI), a group with documented reading difficulties, also experience writing difficulties. In addition, a purpose was to examine if the writing outcomes differed when children had concomitant cognitive deficits in addition to oral language problems. A group of 293 preschool children were administered an assessment battery that included measures to examine oral language, nonverbal cognition, emergent reading, and writing. Children were divided into four groups based on their language and cognitive performance. The findings from this study show that as early as preschool, children with weaker oral language skills lag behind their peers with stronger oral language skills in terms of their writing-related skills. Children with oral language and cognitive deficits performed more poorly than children whose deficits were confined to oral language. A child’s cognitive ability also has an impact on emergent writing skills, but it appears to be moderated by oral language skills. These results are consistent with research documenting links between preschool language and emergent reading in children with a history of LI. PMID:22043027

Cognitive Training and Work Therapy for the Treatment of Verbal Learning and Memory Deficits in Veterans With Alcohol Use Disorders.

PubMed

Bell, Morris D; Vissicchio, Nicholas A; Weinstein, Andrea J

2016-01-01

This study focused on the efficacy of cognitive training for verbal learning and memory deficits in a population of older veterans with alcohol use disorders. Veterans with alcohol use disorders, who were in outpatient treatment at VA facilities and in early-phase recovery (N = 31), were randomized to receive a three-month trial of daily cognitive training plus work therapy (n = 15) or work therapy alone (n = 16), along with treatment as usual. Participants completed assessments at baseline and at three- and six-month follow-ups; the Hopkins Verbal Learning Task (HVLT) was the primary outcome measure. Participants were primarily male (97%) and in their mid-50s (M = 55.16, SD = 5.16) and had been sober for 1.64 (SD = 2.81) months. Study retention was excellent (91% at three-month follow-up) and adherence to treatment in both conditions was very good. On average, participants in the cognitive training condition had more than 41 hours of cognitive training, and both conditions had more than 230 hours of productive activity. HVLT results at three-month follow-up revealed significant condition effects favoring cognitive training for verbal learning (HVLT Trial-3 T-score, p < .005, Cohen's d = 1.3) and verbal memory (HVLT Total T-score, p < .01, Cohen's d = 1.1). Condition effects were sustained at six-month follow-up. At baseline, 55.9% of participants showed a significant deficit in verbal memory and 58.8% showed a deficit in verbal learning compared with a premorbid estimate of verbal IQ. At three-month follow-up there was a significant reduction in the number of participants in the cognitive training condition with clinically significant verbal memory deficits (p < .01, number needed to treat = 3.0) compared with the work therapy alone condition and a trend toward significance for verbal learning deficits, which was not sustained at six-month follow-up. This National Institute on Drug Abuse-funded pilot study demonstrates that cognitive training within the context of another activating intervention (work therapy) may have efficacy in remediating verbal learning and memory deficits in patients with alcohol use disorder. Findings indicate a large effect for cognitive training in this pilot study, which suggests that further research is warranted. This study is registered on ClinicalTrials.gov (NCT 01410110).

Behavioral and cognitive outcomes for clinical trials in children with neurofibromatosis type 1.

PubMed

van der Vaart, Thijs; Rietman, André B; Plasschaert, Ellen; Legius, Eric; Elgersma, Ype; Moll, Henriëtte A

2016-01-12

To evaluate the appropriateness of cognitive and behavioral outcome measures in clinical trials in neurofibromatosis type 1 (NF1) by analyzing the degree of deficits compared to reference groups, test-retest reliability, and how scores correlate between outcome measures. Data were analyzed from the Simvastatin for cognitive deficits and behavioral problems in patients with neurofibromatosis type 1 (NF1-SIMCODA) trial, a randomized placebo-controlled trial of simvastatin for cognitive deficits and behavioral problems in children with NF1. Outcome measures were compared with age-specific reference groups to identify domains of dysfunction. Pearson r was computed for before and after measurements within the placebo group to assess test-retest reliability. Principal component analysis was used to identify the internal structure in the outcome data. Strongest mean score deviations from the reference groups were observed for full-scale intelligence (-1.1 SD), Rey Complex Figure Test delayed recall (-2.0 SD), attention problems (-1.2 SD), and social problems (-1.1 SD). Long-term test-retest reliability were excellent for Wechsler scales (r > 0.88), but poor to moderate for other neuropsychological tests (r range 0.52-0.81) and Child Behavioral Checklist subscales (r range 0.40-0.79). The correlation structure revealed 2 strong components in the outcome measures behavior and cognition, with no correlation between these components. Scores on psychosocial quality of life correlate strongly with behavioral problems and less with cognitive deficits. Children with NF1 show distinct deficits in multiple domains. Many outcome measures showed weak test-retest correlations over the 1-year trial period. Cognitive and behavioral outcomes are complementary. This analysis demonstrates the need to include reliable outcome measures on a variety of cognitive and behavioral domains in clinical trials for NF1. © 2015 American Academy of Neurology.

Regional neuronal network failure and cognition in late-onset sporadic Alzheimer disease.

PubMed

Carter, S F; Embleton, K V; Anton-Rodriguez, J M; Burns, A; Ralph, M A L; Herholz, K

2014-06-01

The severe cognitive deficits in Alzheimer disease are associated with structural lesions in gray and white matter in addition to changes in synaptic function. The current investigation studied the breakdown of the structure and function in regional networks involving the Papez circuit and extended neocortical association areas. Cortical volumetric and diffusion tensor imaging (3T MR imaging), positron-emission tomography with (18)F fluorodeoxyglucose on a high-resolution research tomograph, and comprehensive neuropsychological assessments were performed in patients with late-onset sporadic Alzheimer disease, those with mild cognitive impairment, and elderly healthy controls. Atrophy of the medial temporal lobes was the strongest and most consistent abnormality in patients with mild cognitive impairment and Alzheimer disease. Atrophy in the temporal, frontal, and parietal regions was most strongly related to episodic memory deficits, while deficits in semantic cognition were also strongly related to reductions of glucose metabolism in the posterior cingulate cortex and temporoparietal regions. Changes in fractional anisotropy within white matter tracts, particularly in the left cingulum bundle, uncinate fasciculus, superior longitudinal fasciculus, and inferior fronto-occipital fasciculus, were significantly associated with the cognitive deficits in multiple regression analyses. Posterior cingulate and orbitofrontal metabolic deficits appeared to be related to microstructural changes in projecting white matter tracts. Many lesioned network components within the Papez circuit and extended neocortical association areas were significantly associated with cognitive dysfunction in both mild cognitive impairment and late-onset sporadic Alzheimer disease. Hippocampal atrophy was the most prominent lesion, with associated impairment of the uncinate and cingulum white matter microstructures and hippocampal and posterior cingulate metabolic impairment. © 2014 by American Journal of Neuroradiology.

Primary empathy deficits in frontotemporal dementia.

PubMed

Baez, Sandra; Manes, Facundo; Huepe, David; Torralva, Teresa; Fiorentino, Natalia; Richter, Fabian; Huepe-Artigas, Daniela; Ferrari, Jesica; Montañes, Patricia; Reyes, Pablo; Matallana, Diana; Vigliecca, Nora S; Decety, Jean; Ibanez, Agustin

2014-01-01

Loss of empathy is an early central symptom and diagnostic criterion of the behavioral variant frontotemporal dementia (bvFTD). Although changes in empathy are evident and strongly affect the social functioning of bvFTD patients, few studies have directly investigated this issue by means of experimental paradigms. The current study assessed multiple components of empathy (affective, cognitive and moral) in bvFTD patients. We also explored whether the loss of empathy constitutes a primary deficit of bvFTD or whether it is explained by impairments in executive functions (EF) or other social cognition domains. Thirty-seven bvFTD patients with early/mild stages of the disease and 30 healthy control participants were assessed with a task that involves the perception of intentional and accidental harm. Participants were also evaluated on emotion recognition, theory of mind (ToM), social norms knowledge and several EF domains. BvFTD patients presented deficits in affective, cognitive and moral aspects of empathy. However, empathic concern was the only aspect primarily affected in bvFTD that was neither related nor explained by deficits in EF or other social cognition domains. Deficits in the cognitive and moral aspects of empathy seem to depend on EF, emotion recognition and ToM. Our findings highlight the importance of using tasks depicting real-life social scenarios because of their greater sensitivity in the assessment of bvFTD. Moreover, our results contribute to the understanding of primary and intrinsic empathy deficits of bvFTD and have important theoretical and clinical implications.

Primary empathy deficits in frontotemporal dementia

PubMed Central

Baez, Sandra; Manes, Facundo; Huepe, David; Torralva, Teresa; Fiorentino, Natalia; Richter, Fabian; Huepe-Artigas, Daniela; Ferrari, Jesica; Montañes, Patricia; Reyes, Pablo; Matallana, Diana; Vigliecca, Nora S.; Decety, Jean; Ibanez, Agustin

2014-01-01

Loss of empathy is an early central symptom and diagnostic criterion of the behavioral variant frontotemporal dementia (bvFTD). Although changes in empathy are evident and strongly affect the social functioning of bvFTD patients, few studies have directly investigated this issue by means of experimental paradigms. The current study assessed multiple components of empathy (affective, cognitive and moral) in bvFTD patients. We also explored whether the loss of empathy constitutes a primary deficit of bvFTD or whether it is explained by impairments in executive functions (EF) or other social cognition domains. Thirty-seven bvFTD patients with early/mild stages of the disease and 30 healthy control participants were assessed with a task that involves the perception of intentional and accidental harm. Participants were also evaluated on emotion recognition, theory of mind (ToM), social norms knowledge and several EF domains. BvFTD patients presented deficits in affective, cognitive and moral aspects of empathy. However, empathic concern was the only aspect primarily affected in bvFTD that was neither related nor explained by deficits in EF or other social cognition domains. Deficits in the cognitive and moral aspects of empathy seem to depend on EF, emotion recognition and ToM. Our findings highlight the importance of using tasks depicting real-life social scenarios because of their greater sensitivity in the assessment of bvFTD. Moreover, our results contribute to the understanding of primary and intrinsic empathy deficits of bvFTD and have important theoretical and clinical implications. PMID:25346685

Brain and Behavior in Children with 22Q11.2 Deletion Syndrome: A Volumetric and Voxel-Based Morphometry MRI Study

ERIC Educational Resources Information Center

Campbell, Linda E.; Daly, Eileen; Toal, Fiona; Stevens, Angela; Azuma, Rayna; Catani, Marco; Ng, Virginia; Van Amelsvoort, Therese; Chitnis, Xavier; Cutter, William; Murphy, Declan G. M.; Murphy, Kieran C.

2006-01-01

In people with velo-cardio-facial syndrome [or 22q11.2 deletion syndrome (22qDS)], a single interstitial deletion of chromosome 22q11.2 causes a wide spectrum of cognitive deficits ranging from global learning difficulties to specific cognitive deficits. People with 22qDS are also at high risk of developing attention-deficit hyperactivity disorder…

Early deficits in spatial memory and theta rhythm in experimental temporal lobe epilepsy.

PubMed

Chauvière, Laetitia; Rafrafi, Nadia; Thinus-Blanc, Catherine; Bartolomei, Fabrice; Esclapez, Monique; Bernard, Christophe

2009-04-29

Patients with temporal lobe epilepsy (TLE), the most common form of epilepsy in adults, often display cognitive deficits. The time course and underlying mechanisms of cognitive decline remain unknown during epileptogenesis (the process leading to epilepsy). Using the rat pilocarpine model of TLE, we performed a longitudinal study to assess spatial and nonspatial cognitive performance during epileptogenesis. In parallel, we monitored interictal-like activity (ILA) in the hippocampal CA1 region, as well as theta oscillations, a brain rhythm central to numerous cognitive processes. Here, we report that spatial memory was altered soon after pilocarpine-induced status epilepticus, i.e., already during the seizure-free, latent period. Spatial deficits correlated with a decrease in the power of theta oscillations but not with the frequency of ILA. Spatial deficits persisted when animals had spontaneous seizures (chronic stage) without further modification. In contrast, nonspatial memory performances remained unaffected throughout. We conclude that the reorganization of hippocampal circuitry that immediately follows the initial insult can affect theta oscillation mechanisms, in turn, resulting in deficits in hippocampus-dependent memory tasks. These deficits may be dissociated from the process that leads to epilepsy itself but could instead constitute, as ILA, early markers in at-risk patients and/or provide beneficial therapeutic targets.

Screening of Cognitive Impairment in Schizophrenia: Reliability, Sensitivity, and Specificity of the Repeatable Battery for the Assessment of Neuropsychological Status in a Spanish Sample.

PubMed

De la Torre, Gabriel G; Perez, Maria J; Ramallo, Miguel A; Randolph, Christopher; González-Villegas, Macarena Bernal

2016-04-01

In recent years, a number of studies focusing on the evaluation of neuropsychological deficits in individuals with schizophrenia have shown deficits that include several cognitive functions. Attention deficits as well as memory or executive function deficits are common in this kind of disorder together with sustained attention problems, working memory deficiencies, and problem-solving difficulties, among many others. Currently, the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) is gaining special importance in the evaluation of the cognitive deficits associated with schizophrenia. In this article, we describe an RBANS screening in a sample of 88 Spanish patients diagnosed with schizophrenia. We also aimed to check the battery's reliability, sensitivity, and specificity in the studied sample. We performed a comparative study with 88 healthy participants. The results showed a reliability index value of α = .795 and an item value of α = .762. For total test reliability, we obtained an index value of α = .761 and an item value of α = .762. Sensitivity score was 87.5% and specificity 86.4%. RBANS obtained good reliability, sensitivity, and specificity scores and represents a good screening tool in detecting cognitive deficits associated with schizophrenia. © The Author(s) 2015.

Cognitive Outcomes for Extremely Preterm/Extremely Low Birth Weight Children in Kindergarten

PubMed Central

Orchinik, Leah J.; Taylor, H. Gerry; Espy, Kimberly Andrews; Minich, Nori; Klein, Nancy; Sheffield, Tiffany; Hack, Maureen

2012-01-01

Our objectives were to examine cognitive outcomes for extremely preterm/extremely low birth weight (EPT/ELBW, gestational age <28 weeks and/or birth weight <1000 g) children in kindergarten and the associations of these outcomes with neonatal factors, early childhood neurodevelopmental impairment, and socioeconomic status (SES). The sample comprised a hospital-based 2001-2003 birth cohort of 148 EPT/ELBW children (mean birth weight 818 g; mean gestational age 26 weeks) and a comparison group of 111 term-born normal birth weight (NBW) classmate controls. Controlling for background factors, the EPT/ELBW group had pervasive deficits relative to the NBW group on a comprehensive test battery, with rates of cognitive deficits that were 3 to 6 times higher in the EPT/ELBW group. Deficits on a measure of response inhibition were found in 48% versus 10%, OR (95% CI) = 7.32 (3.32, 16.16), p <.001. Deficits on measures of executive function and motor and perceptual-motor abilities were found even when controlling for acquired verbal knowledge. Neonatal risk factors, early neurodevelopmental impairment, and lower SES were associated with higher rates of deficits within the EPT/ELBW group. The findings document both global and selective cognitive deficits in EPT/ELBW children at school entry and justify efforts at early identification and intervention. PMID:21923973

Cognitive Dysfunction in Major Depressive Disorder. A Translational Review in Animal Models of the Disease

PubMed Central

Darcet, Flavie; Gardier, Alain M.; Gaillard, Raphael; David, Denis J.; Guilloux, Jean-Philippe

2016-01-01

Major Depressive Disorder (MDD) is the most common psychiatric disease, affecting millions of people worldwide. In addition to the well-defined depressive symptoms, patients suffering from MDD consistently complain about cognitive disturbances, significantly exacerbating the burden of this illness. Among cognitive symptoms, impairments in attention, working memory, learning and memory or executive functions are often reported. However, available data about the heterogeneity of MDD patients and magnitude of cognitive symptoms through the different phases of MDD remain difficult to summarize. Thus, the first part of this review briefly overviewed clinical studies, focusing on the cognitive dysfunctions depending on the MDD type. As animal models are essential translational tools for underpinning the mechanisms of cognitive deficits in MDD, the second part of this review synthetized preclinical studies observing cognitive deficits in different rodent models of anxiety/depression. For each cognitive domain, we determined whether deficits could be shared across models. Particularly, we established whether specific stress-related procedures or unspecific criteria (such as species, sex or age) could segregate common cognitive alteration across models. Finally, the role of adult hippocampal neurogenesis in rodents in cognitive dysfunctions during MDD state was also discussed. PMID:26901205

The Origins of Cognitive Deficits in Victimized Children: Implications for Neuroscientists and Clinicians.

PubMed

Danese, Andrea; Moffitt, Terrie E; Arseneault, Louise; Bleiberg, Ben A; Dinardo, Perry B; Gandelman, Stephanie B; Houts, Renate; Ambler, Antony; Fisher, Helen L; Poulton, Richie; Caspi, Avshalom

2017-04-01

Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. The authors used data from two large cohort studies to address these research questions directly. The authors tested the association between prospectively collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.K. E-Risk Study and 1,037 members of the New Zealand Dunedin Study who were followed up from birth until ages 18 and 38 years, respectively. Multiple measures of victimization and cognition were used, and comparisons were made of cognitive scores for twins discordant for victimization. Individuals exposed to childhood victimization had pervasive impairments in clinically relevant cognitive functions, including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks. Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 km apart suggest that the association between childhood violence victimization and later cognition is largely noncausal, in contrast to conventional interpretations. These findings support the adoption of a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment.

THE ORIGINS OF COGNITIVE DEFICITS IN VICTIMIZED CHILDREN: IMPLICATIONS FOR NEUROSCIENTISTS AND CLINICIANS

PubMed Central

Danese, Andrea; Moffitt, Terrie E; Arseneault, Louise; Bleiberg, Ben A; Dinardo, Perry B; Gandelman, Stephanie B; Houts, Renate; Ambler, Antony; Fisher, Helen; Poulton, Richie; Caspi, Avshalom

2016-01-01

OBJECTIVE Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. We directly tested these research gaps. METHOD We tested the association between prospectively-collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the UK E-Risk Study and 1,037 members of the New Zealand Dunedin Study, who were followed-up from birth until ages 18 and 38 years, respectively. We used multiple measures of victimization and cognition, and included comparisons of cognitive scores for twins discordant for victimization. RESULTS We found that individuals exposed to childhood victimization had pervasive impairments in clinically-relevant cognitive functions including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks. CONCLUSIONS Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 kilometers apart suggest that the association between childhood violence victimization and later cognition is largely non-causal, in contrast to conventional interpretations. These findings urge adopting a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment. PMID:27794691

Early Presymptomatic and Long-Term Changes of Rest Activity Cycles and Cognitive Behavior in a MPTP-Monkey Model of Parkinson's Disease

PubMed Central

Vezoli, Julien; Fifel, Karim; Leviel, Vincent; Dehay, Colette; Kennedy, Henry; Cooper, Howard M.; Gronfier, Claude; Procyk, Emmanuel

2011-01-01

Background It is increasingly recognized that non-motor symptoms are a prominent feature of Parkinson's disease and in the case of cognitive deficits can precede onset of the characteristic motor symptoms. Here, we examine in 4 monkeys chronically treated with low doses of the neurotoxin MPTP the early and long-term alterations of rest-activity rhythms in relationship to the appearance of motor and cognitive symptoms. Methodology/Principal Findings Behavioral activity recordings as well as motor and cognitive assessments were carried out continuously and in parallel before, during and for several months following MPTP-treatment (12–56 weeks). Cognitive abilities were assessed using a task that is dependent on the functional integrity of the fronto-striatal axis. Rest-activity cycles were monitored continuously using infrared movement detectors of locomotor activity. Motor impairment was evaluated using standardized scales for primates. Results show that MPTP treatment led to an immediate alteration (within one week) of rest-activity cycles and cognitive deficits. Parkinsonian motor deficits only became apparent 3 to 5 weeks after initiating chronic MPTP administration. In three of the four animals studied, clinical scores returned to control levels 5–7 weeks following cessation of MPTP treatment. In contrast, both cognitive deficits and chronobiological alterations persisted for many months. Levodopa treatment led to an improvement of cognitive performance but did not affect rest-activity rhythms in the two cases tested. Conclusions/Significance Present results show that i) changes in the rest activity cycles constituted early detectable consequences of MPTP treatment and, along with cognitive alterations, characterize the presymptomatic stage; ii) following motor recovery there is a long-term persistence of non-motor symptoms that could reflect differential underlying compensatory mechanisms in these domains; iii) the progressive MPTP-monkey model of presymptomatic ongoing parkinsonism offers possibilities for in-depth studies of early non-motor symptoms including sleep alterations and cognitive deficits. PMID:21887350

Cognitive Function in Prepubertal Children with Obstructive Sleep Apnea: A Modifying Role for NADPH Oxidase p22 Subunit Gene Polymorphisms?

PubMed Central

Khalyfa, Abdelnaby; Capdevila, Oscar Sans; Kheirandish-Gozal, Leila; Khalyfa, Ahamed A.; Kim, Jinkwan

2012-01-01

Abstract Pediatric obstructive sleep apnea (OSA) may lead to neurocognitive dysfunction, but not in everyone affected. The frequencies of NADPH oxidase (NOX) polymorphisms in the p22phox subunit were similar between children with OSA and controls, except for rs6520785 and rs4673, the latter being significantly more frequent among the OSA children without deficits than with deficits (p<0.02). Similarly, 8-hydroxydeoxyguanine urine levels and NOX activity were lower among children without cognitive deficits and particularly among those with the rs4673 polymorphism. Thus, polymorphisms within the NOX gene or its functional subunits may account for important components of the variance in cognitive function deficits associated with OSA in children. Antioxid. Redox Signal. 16, 171–177. PMID:21902598

Broad Cognitive Profile in Children and Adolescents with HF-ASD and in Their Siblings: Widespread Underperformance and Its Clinical and Adaptive Correlates

ERIC Educational Resources Information Center

Rosa, Mireia; Puig, Olga; Lázaro, Luisa; Vallés, Virginia; Lera, Sara; Sánchez-Gistau, Vanesa; Calvo, Rosa

2017-01-01

Despite evidence supporting the presence of cognitive deficits in children and adolescents with high-functioning autism spectrum disorder (HF-ASD), the nature of these deficits and their clinical and adaptive correlates remain unclear. Moreover, there are few cognitive studies of ASD siblings as a high risk population. We compared 50 children and…

The Cognitive Abilities and Skills of Children Who Suffer from Attention Deficit and Hyperactivity Disorder (ADHD) in Kuwait State

ERIC Educational Resources Information Center

Mohammed, Ali Mohammed Haidar

2016-01-01

The present study aims to identify the level of cognitive skills and abilities of children who suffer from the Attention Deficit and Hyperactivity Disorder (ADHD) and the differences in the level of cognitive skills and abilities according to the age group and the level of academic achievement. To achieve the objective of the study, a…

Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice.

PubMed

Kesby, James P; Markou, Athina; Semenova, Svetlana

2015-01-01

Methamphetamine abuse is common among individuals infected by human immunodeficiency virus (HIV). Neurocognitive outcomes tend to be worse in methamphetamine users with HIV. However, it is unclear whether discrete cognitive domains are susceptible to impairment after combined HIV infection and methamphetamine abuse. The expression of HIV/gp120 protein induces neuropathology in mice similar to HIV-induced pathology in humans. We investigated the separate and combined effects of methamphetamine exposure and gp120 expression on cognitive function in transgenic (gp120-tg) and control mice. The mice underwent an escalating methamphetamine binge regimen and were tested in novel object/location recognition, object-in-place recognition, and Barnes maze tests. gp120 expression disrupted performance in the object-in-place test (i.e. similar time spent with all objects, regardless of location), indicating deficits in associative recognition memory. gp120 expression also altered reversal learning in the Barnes maze, suggesting impairments in executive function. Methamphetamine exposure impaired spatial strategy in the Barnes maze, indicating deficits in spatial learning. Methamphetamine-exposed gp120-tg mice had the lowest spatial strategy scores in the final acquisition trials in the Barnes maze, suggesting greater deficits in spatial learning than all of the other groups. Although HIV infection involves interactions between multiple proteins and processes, in addition to gp120, our findings in gp120-tg mice suggest that humans with the dual insult of HIV infection and methamphetamine abuse may exhibit a broader spectrum of cognitive deficits than those with either factor alone. Depending on the cognitive domain, the combination of both insults may exacerbate deficits in cognitive performance compared with each individual insult. Copyright © 2014 Elsevier B.V. and ECNP. All rights reserved.

Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice

PubMed Central

Kesby, James P.; Markou, Athina; Semenova, Svetlana

2014-01-01

Methamphetamine abuse is common among individuals infected by human immunodeficiency virus (HIV). Neurocognitive outcomes tend to be worse in methamphetamine users with HIV. However, it is unclear whether discrete cognitive domains are susceptible to impairment after combined HIV infection and methamphetamine abuse. The expression of HIV/gp120 protein induces neuropathology in mice similar to HIV-induced pathology in humans. We investigated the separate and combined effects of methamphetamine exposure and gp120 expression on cognitive function in transgenic (gp120-tg) and control mice. The mice underwent an escalating methamphetamine binge regimen and were tested in novel object/location recognition, object-in-place recognition, and Barnes maze tests. gp120 expression disrupted performance in the object-in-place test (i.e., similar time spent with all objects, regardless of location), indicating deficits in associative recognition memory. gp120 expression also altered reversal learning in the Barnes maze, suggesting impairments in executive function. Methamphetamine exposure impaired spatial strategy in the Barnes maze, indicating deficits in spatial learning. Methamphetamine-exposed gp120-tg mice had the lowest spatial strategy scores in the final acquisition trials in the Barnes maze, suggesting greater deficits in spatial learning than all of the other groups. Although HIV infection involves interactions between multiple proteins and processes, in addition to gp120, our findings in gp120-tg mice suggest that humans with the dual insult of HIV infection and methamphetamine abuse may exhibit a broader spectrum of cognitive deficits than those with either factor alone. Depending on the cognitive domain, the combination of both insults may exacerbate deficits in cognitive performance compared with each individual insult. PMID:25476577

The effects of sigma (σ1) receptor-selective ligands on muscarinic receptor antagonist-induced cognitive deficits in mice

PubMed Central

Malik, Maninder; Rangel-Barajas, Claudia; Sumien, Nathalie; Su, Chang; Singh, Meharvan; Chen, Zhenglan; Huang, Ren-Qi; Meunier, Johann; Maurice, Tangui; Mach, Robert H; Luedtke, Robert R

2015-01-01

Background and Purpose Cognitive deficits in patients with Alzheimer's disease, Parkinson's disease, traumatic brain injury and stroke often involve alterations in cholinergic signalling. Currently available therapeutic drugs provide only symptomatic relief. Therefore, novel therapeutic strategies are needed to retard and/or arrest the progressive loss of memory. Experimental Approach Scopolamine-induced memory impairment provides a rapid and reversible phenotypic screening paradigm for cognition enhancement drug discovery. Male C57BL/6J mice given scopolamine (1 mg·kg−1) were used to evaluate the ability of LS-1–137, a novel sigma (σ1) receptor-selective agonist, to improve the cognitive deficits associated with muscarinic antagonist administration. Key Results LS-1–137 is a high-affinity (Ki = 3.2 nM) σ1 receptor agonist that is 80-fold selective for σ1, compared with σ2 receptors. LS-1–137 binds with low affinity at D2-like (D2, D3 and D4) dopamine and muscarinic receptors. LS-1–137 was found to partially reverse the learning deficits associated with scopolamine administration using a water maze test and an active avoidance task. LS-1–137 treatment was also found to trigger the release of brain-derived neurotrophic factor from rat astrocytes. Conclusions and Implications The σ1 receptor-selective compound LS-1–137 may represent a novel candidate cognitive enhancer for the treatment of muscarinic receptor-dependent cognitive deficits. PMID:25573298

Deficits in Domains of Social Cognition in Schizophrenia: A Meta-Analysis of the Empirical Evidence

PubMed Central

Savla, Gauri N.

2013-01-01

Objective: Social cognition is strongly associated with functional outcome in schizophrenia, making it an important target for treatment. Our goal was to examine the average magnitude of differences between schizophrenia patients (SCs) and normal comparison (NCs) patients across multiple domains of social cognition recognized by the recent NIMH consensus statement: theory of mind (ToM), social perception, social knowledge, attributional bias, emotion perception, and emotion processing. Method: We conducted a meta-analysis of peer-reviewed studies of social cognition in schizophrenia, published between 1980 and November, 2011. Results: 112 studies reporting results from 3908 SCs and 3570 NCs met our inclusion criteria. SCs performed worse than NCs across all domains, with large effects for social perception (g = 1.04), ToM (g = 0.96), emotion perception (g = 0.89), and emotion processing (g = 0.88). Regression analyses showed that statistically significant heterogeneity in effects within domains was not explained by age, education, or gender. Greater deficits in social and emotion perception were associated with inpatient status, and greater deficits in emotion processing were associated with longer illness duration. Conclusions: Despite the limitations of existing studies, including lack of standardization or psychometric validation of measures, the evidence for deficits across multiple social cognitive domains in schizophrenia is clear. Future research should examine the role of neurobiological and psychosocial factors in models linking various aspects of deficit in schizophrenia, including social cognition, in order to identify targets for intervention. PMID:22949733

Does atrioventricular reentry tachycardia (AVRT) or atrioventricular nodal reentry tachycardia (AVNRT) in children affect their cognitive and emotional development?

PubMed

Maryniak, Agnieszka; Bielawska, Alicja; Bieganowska, Katarzyna; Miszczak-Knecht, Maria; Walczak, Franciszek; Szumowski, Lukasz

2013-04-01

The current study sought to assess cognitive and emotional functions among children and adolescents with atrioventricular reentry tachycardia (AVRT) and atrioventricular nodal reentry tachycardia (AVNRT). 113 patients (62 girls and 51 boys ages, 9-18 years) scheduled for radiofrequency ablation due to AVRT or AVNRT underwent neuropsychologic examination. The study excluded patients who had experienced cardiac arrest, congenital heart defects, neurologic disorders, or other diseases affecting cognitive or emotional development. Standardized tests for examining verbal and visual memory as well as visual-spatial functioning were performed. For patients exhibiting deficits in two or more tests, a diagnosis of "cognitive deficits" was determined. Levels of anxiety were tested using the State-Trait Anxiety Inventory. Cognitive deficits were found in 47.8 % of the patients. The age at first arrhythmia attack was related to memory dysfunction. The mean age at which the first symptoms occurred was significantly lower for patients with deficits (8.3 years) than for patients who had no deficit (10.2 years) (t = 2.15; p = 0.03). Boys exhibited a significantly higher level of trait anxiety than girls (t = 3.42; p = 0.0009). A significant negative correlation was found between anxiety and the age at appearance of the first symptoms (r = -0.26; p = 0.005). These findings led us to conclude that cognitive and emotional developments can be negatively affected by AVNRT and AVRT, particularly if tachycardia appears early in life.

Exposure to severe urban air pollution influences cognitive outcomes, brain volume and systemic inflammation in clinically healthy children.

PubMed

Calderón-Garcidueñas, Lilian; Engle, Randall; Mora-Tiscareño, Antonieta; Styner, Martin; Gómez-Garza, Gilberto; Zhu, Hongtu; Jewells, Valerie; Torres-Jardón, Ricardo; Romero, Lina; Monroy-Acosta, Maria E; Bryant, Christopher; González-González, Luis Oscar; Medina-Cortina, Humberto; D'Angiulli, Amedeo

2011-12-01

Exposure to severe air pollution produces neuroinflammation and structural brain alterations in children. We tested whether patterns of brain growth, cognitive deficits and white matter hyperintensities (WMH) are associated with exposures to severe air pollution. Baseline and 1 year follow-up measurements of global and regional brain MRI volumes, cognitive abilities (Wechsler Intelligence Scale for Children-Revised, WISC-R), and serum inflammatory mediators were collected in 20 Mexico City (MC) children (10 with white matter hyperintensities, WMH(+), and 10 without, WMH(-)) and 10 matched controls (CTL) from a low polluted city. There were significant differences in white matter volumes between CTL and MC children - both WMH(+) and WMH(-) - in right parietal and bilateral temporal areas. Both WMH(-) and WMH(+) MC children showed progressive deficits, compared to CTL children, on the WISC-R Vocabulary and Digit Span subtests. The cognitive deficits in highly exposed children match the localization of the volumetric differences detected over the 1 year follow-up, since the deficits observed are consistent with impairment of parietal and temporal lobe functions. Regardless of the presence of prefrontal WMH, Mexico City children performed more poorly across a variety of cognitive tests, compared to CTL children, thus WMH(+) is likely only partially identifying underlying white matter pathology. Together these findings reveal that exposure to air pollution may perturb the trajectory of cerebral development and result in cognitive deficits during childhood. Copyright © 2011 Elsevier Inc. All rights reserved.

GLYX-13 (rapastinel) ameliorates subchronic phencyclidine- and ketamine-induced declarative memory deficits in mice

PubMed Central

Rajagopal, Lakshmi; Burgdorf, Jeffrey S.; Moskal, Joseph R.; Meltzer, Herbert Y.

2016-01-01

GLYX-13 (rapastinel), a tetrapeptide (Thr-Pro-Pro-Thr-amide), has been reported to have fast acting antidepressant properties in man based upon its N-methyl-d-aspartate receptor (NMDAR) glycine site functional partial agonism. Ketamine, a non-competitive NMDAR antagonist, also reported to have fast acting antidepressant properties, produces cognitive impairment in rodents and man, whereas rapastinel has been reported to have cognitive enhancing properties in rodents, without impairing cognition in man, albeit clinical testing has been limited. The goal of this study was to compare the cognitive impairing effects of rapastinel and ketamine in novel object recognition (NOR), a measure of declarative memory, in male C57BL/6J mice treated with phencyclidine (PCP), another NMDAR noncompetitive antagonist known to severely impair cognition, in both rodents and man. C57BL/6J mice given a single dose or subchronic ketamine (30 mg/kg. i.p.) showed acute or persistent deficits in NOR, respectively. Acute i.v. rapastinel (1.0 mg/kg), did not induce NOR deficit. Pre-treatment with rapastinel significantly prevented acute ketamine-induced NOR deficit. Rapastinel (1.0 mg/kg, but not 0.3 mg/kg, iv) significantly reversed both subchronic ketamine- and subchronic PCP-induced NOR deficits. Rapastinel also potentiated the atypical antipsychotic drug with antidepressant properties, lurasidone, to restore NOR in subchronic ketamine-treated mice. These findings indicate that rapastinel, unlike ketamine, does not induce a declarative memory deficit in mice, and can prevent or reverse the ketamine-induced NOR deficit. Further study is required to determine if these differences translate during clinical use of ketamine and rapastinel as fast acting antidepressant drugs and if rapastinel could have non-ionotropic effects as an add-on therapy with antipsychotic/antidepressant medications. PMID:26632337

Improvement of dizocilpine-induced social recognition deficits in mice by brexpiprazole, a novel serotonin-dopamine activity modulator.

PubMed

Yoshimi, Noriko; Futamura, Takashi; Hashimoto, Kenji

2015-03-01

Cognitive impairment, including impaired social cognition, is largely responsible for the deterioration in social life suffered by patients with psychiatric disorders, such as schizophrenia and major depressive disorder (MDD). Brexpiprazole (7-{4-[4-(1-benzothiophen-4-yl)piperazin-1-yl]butoxy}quinolin-2(1H)-one), a novel serotonin-dopamine activity modulator, was developed to offer efficacious and tolerable therapy for different psychiatric disorders, including schizophrenia and adjunctive treatment of MDD. In this study, we investigated whether brexpiprazole could improve social recognition deficits (one of social cognition deficits) in mice, after administration of the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 (dizocilpine). Dosing with dizocilpine (0.1mg/kg) induced significant impairment of social recognition in mice. Brexpiprazole (0.01, 0.03, 0.1mg/kg, p.o.) significantly ameliorated dizocilpine-induced social recognition deficits, without sedation or a reduction of exploratory behavior. In addition, brexpiprazole alone had no effect on social recognition in untreated control mice. By contrast, neither risperidone (0.03mg/kg, p.o.) nor olanzapine (0.03mg/kg, p.o.) altered dizocilpine-induced social recognition deficits. Finally, the effect of brexpiprazole on dizocilpine-induced social recognition deficits was antagonized by WAY-100,635, a selective serotonin 5-HT1A antagonist. These results suggest that brexpiprazole could improve dizocilpine-induced social recognition deficits via 5-HT1A receptor activation in mice. Therefore, brexpiprazole may confer a beneficial effect on social cognition deficits in patients with psychiatric disorders. Copyright © 2015 Elsevier B.V. and ECNP. All rights reserved.

Cognitive and behavior deficits in sickle cell mice are associated with profound neuropathologic changes in hippocampus and cerebellum

PubMed Central

Wang, Li; Almeida, Luis E.F.; de Souza Batista, Celia M.; Khaibullina, Alfia; Xu, Nuo; Albani, Sarah; Guth, Kira A.; Seo, Ji Sung; Quezado, Martha; Quezado, Zenaide M.N.

2015-01-01

Strokes are perhaps the most serious complications of sickle cell disease (SCD) and by the fifth decade occur in approximately 25% of patients. While most patients do not develop strokes, mounting evidence indicates that even without brain abnormalities on imaging studies, SCD patients can present profound neurocognitive dysfunction. We sought to evaluate the neurocognitive behavior profile of humanized SCD mice (Townes, BERK) and to identify hematologic and neuropathologic abnormalities associated with the behavioral alterations observed in these mice. Heterozygous and homozygous Townes mice displayed severe cognitive deficits shown by significant delays in spatial learning compared to controls. Homozygous Townes also had increased depression- and anxiety-like behaviors as well as reduced performance on voluntary wheel running compared to controls. Behavior deficits observed in Townes were also seen in BERKs. Interestingly, most deficits in homozygotes were observed in older mice and were associated with worsening anemia. Further, neuropathologic abnormalities including the presence of large bands of dark/pyknotic (shrunken) neurons in CA1 and CA3 fields of hippocampus and evidence of neuronal dropout in cerebellum were present in homozygotes but not control Townes. These observations suggest that cognitive and behavioral deficits in SCD mice mirror those described in SCD patients and that aging, anemia, and profound neuropathologic changes in hippocampus and cerebellum are possible biologic correlates of those deficits. These findings support using SCD mice for studies of cognitive deficits in SCD and point to vulnerable brain areas with susceptibility to neuronal injury in SCD and to mechanisms that potentially underlie those deficits. PMID:26462816

Deficits in Social Cognition: An Unveiled Signature of Multiple Sclerosis.

PubMed

Chalah, Moussa A; Ayache, Samar S

2017-03-01

Multiple sclerosis (MS) is a chronic progressive inflammatory disease of the central nervous system, representing the primary cause of non-traumatic disability in young adults. Cognitive dysfunction can affect patients at any time during the disease process and might alter the six core functional domains. Social cognition is a multi-component construct that includes the theory of mind, empathy and social perception of emotions from facial, bodily and vocal cues. Deficits in this cognitive faculty might have a drastic impact on interpersonal relationships and quality of life (QoL). Although exhaustive data exist for non-social cognitive functions in MS, only a little attention has been paid for social cognition. The objectives of the present work are to reappraise the definition and anatomy of social cognition and evaluate the integrity of this domain across MS studies. We will put special emphasis on neuropsychological and neuroimaging studies concerning social cognitive performance in MS. Studies were selected in conformity with PRISMA guidelines. We looked for computerized databases (PubMed, Medline, and Scopus) that index peer-reviewed journals to identify published reports in English and French languages that mention social cognition and multiple sclerosis, regardless of publication year. We combined keywords as follows: (facial emotion or facial expression or emotional facial expressions or theory of mind or social cognition or empathy or affective prosody) AND multiple sclerosis AND (MRI or functional MRI or positron emission tomography or functional imaging or structural imaging). We also scanned references from articles aiming to get additional relevant studies. In total, 26 studies matched the abovementioned criteria (26 neuropsychological studies including five neuroimaging studies). Available data support the presence of social cognitive deficits even at early stages of MS. The increase in disease burden along with the "multiple disconnection syndrome" resulting from gray and white matters pathology might exceed the "threshold for cerebral tolerance" and can manifest as deficits in social cognition. Admitting the impact of the latter on patients' social functioning, a thorough screening for such deficits is crucial to improving patients' QoL. (JINS, 2017, 23, 266-286).

Bacopa monnieri (Brahmi) Enhanced Cognitive Function and Prevented Cognitive Impairment by Increasing VGLUT2 Immunodensity in Prefrontal Cortex of Sub-Chronic Phencyclidine Rat Model of Schizophrenia.

PubMed

Piyabhan, Pritsana; Wetchateng, Thanitsara

2015-04-01

Glutamatergic hypofunction is affected in schizophrenia. The decrement ofpresynaptic glutamatergic marker remarkably vesicular glutamate transporter type 1 (VGLUT1) indicates the deficit ofglutamatergic and cognitive function in schizophrenic brain. However there have been afew studies in VGLUT2. Brahmi, a traditional herbal medicine, might be a new frontier of cognitive deficit treatment and prevention in schizophrenia by changing cerebral VGLUT2 density. To study cognitive enhancement- and neuroprotective-effects of Brahmi on novel object recognition task and cerebral VGLUT2 immunodensity in sub-chronic phencyclidine (PCP) rat model of schizophrenia. Cognitive enhancement effect study; rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: PCP + Brahmi. Neuroprotective effect study; rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: Brahmi + PCP Discrimination ratio (DR) representing cognitive ability was obtained from novel object recognition task. VGLUT2 immunodensity was measured in prefrontal cortex, striatum, cornu ammonis fields 1 (CA1) and 2/3 (CA2/3) of hippocampus using immunohistochemistry. DR was significantly reduced in PCP group compared with control. This occurred alongside VGLUT2 reduction in prefrontal cortex, but not in striatum, CA1 or CA2/3. Both PCP + Brahmi and Brahmi + PCP groups showed an increased DR score up to normal, which occurred alongside a significantly increased VGLUT2 immunodensity in the prefrontal cortex, compared with PCP group. The decrement of VGLUT2 density in prefrontal cortex resulted in cognitive deficit in rats receiving PCP. Interestingly, receiving Brahmi after PCP administration can restore this cognitive deficit by increasing VGLUT2 density in prefrontal cortex. This investigation is defined as Brahmi's cognitive enhancement effect. Additionally, receiving Brahmi before PCP administration can also prevent cognitive impairment by elevating VGLUT2 density in prefrontal cortex. This observation indicates neuroprotective effect of Brahmi. Therefore, Brahmi could be a new frontier of restoration and prevention of cognitive deficit in schizophrenia.

Neurological sequelae of bacterial meningitis.

PubMed

Lucas, Marjolein J; Brouwer, Matthijs C; van de Beek, Diederik

2016-07-01

We reported on occurrence and impact of neurological sequelae after bacterial meningitis. We reviewed occurrence of neurological sequelae in children and adults after pneumococcal and meningococcal meningitis. Most frequently reported sequelae are focal neurological deficits, hearing loss, cognitive impairment and epilepsy. Adults with pneumococcal meningitis have the highest risk of developing focal neurological deficits, which are most commonly caused by cerebral infarction, but can also be due to cerebritis, subdural empyema, cerebral abscess or intracerebral bleeding. Focal deficits may improve during clinical course and even after discharge, but a proportion of patients will have persisting focal neurological deficits that often interfere in patient's daily life. Hearing loss occurs in a high proportion of patients with pneumococcal meningitis and has been associated with co-existing otitis. Children and adults recovering from bacterial meningitis without apparent neurological deficits are at risk for long-term cognitive deficits. Early identification of neurological sequelae is important for children to prevent additional developmental delay, and for adults to achieve successful return in society after the disease. Neurological sequelae occur in a substantial amount of patients following bacterial meningitis. Most frequently reported sequelae are focal neurological deficits, hearing loss, cognitive impairment and epilepsy. Copyright © 2016 The British Infection Association. Published by Elsevier Ltd. All rights reserved.

Psychological factors are associated with subjective cognitive complaints 2 months post-stroke.

PubMed

Nijsse, Britta; van Heugten, Caroline M; van Mierlo, Marloes L; Post, Marcel W M; de Kort, Paul L M; Visser-Meily, Johanna M A

2017-01-01

The aim of this study was to investigate which psychological factors are related to post-stroke subjective cognitive complaints, taking into account the influence of demographic and stroke-related characteristics, cognitive deficits and emotional problems. In this cross-sectional study, 350 patients were assessed at 2 months post-stroke, using the Checklist for Cognitive and Emotional consequences following stroke (CLCE-24) to identify cognitive complaints. Psychological factors were: proactive coping, passive coping, self-efficacy, optimism, pessimism, extraversion, and neuroticism. Associations between CLCE-24 cognition score and psychological factors, emotional problems (depressive symptoms and anxiety), cognitive deficits, and demographic and stroke characteristics were examined using Spearman correlations and multiple regression analyses. Results showed that 2 months post-stroke, 270 patients (68.4%) reported at least one cognitive complaint. Age, sex, presence of recurrent stroke(s), comorbidity, cognitive deficits, depressive symptoms, anxiety, and all psychological factors were significantly associated with the CLCE-24 cognition score in bivariate analyses. Multiple regression analysis showed that psychological factors explained 34.7% of the variance of cognitive complaints independently, and 8.5% (p < .001) after taking all other factors into account. Of all psychological factors, proactive coping was independently associated with cognitive complaints (p < .001), showing that more proactive coping related to less cognitive complaints. Because cognitive complaints are common after stroke and are associated with psychological factors, it is important to focus on these factors in rehabilitation programmes.

A distinct pattern of memory and attention deficiency in patients with depression.

PubMed

Luo, Lan-Lan; Chen, Xin; Chai, Yan; Li, Jin-Hong; Zhang, Mian; Zhang, Jian-Ning

2013-03-01

Depression related cognitive deficits are frequently considered as simple epiphenomena of the disorder. However, whether or not the depression might directly bring about cognitive deficits is still under investigation. This study was to investigate the distinct pattern of cognitive deficits in patients with depression by comparing the cognitive function before and after anti-depressive drug therapy. Sixty cases of patients, first-time diagnosed with depression, were assessed by 17-item Hamilton Rating Scale for Depression (HAMD17scale). The memory ability was tested by quantitatively clinical memory scale, while the attention ability by modified Ruff 2&7 Selective Attention Test. Forty-two healthy volunteers were recruited as controls. The depressive patients were treated with Venlafaxine (75 - 300 mg/d), Fluoxetine (20 - 40 mg/d), Paroxetine (20 - 40 mg/d), and Sertraline (50 - 150 mg/d). After 12 weeks treatment, patients were tested again by HAMD17scale, quantitatively clinical memory scale, and modified Ruff 2&7 selective attention test to assess the effect of anti-depressive drugs on cognitive deficits. The memory quotient (MQ) was significantly lowered in depressive patients. The selection speed was also significantly decreased and the number of missing and error hits increased in the depression group as compared to control. However, there was no significant difference in clinical memory scale and Ruff 2&7 selective attention test between mild-to-moderate and severe depression group. Importantly, after anti-depressive drug therapy, the HAMD17 scale scores in depressive patients were significantly decreased, but the MQ, directional memory (DM), free recall (FR), associative learning (AL), and face recognition were comparable with those before the treatment. Furthermore, the selection speed and the number of missing and error hits were also not significantly different after anti-depressive drugs treatment. Depressive patients suffer from short-term memory deficits, and attention extent, stability and rearrangement deficiency. Even though anti-depressive drugs sufficiently relieve the cardinal presentation of depression, they could not successfully alleviate the accompanying cognitive deficits. This might indicate a distinct pattern of cognitive deficits in patients with depression.

Self-perceived cognitive deficits and occupational outcome in persons with schizophrenia.

PubMed

Verdoux, Hélène; Monello, Florence; Goumilloux, Régis; Cougnard, Audrey; Prouteau, Antoinette

2010-07-30

A two-year prospective follow-up study was used to explore whether self-perceived cognitive deficits (SPCD) predict occupational outcome in persons with schizophrenia. Cognitive complaints were assessed using the Scale to Investigate Cognition in Schizophrenia (SSTICS) in persons with schizophrenia requesting disability status. A higher level of SPCD was associated with better occupational outcome, independently from other characteristics. Persons with better social functioning may have a higher level of metacognition allowing a greater awareness of their cognitive difficulties. Measures of cognitive complaints should be complemented by objective testing to assess potential for vocational rehabilitation. Copyright 2010 Elsevier Ltd. All rights reserved.

Cognitive impairment and medial temporal lobe structure in young adults with a depressive episode.

PubMed

Donix, Markus; Haussmann, Robert; Helling, Franziska; Zweiniger, Anne; Lange, Jan; Werner, Annett; Donix, Katharina L; Brandt, Moritz D; Linn, Jennifer; Bauer, Michael; Buthut, Maria

2018-09-01

Cognitive deficits are common in patients with a depressive episode although the predictors for their development and severity remain elusive. We investigated whether subjective and objective cognitive impairment in young depressed adults would be associated with cortical thinning in medial temporal subregions. High-resolution magnetic resonance imaging, cortical unfolding data analysis, and comprehensive assessments of subjective and objective cognitive abilities were performed on 27 young patients with a depressive episode (mean age: 29.0 ± 5.8 years) and 23 older participants without a history of a depressive disorder but amnestic mild cognitive impairment (68.5 ± 6.6 years) or normal cognition (65.2 ± 8.7 years). Thickness reductions in parahippocampal, perirhinal and fusiform cortices were associated with subjective memory deficits only among young patients with a depressive episode and a measurable cognitive impairment. Long-term longitudinal data would be desirable to determine the trajectories of cognitive impairment associated with depression in patients with or without cortical structure changes. The presence of clinically significant cognitive deficits in young people with a depressive episode may identify a patient population with extrahippocampal cortical thinning. Copyright © 2018 Elsevier B.V. All rights reserved.

Successful evaluation of cognitive function and the nature of cognitive deficits among people with schizophrenia in clinical rehabilitation settings.

PubMed

John, Alexander Panickacheril; Yeak, Kim; Ayres, Helen; Sevastos, Marie; Moore, Elizabeth

2016-08-01

Despite possessing considerable relevance for planning and delivery of effective rehabilitation interventions, systematic evaluation of cognitive function is often ignored in clinical practice. This paper describes a successful method for measuring cognitive function and the nature of cognitive deficits (CD) in people with schizophrenia admitted to psychiatric rehabilitation services. Data on the cognitive functioning of consecutive patients with schizophrenia / schizoaffective disorder admitted during a 5-year period to a public in-patient rehabilitation facility was collated retrospectively and analysed. The Brief Assessment of Cognition in Schizophrenia (BACS) was used to evaluate cognitive function. It was possible to administer the BACS to 122 of 135 consecutive admissions. The mean composite score on the BACS was 1.8 standard deviations below the norm, and 43% had moderate or severe CD. The BACS sub-tests of list learning and symbol coding revealed more severe deficits. The study indicates that evaluation of cognitive function using brief instruments is feasible in psychiatric rehabilitation settings. Global and domain-specific CD were prevalent among people with schizophrenia. In view of the strong association of cognitive functioning with community functioning and rehabilitation outcomes, further studies exploring the feasibility and utility of routinely evaluating cognitive function are warranted. © The Royal Australian and New Zealand College of Psychiatrists 2016.

Response-Conflict Moderates the Cognitive Control of Episodic and Contextual Load in Older Adults

PubMed Central

Eich, Teal S.; Rakitin, Brian C.

2016-01-01

Objectives: Decline in cognitive control is one of the primary cognitive changes in normal aging. Reaching a consensus regarding the nature of these age-related changes, however, is complicated by the complexity of cognitive control as a construct. Methods: Healthy older and younger adults participated in a multifactorial test of cognitive control. Within participants, the procedure varied as a function of the amount contextual load, episodic load, and response-conflict load present. Results: We found that older adults showed impaired performance relative to younger adults. We also found, however, that the response selection process underlying the response-conflict manipulation was a major moderator of age-related differences in both the contextual and episodic load conditions—suggesting a hierarchical organization. Discussion: These findings are consistent with previous findings, suggesting that deficits in cognitive control in older adults are directly related to the resolution of response-conflict and that other apparent deficits may be derivative upon the more basic response-conflict related deficit. PMID:26224757

Hypoglycemia Induced by Insulin as a Triggering Factor of Cognitive Deficit in Diabetic Children

PubMed Central

Rodrigues Vilela, Vanessa; de Castro Ruiz Marques, Any; Schamber, Christiano Rodrigues

2014-01-01

This paper provides an overview of insulin-induced hypoglycemia as a triggering factor of cognitive deficit in children with type 1 diabetes mellitus. For this purpose, databases from 1961 to 2013 were used with the objective of detecting the primary publications that address the impact of hypoglycemia on cognitive performance of diabetic children. The results obtained from experimental animals were excluded. The majority of studies demonstrated that the cognitive deficit in diabetic children involves multiple factors including duration, intensity, severity, and frequency of hypoglycemia episodes. Additionally, age at the onset of type 1 diabetes also influences the cognitive performance, considering that early inception of the disease is a predisposing factor for severe hypoglycemia. Furthermore, the results suggest that there is a strong correlation between brain damage caused by hypoglycemia and cognitive deterioration. Therefore, a more cautious follow-up and education are needed to impede and treat hypoglycemia in children with diabetes mellitus. PMID:24790575

Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model.

PubMed

Qi, Zhonghua; Xu, Yinghui; Liang, Zhanhua; Li, Sheng; Wang, Jie; Wei, Yi; Dong, Bin

2015-11-01

Naringenin is a flavonoid polyphenolic compound, which facilitates the removal of free radicals, oxidative stress and inflammation. The present study aimed to obtain a better understanding of the effects of curcumin on the regulation of diabetes‑associated cognitive decline, and its underlying mechanisms. An experimental diabetes mellitus (DM) rat model was induced by streptozoticin (50 mg/kg). Following treatment with naringin (100 and 200 mg/kg) for 16 weeks, the body weight and blood glucose levels of the DM rats were measured. A morris water maze test was used to analyze the effects of naringin on the cognitive deficit of the DM rats. The levels of oxidative stress, proinflammatory factors, caspase‑3 and caspase‑9, and the protein expression of peroxisome proliferator‑activated receptor γ (PPARγ) were quantified in the DM rats using a commercially‑available kit and western blot assay, respectively. In addition, a GW9662 PPARγ inhibitor (0.3 mg/kg) was administered to the DM rats to determine whether PPARγ affected the effects of naringin on the cognitive deficit of the DM rats. The results demonstrated that naringin increased the body weight, blood glucose levels, and cognitive deficits of the DM rats. The levels of oxidative stress and proinflammatory factors in the naringin‑treated rats were significantly lower, compared with those of the DM rats. In addition, naringin activated the protein expression of PPARγ, and administration of the PPARγ inhibitor decreased the protein expression of PPARγ, and attenuated the effects of naringin on cognitive deficit. The results also demonstrated that naringin decreased the expression levels of caspase‑3 and caspase‑9 in the DM rats. These results suggested that naringin ameliorated cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in the type 2 diabetic rat model. Furthermore, oxidative stress, proinflammatory factors and PPARγ signaling may be involved in mediating these effects.

Cognitive Functioning of Adolescent and Young Adult Cannabis Users in the Philadelphia Neurodevelopmental Cohort

PubMed Central

Scott, J. Cobb; Wolf, Daniel H.; Calkins, Monica E.; Bach, Emily C.; Weidner, Jennifer; Ruparel, Kosha; Moore, Tyler M.; Jones, Jason D.; Jackson, Chad T.; Gur, Raquel E.; Gur, Ruben C.

2017-01-01

Cannabis use in youth is rising and has been linked to deficits in cognitive functioning. However, cognitive findings have primarily been based on small samples of users seeking treatment, and few studies have evaluated cognition in occasional cannabis users. Here, we examined 4,568 adolescents and young adults (ages 14–21) drawn from the Philadelphia Neurodevelopmental Cohort, a prospective, population-based study. Participants were classified as cannabis Non-Users (n=3,401), Occasional Users (twice per week or less; n=940), or Frequent Users (>3 times per week; n=227). Mixed-model analyses examined main effects of cannabis use and interactions between age and cannabis use on cognitive functioning. There was a significant interaction between cannabis group and age, such that adolescent (but not young adult) Frequent Users performed worse than Non-Users on measures of executive control (p=0.002). Earlier age of cannabis use was associated with worse performance in executive control in Occasional Users (p=0.04). Unexpectedly, Occasional Users exhibited better executive control, memory, and social cognition than Non-Users (ps<.05). Although mild executive control deficits in adolescent frequent users and a relation between early cannabis initiation and cognitive performance are partially consistent with prior research, cognitive deficits were not found in other hypothesized domains in this community-based sample. Moreover, occasional cannabis users displayed equivalent or even slightly better executive control, social cognitive, and memory abilities compared to non-users, suggesting complex relationships between cannabis use and cognition in youth. Longitudinal studies with community samples are needed to identify variables affecting risk and resilience to cognitive deficits associated with cannabis. PMID:28414475

Basic Information Processing Abilities at 11 years Account for Deficits in IQ Associated with Preterm Birth.

PubMed

Rose, Susan A; Feldman, Judith F; Jankowski, Jeffery J; Van Rossem, Ronan

2011-07-01

Although it is well established that preterms as a group do poorly relative to their full-term peers on tests of global cognitive functioning, the basis for this relative deficiency is less understood. The present paper examines preterm deficits in core cognitive abilities and determines their role in mediating preterm/full-term differences in IQ. The performance of 11-year-old children born preterm (birth weight <1750g) and their full-term controls were compared on a large battery of 15 tasks, covering four basic cognitive domains -- memory, attention, speed of processing and representational competence. The validity of these four domains was established using latent variables and confirmatory factor analysis (CFA). Preterms showed pervasive deficits within and across domains. Additionally, preterm deficits in IQ were completely mediated by these four cognitive domains in a structural equation model involving a cascade from elementary abilities (attention and speed), to more complex abilities (memory and representational competence), to IQ. The similarity of findings to those obtained with this cohort in infancy and toddlerhood suggest that preterm deficits persist - across time, across task, and from the non-verbal to the verbal period.

Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission.

PubMed

Han, Sung; Tai, Chao; Westenbroek, Ruth E; Yu, Frank H; Cheah, Christine S; Potter, Gregory B; Rubenstein, John L; Scheuer, Todd; de la Iglesia, Horacio O; Catterall, William A

2012-09-20

Haploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel Na(V)1.1 causes Dravet's syndrome, a childhood neuropsychiatric disorder including recurrent intractable seizures, cognitive deficit and autism-spectrum behaviours. The neural mechanisms responsible for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome are poorly understood. Here we report that mice with Scn1a haploinsufficiency exhibit hyperactivity, stereotyped behaviours, social interaction deficits and impaired context-dependent spatial memory. Olfactory sensitivity is retained, but novel food odours and social odours are aversive to Scn1a(+/-) mice. GABAergic neurotransmission is specifically impaired by this mutation, and selective deletion of Na(V)1.1 channels in forebrain interneurons is sufficient to cause these behavioural and cognitive impairments. Remarkably, treatment with low-dose clonazepam, a positive allosteric modulator of GABA(A) receptors, completely rescued the abnormal social behaviours and deficits in fear memory in the mouse model of Dravet's syndrome, demonstrating that they are caused by impaired GABAergic neurotransmission and not by neuronal damage from recurrent seizures. These results demonstrate a critical role for Na(V)1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome.

Autistic behavior in Scn1a+/− mice and rescue by enhanced GABAergic transmission

PubMed Central

Han, Sung; Tai, Chao; Westenbroek, Ruth E.; Yu, Frank H.; Cheah, Christine S.; Potter, Gregory B.; Rubenstein, John L.; Scheuer, Todd; de la Iglesia, Horacio O; Catterall, William A

2012-01-01

Haploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel NaV1.1 causes Dravet Syndrome (DS), a childhood neuropsychiatric disorder including recurrent intractable seizures, cognitive deficit, and autism-spectrum behaviors. The neural mechanisms responsible for cognitive deficit and autism-spectrum behaviors in DS are poorly understood. Here we show that mice with Scn1a haploinsufficiency display hyperactivity, stereotyped behaviors, social interaction deficits, and impaired context-dependent spatial memory. Olfactory sensitivity is retained, but novel food odors and social odors are aversive to Scn1a+/− mice. GABAergic neurotransmission is specifically impaired by this mutation, and selective deletion of NaV1.1 channels in forebrain interneurons is sufficient to cause these behavioral and cognitive impairments. Remarkably, treatment with low-dose clonazepam, a positive allosteric modulator of GABAA receptors, completely rescued the abnormal social behaviors and deficits in fear memory in DS mice, demonstrating that they are caused by impaired GABAergic neurotransmission and not by neuronal damage from recurrent seizures. These results demonstrate a critical role for NaV1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviors in DS. PMID:22914087

Basic Information Processing Abilities at 11 years Account for Deficits in IQ Associated with Preterm Birth

PubMed Central

Rose, Susan A.; Feldman, Judith F.; Jankowski, Jeffery J.; Van Rossem, Ronan

2011-01-01

Although it is well established that preterms as a group do poorly relative to their full-term peers on tests of global cognitive functioning, the basis for this relative deficiency is less understood. The present paper examines preterm deficits in core cognitive abilities and determines their role in mediating preterm/full-term differences in IQ. The performance of 11-year-old children born preterm (birth weight <1750g) and their full-term controls were compared on a large battery of 15 tasks, covering four basic cognitive domains -- memory, attention, speed of processing and representational competence. The validity of these four domains was established using latent variables and confirmatory factor analysis (CFA). Preterms showed pervasive deficits within and across domains. Additionally, preterm deficits in IQ were completely mediated by these four cognitive domains in a structural equation model involving a cascade from elementary abilities (attention and speed), to more complex abilities (memory and representational competence), to IQ. The similarity of findings to those obtained with this cohort in infancy and toddlerhood suggest that preterm deficits persist – across time, across task, and from the non-verbal to the verbal period. PMID:21643482

Sleep and nutritional deprivation and performance of house officers.

PubMed

Hawkins, M R; Vichick, D A; Silsby, H D; Kruzich, D J; Butler, R

1985-07-01

A study was conducted by the authors to compare cognitive functioning in acutely and chronically sleep-deprived house officers. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills as well as in tasks requiring high-order cognitive functioning and traditional intellective abilities. These deficits existed only for the acutely sleep-deprived group. The finding of deficits in individuals who reported five hours or less of sleep in a 24-hour period suggests that the minimum standard of four hours that has been considered by some to be adequate for satisfactory performance may be insufficient for more complex cognitive functioning.

Polygenic risk score, genome-wide association, and gene set analyses of cognitive domain deficits in schizophrenia.

PubMed

Nakahara, Soichiro; Medland, Sarah; Turner, Jessica A; Calhoun, Vince D; Lim, Kelvin O; Mueller, Bryon A; Bustillo, Juan R; O'Leary, Daniel S; Vaidya, Jatin G; McEwen, Sarah; Voyvodic, James; Belger, Aysenil; Mathalon, Daniel H; Ford, Judith M; Guffanti, Guia; Macciardi, Fabio; Potkin, Steven G; van Erp, Theo G M

2018-06-12

This study assessed genetic contributions to six cognitive domains, identified by the MATRICS Cognitive Consensus Battery as relevant for schizophrenia, cognition-enhancing, clinical trials. Psychiatric Genomics Consortium Schizophrenia polygenic risk scores showed significant negative correlations with each cognitive domain. Genome-wide association analyses identified loci associated with attention/vigilance (rs830786 within HNF4G), verbal memory (rs67017972 near NDUFS4), and reasoning/problem solving (rs76872642 within HDAC9). Gene set analysis identified unique and shared genes across cognitive domains. These findings suggest involvement of common and unique mechanisms across cognitive domains and may contribute to the discovery of new therapeutic targets to treat cognitive deficits in schizophrenia. Copyright © 2018 Elsevier B.V. All rights reserved.

Memory deficits for facial identity in patients with amnestic mild cognitive impairment (MCI).

PubMed

Savaskan, Egemen; Summermatter, Daniel; Schroeder, Clemens; Schächinger, Hartmut

2018-01-01

Faces are among the most relevant social stimuli revealing an encounter's identity and actual emotional state. Deficits in facial recognition may be an early sign of cognitive decline leading to social deficits. The main objective of the present study is to investigate if individuals with amnestic mild cognitive impairment show recognition deficits in facial identity. Thirty-seven individuals with amnestic mild cognitive impairment, multiple-domain (15 female; age: 75±8 yrs.) and forty-one healthy volunteers (24 female; age 71±6 yrs.) participated. All participants completed a human portrait memory test presenting unfamiliar faces with happy and angry emotional expressions. Five and thirty minutes later, old and new neutral faces were presented, and discrimination sensitivity (d') and response bias (C) were assessed as signal detection parameters of cued facial identity recognition. Memory performance was lower in amnestic mild cognitive impairment as compared to control subjects, mainly because of an altered response bias towards an increased false alarm rate (favoring false OLD ascription of NEW items). In both groups, memory performance declined between the early and later testing session, and was always better for acquired happy than angry faces. Facial identity memory is impaired in patients with amnestic mild cognitive impairment. Liberalization of the response bias may reflect a socially motivated compensatory mechanism maintaining an almost identical recognition hit rate of OLD faces in individuals with amnestic mild cognitive impairment.

Social cognition and underlying cognitive mechanisms in children with an extra X chromosome: a comparison with autism spectrum disorder.

PubMed

van Rijn, S; Stockmann, L; van Buggenhout, G; van Ravenswaaij-Arts, C; Swaab, H

2014-06-01

Individuals with an extra X chromosome are at increased risk for autism symptoms. This study is the first to assess theory of mind and facial affect labeling in children with an extra X chromosome. Forty-six children with an extra X chromosome (29 boys with Klinefelter syndrome and 17 girls with Trisomy X), 56 children with autism spectrum disorder (ASD) and 88 non-clinical controls, aged 9-18 years, were included. Similar to children with ASD, children with an extra X chromosome showed significant impairments in social cognition. Regression analyses showed that different cognitive functions predicted social cognitive skills in the extra X and ASD groups. The social cognitive deficits were similar for boys and girls with an extra X chromosome, and not specific for a subgroup with high Autism Diagnostic Interview Revised autism scores. Thus, children with an extra X chromosome show social cognitive deficits, which may contribute to social dysfunction, not only in children showing a developmental pattern that is 'typical' for autism but also in those showing mild or late presenting autism symptoms. Our findings may also help explain variance in type of social deficit: children may show similar social difficulties, but these may arise as a consequence of different underlying information processing deficits. © 2014 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.

Computer-based cognitive retraining for adults with chronic acquired brain injury: a pilot study.

PubMed

Li, Kitsum; Robertson, Julie; Ramos, Joshua; Gella, Stephanie

2013-10-01

This study evaluated the effectiveness of a computer-based cognitive retraining (CBCR) program on improving memory and attention deficits in individuals with a chronic acquired brain injury (ABI). Twelve adults with a chronic ABI demonstrating deficits in memory and attention were recruited from a convenience sample from the community. Using a quasi-experimental one-group pretest-posttest design, a significant improvement was found in both memory and attention scores postintervention using the cognitive screening tool. This study supported the effectiveness of CBCR programs in improving cognitive deficits in memory and attention in individuals with chronic ABI. Further research is recommended to validate these findings with a larger ABI population and to investigate transfer to improvement in occupational performance that supports daily living skills.

A specific cognitive deficit within semantic cognition across a multi-generational family

PubMed Central

Briscoe, Josie; Chilvers, Rebecca; Baldeweg, Torsten; Skuse, David

2012-01-01

We report a study of eight members of a single family (aged 8–72 years), who all show a specific deficit in linking semantic knowledge to language. All affected members of the family had high levels of overall intelligence; however, they had profound difficulties in prose and sentence recall, listening comprehension and naming. The behavioural deficit was remarkably consistent across affected family members. Structural neuroimaging data revealed grey matter abnormalities in the left infero-temporal cortex and fusiform gyri: brain areas that have been associated with integrative semantics. This family demonstrates, to our knowledge, the first example of a heritable, highly specific abnormality affecting the interface between language and cognition in humans and has important implications for our understanding of the genetic basis of cognition. PMID:22719041

Comparison of the Recovery Patterns of Language and Cognitive Functions in Patients with Post-Traumatic Language Processing Deficits and in Patients with Aphasia Following a Stroke

ERIC Educational Resources Information Center

Vukovic, Mile; Vuksanovic, Jasmina; Vukovic, Irena

2008-01-01

In this study we investigated the recovery patterns of language and cognitive functions in patients with post-traumatic language processing deficits and in patients with aphasia following a stroke. The correlation of specific language functions and cognitive functions was analyzed in the acute phase and 6 months later. Significant recovery of the…

Impact of statins on cognitive deficits in adult male rodents after traumatic brain injury: a systematic review.

PubMed

Peng, Weijun; Yang, Jingjing; Yang, Bo; Wang, Lexing; Xiong, Xin-gui; Liang, Qinghua

2014-01-01

The efficacy of statin treatment on cognitive decline is controversial, and the effect of statins on cognitive deficits in individuals with traumatic brain injury (TBI) has yet to be investigated. Therefore, we systematically reviewed the effect of statins on cognitive deficits in adult male rodents after TBI. After identifying eligible studies by searching four electronic databases on February 28, 2014, we assessed study quality, evaluated the efficacy of statin treatment, and performed stratified metaregression and metaregression to assess the influence of study design on statin efficacy. Eleven studies fulfilled our inclusion criteria from a total of 183 publications. The overall methodological quality of these studies was poor. Meta-analysis showed that statins exert statistically significant positive effects on cognitive performance after TBI. Stratified analysis showed that atorvastatin has the greatest effect on acquisition memory, simvastatin has the greatest effect on retention memory, and statin effects on acquisition memory are higher in closed head injury models. Metaregression analysis further showed that that animal species, study quality, and anesthetic agent impact statin effects on retention memory. We conclude that statins might reduce cognitive deficits after TBI. However, additional well-designed and well-reported animal studies are needed to inform further clinical study.

Theory of mind in a first-episode psychosis population using the Hinting Task.

PubMed

Lindgren, Maija; Torniainen-Holm, Minna; Heiskanen, Inkeri; Voutilainen, Greta; Pulkkinen, Ulla; Mehtälä, Tuukka; Jokela, Markus; Kieseppä, Tuula; Suvisaari, Jaana; Therman, Sebastian

2018-05-01

Deficiencies in theory of mind (ToM) are common in psychosis and may largely explain impaired social functioning. Currently, it is unclear whether impairments in ToM are explained by the more general cognitive deficits related to psychosis or whether ToM is impaired in psychosis independently of other cognitive deficits. This study examined ToM using the Hinting Task in young adults (n = 66) with first-episode psychosis and matched controls (n = 62). The participants were administered a broad neuropsychological assessment. Participants with psychosis performed worse than controls on the Hinting Task. However, 75% of the variance between the groups was explained by general cognitive deficits, especially impaired processing speed and episodic memory. Hinting Task performance of the best functioning patient group did not differ from that of the control group. When the psychosis group was divided according to diagnosis, the Hinting Task difference between individuals with schizophrenia and controls remained significant even when general cognitive performance was controlled for, suggesting specific verbal ToM deficits in schizophrenia. In contrast, those with other psychotic disorders did not differ from controls. Our results suggest that ToM deficits can be seen in early phases of psychotic disorders, schizophrenia in particular, and are partly independent of other cognitive functions. Copyright © 2018 Elsevier B.V. All rights reserved.

Cognitive flexibility impairment and reduced frontal cortex BDNF expression in the ouabain model of mania

PubMed Central

Amodeo, Dionisio A.; Grospe, Gena; Zang, Hui; Dwivedi, Yogesh; Ragozzino, Michael E.

2016-01-01

Central infusion of the Na+/K+-ATPase inhibitor, ouabain in rats serves as an animal model of mania because it leads to hyperactivity, as well as reproduces ion dysregulation and reduced BDNF levels similar to that observed in bipolar disorder. Bipolar disorder is also associated with cognitive inflexibility and working memory deficits. It is unknown whether ouabain treatment in rats leads to similar cognitive flexibility and working memory deficits. The present study examined the effects of an intracerebral ventricular infusion of ouabain in rats on spontaneous alternation, probabilistic reversal learning and BDNF expression levels in the frontal cortex. Ouabain treatment significantly increased locomotor activity, but did not affect alternation performance in a Y-maze. Ouabain treatment selectively impaired reversal learning in a spatial discrimination task using an 80/20 probabilistic reinforcement procedure. The reversal learning deficit in ouabain-treated rats resulted from an impaired ability to maintain a new choice pattern (increased regressive errors). Ouabain treatment also decreased sensitivity to negative feedback during the initial phase of reversal learning. Expression of BDNF mRNA and protein levels was downregulated in the frontal cortex which also negatively correlated with regressive errors. These findings suggest that the ouabain model of mania may be useful in understanding the neuropathophysiology that contributes to cognitive flexibility deficits and test potential treatments to alleviate cognitive deficits in bipolar disorder. PMID:27267245

The cognitive cost of sleep lost

PubMed Central

McCoy, John G.; Strecker, Robert E.

2013-01-01

A substantial body of literature supports the intuitive notion that a good night’s sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances. PMID:21875679

Cognitive Control of Auditory Distraction: Impact of Task Difficulty, Foreknowledge, and Working Memory Capacity Supports Duplex-Mechanism Account

ERIC Educational Resources Information Center

Hughes, Robert W.; Hurlstone, Mark J.; Marsh, John E.; Vachon, Francois; Jones, Dylan M.

2013-01-01

The influence of top-down cognitive control on 2 putatively distinct forms of distraction was investigated. Attentional capture by a task-irrelevant auditory deviation (e.g., a female-spoken token following a sequence of male-spoken tokens)--as indexed by its disruption of a visually presented recall task--was abolished when focal-task engagement…

Increased stress reactivity is associated with cognitive deficits and decreased hippocampal brain-derived neurotrophic factor in a mouse model of affective disorders.

PubMed

Knapman, A; Heinzmann, J-M; Hellweg, R; Holsboer, F; Landgraf, R; Touma, C

2010-07-01

Cognitive deficits are a common feature of major depression (MD), with largely unknown biological underpinnings. In addition to the affective and cognitive symptoms of MD, a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is commonly observed in these patients. Increased plasma glucocorticoid levels are known to render the hippocampus susceptible to neuronal damage. This structure is important for learning and memory, creating a potential link between HPA axis dysregulation and cognitive deficits in depression. In order to further elucidate how altered stress responsiveness may contribute to the etiology of MD, three mouse lines with high (HR), intermediate (IR), or low (LR) stress reactivity were generated by selective breeding. The aim of the present study was to investigate whether increased stress reactivity is associated with deficits in hippocampus-dependent memory tests. To this end, we subjected mice from the HR, IR, and LR breeding lines to tests of recognition memory, spatial memory, and depression-like behavior. In addition, measurements of brain-derived neurotrophic factor (BDNF) in the hippocampus and plasma of these animals were conducted. Our results demonstrate that HR mice exhibit hippocampus-dependent memory deficits along with decreased hippocampal, but not plasma, BDNF levels. Thus, the stress reactivity mouse lines are a promising animal model of the cognitive deficits in MD with the unique feature of a genetic predisposition for an altered HPA axis reactivity, which provides the opportunity to explore the progression of the symptoms of MD, predisposing genetic factors as well as new treatment strategies. Copyright 2009 Elsevier Ltd. All rights reserved.

Neuropsychological functioning and brain structure in schizophrenia.

PubMed

Crespo-Facorro, Benedicto; Barbadillo, Laura; Pelayo-Terán, José Maria; Rodríguez-Sánchez, José Manuel

2007-08-01

Cognitive deficits are core features of schizophrenia that are already evident at early phases of the illness. The study of specific relationships between cognition and brain structure might provide valuable clues about neural basis of schizophrenia and its phenomenology. The aim of this article was to review the most consistent findings of the studies exploring the relationships between cognitive deficits and brain anomalies in schizophrenia. Besides several important methodological shortcomings to bear in mind before drawing any consistent conclusion from the revised literature, we have attempted to systematically summarize these findings. Thus, this review has revealed that whole brain volume tends to positively correlate with a range of cognitive domains in healthy volunteers and female patients. An association between prefrontal morphological characteristics and general inability to control behaviour seems to be present in schizophrenia patients. Parahippocampal volume is related to semantic cognitive functions. Thalamic anomalies have been associated with executive deficits specifically in patients. Available evidence on the relationship between cognitive functions and cerebellar structure is still contradictory. Nonetheless, a larger cerebellum appears to be associated with higher IQ in controls and in female patients. Enlarged ventricles, including lateral and third ventricles, are associated with deficits in attention, executive and premorbid cognitive functioning in patients. Several of these reported findings seem to be counterintuitive according to neural basis of cognitive functioning drawn from animal, lesion, and functional imaging investigations. Therefore, there is still a great need for more methodologically stringent investigations that would help in the advance of our understanding of the cognition/brain structure relationships in schizophrenia.

Cognitive functioning in the first-episode of major depressive disorder: A systematic review and meta-analysis.

PubMed

Ahern, Elayne; Semkovska, Maria

2017-01-01

Cognitive deficits are frequently observed in major depression. Yet, when these deficits emerge and how they relate to the depressed state is unclear. The aim of this 2-part systematic review and meta-analysis is to determine the pattern and extent of cognitive deficits during a first-episode of depression (FED) and their persistence following FED remission. Published, peer-reviewed articles on cognitive function in FED patients through October 2015 were searched. Meta-analyses with random-effects modeling were conducted. Part 1 assessed weighted, mean effect sizes of cognitive function in FED patients relative to healthy controls. Moderator analyses of clinical and demographical variables effects were conducted. Part 2 assessed weighted, mean effect sizes of change in cognitive function at remission compared with acute FED performance in longitudinal studies. Thirty-one studies including 994 FED patients were retained in Part 1. Relative to healthy controls, small to large impairments were observed across most cognitive domains. Remission was associated with a normalization of function in processing speed, learning and memory, autobiographical memory, shifting, and IQ. Lower FED age was associated with higher IQ, but more impairment in word-list delayed memory. Four studies including 92 FED patients were retained in Part 2. Following remission, FED patients showed small improvements in processing speed and shifting but persistent impairment in inhibition and verbal fluency. Significant cognitive deficits are already identifiable during a FED, with some functions showing persistent impairment upon remission. Clinicians must consider cognitive impairment alongside mood symptoms to ensure functional recovery from the FED. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

Psychosocial support and cognitive deficits in adults with schizophrenia.

PubMed

Dalagdi, Aikaterini; Arvaniti, Aikaterini; Papatriantafyllou, John; Xenitidis, Kiriakos; Samakouri, Maria; Livaditis, Miltos

2014-08-01

In recent decades there has been an increasing interest in cognitive deficits in schizophrenia. However, only a few studies have examined the impact of psychosocial support on the prevention of cognitive deterioration in patients who suffer from schizophrenia. The aims of the present study are: (1) to confirm the presence of cognitive deficits among patients with schizophrenia; (2) to explore any correlations between such deficits and a range of clinical and/or demographic characteristics of the patients; and (3) to investigate any association between cognitive deficits and psychosocial support. A total of 118 patients with schizophrenia (the patient group) and 102 healthy volunteers (the control group) had a cognitive assessment using a battery of neuropsychological tests. The patients were allocated to one of the following groups: (1) patients under routine outpatient follow-up; or (2) patients receiving or having recently received intensive psychosocial support, in addition to follow-up. This included daily participation in vocational and recreational activities provided by dedicated mental health day centers. The findings of the neuropsychological testing of individuals in all groups were compared, after controlling for clinical or demographic factors. The scores in the neuropsychological tests were lower overall in the patients group compared to healthy volunteers. Within the patients group, those receiving/having received psychosocial support had higher scores compared to those on routine follow-up alone. There were no significant differences between patients currently receiving psychosocial support and those having received it in the past. Lower education, age and illness duration (but not severity of positive or negative symptoms) were factors associated with lower test scores. The study provides some evidence that psychosocial support may be beneficial for the cognitive functioning of patients with schizophrenia and this benefit may be a lasting one. © The Author(s) 2013.

Curcumin attenuates inflammatory response and cognitive deficits in experimental model of chronic epilepsy.

PubMed

Kaur, Harpreet; Patro, Ishan; Tikoo, Kulbhushan; Sandhir, Rajat

2015-10-01

Evidence suggests that glial cells play a critical role in inflammation in chronic epilepsy, contributing to perpetuation of seizures and cognitive dysfunctions. The present study was designed to evaluate the beneficial effect of curcumin, a polyphenol with pleiotropic properties, on cognitive deficits and inflammation in chronic epilepsy. Kindled model of epilepsy was induced by administering sub-convulsive dose of pentylenetetrazole (PTZ) at 40 mg/kg, i.p. every alternative day for 30 days to Wistar rats. The animals were assessed for cognitive deficits by Morris water maze and inflammatory response in terms of microglial and astrocyte activation. PTZ treated animals had increased escape latency suggesting impaired cognitive functions. Further, an increased expression of astrocyte (GFAP) and microglial (Iba-1) activation markers were observed in terms of mRNA and protein levels in the PTZ treated animals. Concomitantly, mRNA and protein levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and chemokine (MCP-1) were increased in hippocampus and cortex. Immunoreactivity to anti-GFAP and anti-Iba-1 antibodies was also enhanced in hippocampus and cortex suggesting gliosis in PTZ treated animals. However, curcumin administration at a dose of 100 mg/kg to PTZ animals prevented cognitive deficits. A significant decrease in pro-inflammatory cytokines and chemokine expression was observed in hippocampus and cortex of PTZ treated rats supplemented with curcumin. In addition, curcumin also attenuated increased expression of GFAP and Iba-1 in animals with PTZ induced chronic epilepsy. Moreover, immunohistochemical analysis also showed significant reduction in number of activated glial cells on curcumin administration to PTZ treated animals. Taken together, these findings suggest that curcumin is effective in attenuating glial activation and ameliorates cognitive deficits in chronic epilepsy. Copyright © 2015 Elsevier Ltd. All rights reserved.

Cocaine self-administration abolishes associative neural encoding in the nucleus accumbens necessary for higher-order learning.

PubMed

Saddoris, Michael P; Carelli, Regina M

2014-01-15

Cocaine use is often associated with diminished cognitive function, persisting even after abstinence from the drug. Likely targets for these changes are the core and shell of the nucleus accumbens (NAc), which are critical for mediating the rewarding aspects of drugs of abuse as well as supporting associative learning. To understand this deficit, we recorded neural activity in the NAc of rats with a history of cocaine self-administration or control subjects while they learned Pavlovian first- and second-order associations. Rats were trained for 2 weeks to self-administer intravenous cocaine or water. Later, rats learned a first-order Pavlovian discrimination where a conditioned stimulus (CS)+ predicted food, and a control (CS-) did not. Rats then learned a second-order association where, absent any food reinforcement, a novel cued (SOC+) predicted the CS+ and another (SOC-) predicted the CS-. Electrophysiological recordings were taken during performance of these tasks in the NAc core and shell. Both control subjects and cocaine-experienced rats learned the first-order association, but only control subjects learned the second-order association. Neural recordings indicated that core and shell neurons encoded task-relevant information that correlated with behavioral performance, whereas this type of encoding was abolished in cocaine-experienced rats. The NAc core and shell perform complementary roles in supporting normal associative learning, functions that are impaired after cocaine experience. This impoverished encoding of motivational behavior, even after abstinence from the drug, might provide a key mechanism to understand why addiction remains a chronically relapsing disorder despite repeated attempts at sobriety. Copyright © 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Experimental Training of Children with Attention Deficit/Hyperactivity Disorder

ERIC Educational Resources Information Center

Piscalkiene, Viktorija

2009-01-01

Attention-deficit/hyperactivity disorder (AD/HD) negatively affects the cognitive and psychomotoric spheres of the pupil's social behavior and social adaptation. The review of many studies states that pupils with AD/HD achieve worse learning results because of insufficiently functioning cognitive processes, such as attention, (work) memory,…

Parkinson's Disease and Dopaminergic Therapy--Differential Effects on Movement, Reward and Cognition

ERIC Educational Resources Information Center

Rowe, J. B.; Hughes, L.; Ghosh, B. C. P.; Eckstein, D.; Williams-Gray, C. H.; Fallon, S.; Barker, R. A.; Owen, A. M.

2008-01-01

Cognitive deficits are very common in Parkinson's disease particularly for "executive functions" associated with frontal cortico-striatal networks. Previous work has identified deficits in tasks that require attentional control like task-switching, and reward-based tasks like gambling or reversal learning. However, there is a complex…

Understanding Cognitive Deficits in Parkinson's Disease: Lessons from Preclinical Animal Models

ERIC Educational Resources Information Center

Solari, Nicola; Bonito-Oliva, Alessandra; Fisone, Gilberto; Brambilla, Riccardo

2013-01-01

Parkinson's disease (PD) has been, until recently, mainly defined by the presence of characteristic motor symptoms, such as rigidity, tremor, bradykinesia/akinesia, and postural instability. Accordingly, pharmacological and surgical treatments have so far addressed these motor disturbances, leaving nonmotor, cognitive deficits an unmet…

Visuospatial Attention Disturbance in Duchenne Muscular Dystrophy

ERIC Educational Resources Information Center

De Moura, Maria Clara Drummond Soares; do Valle, Luiz Eduardo Ribeiro; Resende, Maria Bernadete Dutra; Pinto, Katia Osternack

2010-01-01

Aim: The cognitive deficits present in the Duchenne muscular dystrophy (DMD) are not yet well characterized. Attention, considered to be the brain mechanism responsible for the selection of sensory stimuli, could be disturbed in DMD, contributing, at least partially, to the observed global cognitive deficit. The aim of this study was to…

Berry fruit can improve age-associated neuronal and cognitive deficits: from the laboratory to the clinic

USDA-ARS?s Scientific Manuscript database

Research has demonstrated, in both human and animals, that cognitive functioning decreases with age, to include deficits in processing speed, executive function, memory, and spatial learning. The cause of these functional declines is not entirely understood; however, neuronal losses and the associat...

An Integrative, Cognitive-Behavioral, Systemic Approach to Working with Students Diagnosed with Attention Deficit Hyperactive Disorder

ERIC Educational Resources Information Center

Shillingford, Margaret Ann; Lambie, Glenn W.; Walter, Sara Meghan

2007-01-01

Attention deficit hyperactive disorder (ADHD) is a prevalent diagnostic disorder for many students, which correlates with negative academic, social, and personal consequences. This article presents an integrative, cognitive-behavioral, systemic approach that offers behaviorally based interventions for professional school counselors to support…

Cognitive Screening in Brain Tumors: Short but Sensitive Enough?

PubMed Central

Robinson, Gail A.; Biggs, Vivien; Walker, David G.

2015-01-01

Cognitive deficits in brain tumors are generally thought to be relatively mild and non-specific, although recent evidence challenges this notion. One possibility is that cognitive screening tools are being used to assess cognitive functions but their sensitivity to detect cognitive impairment may be limited. For improved sensitivity to recognize mild and/or focal cognitive deficits in brain tumors, neuropsychological evaluation tailored to detect specific impairments has been thought crucial. This study investigates the sensitivity of a cognitive screening tool, the Montreal Cognitive Assessment (MoCA), compared to a brief but tailored cognitive assessment (CA) for identifying cognitive deficits in an unselected primary brain tumor sample (i.e., low/high-grade gliomas, meningiomas). Performance is compared on broad measures of impairment: (a) number of patients impaired on the global screening measure or in any cognitive domain; and (b) number of cognitive domains impaired and specific analyses of MoCA-Intact and MoCA-Impaired patients on specific cognitive tests. The MoCA-Impaired group obtained lower naming and word fluency scores than the MoCA-Intact group, but otherwise performed comparably on cognitive tests. Overall, based on our results from patients with brain tumor, the MoCA has extremely poor sensitivity for detecting cognitive impairments and a brief but tailored CA is necessary. These findings will be discussed in relation to broader issues for clinical management and planning, as well as specific considerations for neuropsychological assessment of brain tumor patients. PMID:25815273

Abnormal frontal theta oscillations underlie the cognitive flexibility deficits in children with high-functioning autism spectrum disorders.

PubMed

Yeung, Michael K; Han, Yvonne M Y; Sze, Sophia L; Chan, Agnes S

2016-03-01

Deficits in cognitive flexibility have been suggested to underlie the repetitive and stereotyped behavior in individuals with autism spectrum disorders (ASD). Because cognitive flexibility is primarily mediated by the frontal lobe, where structural and functional abnormalities have been extensively found in these individuals, it is conceivable that their deficits in cognitive flexibility are related to abnormal activations of the frontal lobe. The present study investigates cognitive flexibility and its underlying neurophysiological activities as indicated by theta oscillations in children with ASD. Twenty-five children with high-functioning ASD and 25 IQ- and age-matched typically developing (TD) children were subjected to neuropsychological assessments on cognitive flexibility and electroencephalography recordings. The children with ASD performed significantly worse than the TD children across the tasks of cognitive flexibility, including the modified Wisconsin Card Sorting Test (WCST). These children also demonstrated a reduced increase of the theta power localized in multiple brain regions, including various sectors of the frontal lobe at the late stage (i.e., 600 ms-900 ms poststimulus interval) but not the early stage (i.e., 250 ms-550 ms poststimulus interval) of the performance of the modified WCST. The suppressed late frontal theta activities were further shown to be significantly correlated with a poorer performance on the cognitive flexibility measures. Our findings suggest that abnormal activations of multiple cortical regions, especially the frontal lobe, form the neural basis of the cognitive flexibility deficits in children with ASD. In addition, we found an EEG marker of cognitive flexibility which could be used to monitor treatment outcomes objectively. (c) 2016 APA, all rights reserved).

Social cognition, social skill, and the broad autism phenotype.

PubMed

Sasson, Noah J; Nowlin, Rachel B; Pinkham, Amy E

2013-11-01

Social-cognitive deficits differentiate parents with the "broad autism phenotype" from non-broad autism phenotype parents more robustly than other neuropsychological features of autism, suggesting that this domain may be particularly informative for identifying genetic and brain processes associated with the phenotype. The current study examined whether the social-cognitive deficits associated with the broad autism phenotype extend to the general population and relate to reduced social skill. A total of 74 undergraduates completed the Broad Autism Phenotype Questionnaire, three standardized social-cognitive tasks, and a live social interaction with an unfamiliar research assistant. Social broad autism phenotype traits were significantly associated with deficits in social cognition and reduced social skill. In addition, the relationship between social broad autism phenotype traits and social skill was partially mediated by social cognition, suggesting that the reduced interpersonal ability associated with the broad autism phenotype occurs in part because of poorer social-cognitive ability. Together, these findings indicate that the impairments in social cognition and social skill that characterize autism spectrum disorder extend in milder forms to the broad autism phenotype in the general population and suggest a framework for understanding how social broad autism phenotype traits may manifest in diminished social ability.

Acute neuroinflammation impairs context discrimination memory and disrupts pattern separation processes in hippocampus.

PubMed

Czerniawski, Jennifer; Guzowski, John F

2014-09-10

Although it is known that immune system activation can impair cognition, no study to date has linked cognitive deficits during acute neuroinflammation to dysregulation of task-relevant neuronal ensemble activity. Here, we assessed both neural circuit activity and context discrimination memory retrieval, in a within-subjects design, of male rats given systemic administration of saline or lipopolysaccharide (LPS). Rats were exposed over several days to two similar contexts: one of which was paired with weak foot shock and the other was not. After reaching criteria for discriminative freezing, rats were given systemic LPS or saline injection and tested for retrieval of context discrimination 6 h later. Importantly, LPS administration produced an acute neuroinflammatory response in dorsal hippocampus at this time (as assessed by elevation of proinflammatory cytokine mRNA levels) and abolished retrieval of the previously acquired discrimination. The impact of neuroinflammation on hippocampal CA3 and CA1 neural circuit activity was assessed using the Arc/Homer1a cellular analysis of temporal activity by fluorescence in situ hybridization imaging method. Whereas the saline-treated subjects discriminated and had low overlap of hippocampal ensembles activated in the two contexts, LPS-treated subjects did not discriminate and had greater ensemble overlap (i.e., reduced orthogonalization). Additionally, retrieval of standard contextual fear conditioning, which does not require context discrimination, was not affected by pretesting LPS administration. Together, the behavioral and circuit analyses data provide compelling evidence that LPS administration impairs context discrimination memory by disrupting cellular pattern separation processes within the hippocampus, thus linking acute neuroinflammation to disruption of specific neural circuit functions and cognitive impairment. Copyright © 2014 the authors 0270-6474/14/3412470-11$15.00/0.

Acute Neuroinflammation Impairs Context Discrimination Memory and Disrupts Pattern Separation Processes in Hippocampus

PubMed Central

Czerniawski, Jennifer

2014-01-01

Although it is known that immune system activation can impair cognition, no study to date has linked cognitive deficits during acute neuroinflammation to dysregulation of task-relevant neuronal ensemble activity. Here, we assessed both neural circuit activity and context discrimination memory retrieval, in a within-subjects design, of male rats given systemic administration of saline or lipopolysaccharide (LPS). Rats were exposed over several days to two similar contexts: one of which was paired with weak foot shock and the other was not. After reaching criteria for discriminative freezing, rats were given systemic LPS or saline injection and tested for retrieval of context discrimination 6 h later. Importantly, LPS administration produced an acute neuroinflammatory response in dorsal hippocampus at this time (as assessed by elevation of proinflammatory cytokine mRNA levels) and abolished retrieval of the previously acquired discrimination. The impact of neuroinflammation on hippocampal CA3 and CA1 neural circuit activity was assessed using the Arc/Homer1a cellular analysis of temporal activity by fluorescence in situ hybridization imaging method. Whereas the saline-treated subjects discriminated and had low overlap of hippocampal ensembles activated in the two contexts, LPS-treated subjects did not discriminate and had greater ensemble overlap (i.e., reduced orthogonalization). Additionally, retrieval of standard contextual fear conditioning, which does not require context discrimination, was not affected by pretesting LPS administration. Together, the behavioral and circuit analyses data provide compelling evidence that LPS administration impairs context discrimination memory by disrupting cellular pattern separation processes within the hippocampus, thus linking acute neuroinflammation to disruption of specific neural circuit functions and cognitive impairment. PMID:25209285

A comparison of discrimination learning in touchscreen and 2-choice swim tank using an allelic series of Huntington's disease mice.

PubMed

Glynn, Dervila; Skillings, Elizabeth A; Morton, A Jennifer

2016-05-30

Progressive cognitive impairments are a major, debilitating symptom of neurodegenerative disorders such as Alzheimer's disease (AD) and Huntington's disease (HD). Developing treatments to slow or prevent cognitive decline is a key challenge for these fields. Unfortunately, preclinical therapeutic testing has not kept pace with molecular advances, and the methods for systematic cognitive testing in mice remain largely unchanged. Although higher throughput semi-automated systems exist, the lack of a 'positive control' (i.e. a drug or treatment that works) makes it challenging to test their sensitivity and predict usefulness for preclinical drug testing. We used an allelic series of transgenic HD mice to test the sensitivity and flexibility of two cognitive testing systems; a semi-automated touchscreen system and a traditional water-based task, the 2-choice swim tank. We found significant differences in performance of HD mice with different CAG repeats, with timing and severity of deficits dependent on CAG repeat length. We also found deficits in long-term memory retention that have not been reported previously. Both systems were useful for detecting deficits, and were sensitive enough to detect small changes (10-20%) in cognitive performance. While the touchscreen system is more sensitive and can identify deficits up to 10 weeks earlier than the 2-choice swim tank, both tests detected similar patterns of deficit progression in HD mice, regardless of CAG repeat length. Thus, although it has its limitations, the 2-choice swim tank remains a simple, cheap and accessible system for assessing cognitive function. Copyright © 2015 Elsevier B.V. All rights reserved.

Cognitive deficits and predictors 3 years after diagnosis of a pilocytic astrocytoma in childhood.

PubMed

Aarsen, Femke K; Paquier, Philippe F; Arts, Willem-Frans; Van Veelen, Marie-Lise; Michiels, Erna; Lequin, Maarten; Catsman-Berrevoets, Coriene E

2009-07-20

PURPOSE To prospectively study cognitive deficits and predictors 3 years after diagnosis in a large series of pediatric patients treated for pilocytic astrocytoma (PA). PATIENTS AND METHODS Sixty-one of 67 children were grouped according to infratentorial, supratentorial midline, and supratentorial hemispheric site. Intelligence, memory, attention, language, visual-spatial, and executive functions were assessed. Included predictors were sex, age, relapse, diagnosis-assessment interval, hydrocephalus, kind of treatment, and tumor variables. Results All children with PA had problems with sustained attention and speed. In the infratentorial group, there also were deficits in verbal intelligence, visual-spatial memory, executive functioning, and naming. Verbal intelligence and verbal memory problems occurred in the brainstem tumor group. The supratentorial hemispheric tumor group had additional problems with selective attention and executive functioning, and the supratentorial midline tumor group displayed no extra impairments. More specifically, the dorsal supratentorial midline tumor group displayed problems with language and verbal memory. Predictors for lower cognitive functioning were hydrocephalus, radiotherapy, residual tumor size, and age; predictors for better functioning were chemotherapy or treatment of hydrocephalus. Almost 60% of children had problems with academic achievement, for which risk factors were relapse and younger age at diagnosis. CONCLUSION Despite normal intelligence at long-term follow-up, children treated for PA display invalidating cognitive impairments. Adequate treatment of hydrocephalus is important for a more favorable long-term cognitive outcome. Even children without initial severe deficits may develop cognitive impairments years after diagnosis, partly because of the phenomenon of growing into deficit, which has devastating implications for academic achievement and quality of life (QOL).

Methamphetamine treatment during development attenuates the dopaminergic deficits caused by subsequent high-dose methamphetamine administration.

PubMed

McFadden, Lisa M; Hoonakker, Amanda J; Vieira-Brock, Paula L; Stout, Kristen A; Sawada, Nicole M; Ellis, Jonathan D; Allen, Scott C; Walters, Elliot T; Nielsen, Shannon M; Gibb, James W; Alburges, Mario E; Wilkins, Diana G; Hanson, Glen R; Fleckenstein, Annette E

2011-08-01

Administration of high doses of methamphetamine (METH) causes persistent dopaminergic deficits in both nonhuman preclinical models and METH-dependent persons. Noteworthy, adolescent [i.e., postnatal day (PND) 40] rats are less susceptible to this damage than young adult (PND90) rats. In addition, biweekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a "challenge" high-dose METH regimen when administered at PND90. Mechanisms underlying this "resistance" were thus investigated. Results revealed that biweekly METH treatment throughout development attenuated both the acute and persistent deficits in VMAT2 function, as well as the acute hyperthermia, caused by a challenge METH treatment. Pharmacokinetic alterations did not appear to contribute to the protection afforded by the biweekly treatment. Maintenance of METH-induced hyperthermia abolished the protection against both the acute and persistent VMAT2-associated deficits suggesting that alterations in thermoregulation were caused by exposure of rats to METH during development. These findings suggest METH during development prevents METH-induced hyperthermia and the consequent METH-related neurotoxicity. Copyright © 2011 Wiley-Liss, Inc.

Amantadine Ameliorates Dopamine-Releasing Deficits and Behavioral Deficits in Rats after Fluid Percussion Injury

PubMed Central

Huang, Eagle Yi-Kung; Tsui, Pi-Fen; Kuo, Tung-Tai; Tsai, Jing-Jr.; Chou, Yu-Ching; Ma, Hsin-I; Chiang, Yung-Hsiao; Chen, Yuan-Hao

2014-01-01

Aims To investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI), we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery. Materials and Methods In this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group) or amantadine hydrochloride, with a releasing rate of 3.6mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV) and high-pressure liquid chromatography (HPLC). Novel object recognition (NOR) and fixed-speed rotarod (FSRR) behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury. Results Sequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value) of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion. Conclusion Chronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury. PMID:24497943

[Research progress in mechanisms and clinical application for blonanserin and lurasidone in improving cognitive function of schizophrenia].

PubMed

Zheng, Qi; Liu, Bangshan; Xu, Shuyin; Liao, Mei; Zhang, Yan; Li, Lingjiang

2017-04-28

Cognition deficit is one of the most common symptoms of schizophrenia, including abstract thinking and memory, and attention deficits. Previous studies have suggested that the improvement of cognition is very important for the recovery of disease and social function for the patients. Recent studies indicated that two new atypical antipsychotics, blonanserin and lurasidone, are expected to improve the cognitive impairment in patients with schizophrenia. This review introduces pathogenesis of cognitive impairment in schizophrenia, mechanisms of blonanserin and lurasidone in the improvement of cognitive impairment and progress in their clinical application for schizophrenia. We hope that this review could guide clinical use of antipsychotics and provide new directions for future studies.

Awareness of memory failures and motivation for cognitive training in mild cognitive impairment.

PubMed

Werheid, Katja; Ziegler, Matthias; Klapper, Annina; Kühl, Klaus-Peter

2010-01-01

Awareness of cognitive deficits is considered to be decisive for the effectiveness of cognitive training in mild cognitive impairment (MCI). However, it is unclear in what way awareness influences motivation to participate in cognitive training. Thirty-two elderly adults with MCI and 72 controls completed the 5-scale Memory Functioning Questionnaire (MFQ) and a motivation questionnaire. The predictive value of the MFQ scales on motivation was analyzed using regression analysis. In the MCI group, but not in controls, higher perceived frequency of memory failures was associated with a lower motivation score. Our findings indicate that, in MCI, greater awareness of cognitive deficits does not necessarily increase motivation to participate in cognitive trainings, and suggest that success expectancy may be a moderating factor. Copyright © 2010 S. Karger AG, Basel.

Emotion Perception or Social Cognitive Complexity: What Drives Face Processing Deficits in Autism Spectrum Disorder?

ERIC Educational Resources Information Center

Walsh, Jennifer A.; Creighton, Sarah E.; Rutherford, M. D.

2016-01-01

Some, but not all, relevant studies have revealed face processing deficits among those with autism spectrum disorder (ASD). In particular, deficits are revealed in face processing tasks that involve emotion perception. The current study examined whether either deficits in processing emotional expression or deficits in processing social cognitive…

The relative contributions of processing speed and cognitive load to working memory accuracy in multiple sclerosis.

PubMed

Leavitt, Victoria M; Lengenfelder, Jean; Moore, Nancy B; Chiaravalloti, Nancy D; DeLuca, John

2011-06-01

Cognitive symptoms of multiple sclerosis (MS) include processing-speed deficits and working memory impairment. The precise manner in which these deficits interact in individuals with MS remains to be explicated. We hypothesized that providing more time on a complex working memory task would result in performance benefits for individuals with MS relative to healthy controls. Fifty-three individuals with clinically definite MS and 36 matched healthy controls performed a computerized task that systematically manipulated cognitive load. The interval between stimuli presentations was manipulated to provide increasing processing time. The results confirmed that individuals with MS who have processing-speed deficits significantly improve in performance accuracy when given additional time to process the information in working memory. Implications of these findings for developing appropriate cognitive rehabilitation interventions are discussed.

An index predictive of cognitive outcome in retired professional American Football players with a history of sports concussion.

PubMed

Wright, Mathew J; Woo, Ellen; Birath, J Brandon; Siders, Craig A; Kelly, Daniel F; Wang, Christina; Swerdloff, Ronald; Romero, Elizabeth; Kernan, Claudia; Cantu, Robert C; Guskiewicz, Kevin

2016-01-01

Various concussion characteristics and personal factors are associated with cognitive recovery in athletes. We developed an index based on concussion frequency, severity, and timeframe, as well as cognitive reserve (CR), and we assessed its predictive power regarding cognitive ability in retired professional football players. Data from 40 retired professional American football players were used in the current study. On average, participants had been retired from football for 20 years. Current neuropsychological performances, indicators of CR, concussion history, and play data were used to create an index for predicting cognitive outcome. The sample displayed a range of concussions, concussion severities, seasons played, CR, and cognitive ability. Many of the participants demonstrated cognitive deficits. The index strongly predicted global cognitive ability (R(2) = .31). The index also predicted the number of areas of neuropsychological deficit, which varied as a function of the deficit classification system used (Heaton: R(2) = .15; Wechsler: R(2) = .28). The current study demonstrated that a unique combination of CR, sports concussion, and game-related data can predict cognitive outcomes in participants who had been retired from professional American football for an average of 20 years. Such indices may prove to be useful for clinical decision making and research.

The Association Between Cognitive Function and Subsequent Depression: A Systematic Review and Meta-Analysis

PubMed Central

Scult, Matthew A.; Paulli, Athelia R.; Mazure, Emily S.; Moffitt, Terrie E.; Hariri, Ahmad R.; Strauman, Timothy J.

2016-01-01

Despite a growing interest in understanding the cognitive deficits associated with major depressive disorder (MDD), it is largely unknown whether such deficits exist before disorder onset or how they might influence the severity of subsequent illness. The purpose of the present study was to conduct a systematic review and meta-analysis of longitudinal datasets to determine whether cognitive function acts as a predictor of later MDD diagnosis or change in depression symptoms. Eligible studies included longitudinal designs with baseline measures of cognitive functioning, and later unipolar MDD diagnosis or symptom assessment. The systematic review identified 29 publications, representing 34 unique samples, and 121,749 participants, that met the inclusion/exclusion criteria. Quantitative meta-analysis demonstrated that higher cognitive function was associated with decreased levels of subsequent depression (r=−0.088; 95% CI: −0.121, −0.054; p<0.001). However, sensitivity analyses revealed that this association is likely driven by concurrent depression symptoms at the time of cognitive assessment. Our review and meta-analysis indicate that the association between lower cognitive function and later depression is confounded by the presence of contemporaneous depression symptoms at the time of cognitive assessment. Thus, cognitive deficits predicting MDD likely represent deleterious effects of subclinical depression symptoms on performance rather than premorbid risk factors for disorder. PMID:27624847

Memantine Protects Rats Treated with Intrathecal Methotrexate from Developing Spatial Memory Deficits

PubMed Central

Cole, Peter D.; Vijayanathan, Veena; Ali, Nafeeza F.; Wagshul, Mark E.; Tanenbaum, Eric J.; Price, Jeremy; Dalal, Vidhi; Gulinello, Maria E.

2014-01-01

Purpose To test whether memantine can prevent methotrexate-induced cognitive deficits in a preclinical model. Experimental Design After noting that methotrexate exposure induces prolonged elevations of the glutamate analog homocysteic acid (HCA) within cerebrospinal fluid, we tested whether intrathecal injection of HCA would produce memory deficits similar to those observed after intrathecal methotrexate. We then tested whether memantine, an antagonist of the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors, could protect animals treated with clinically relevant doses of intrathecal methotrexate against developing memory deficits. Finally, we asked whether memantine affected this pathway beyond inhibiting the NMDA receptor by altering expression of the NMDA receptor or affecting concentrations of HCA or glutamate within the central nervous system. Results Four intrathecal doses of methotrexate induced deficits in spatial memory, persisting at least one month following the final injection. Intrathecal HCA was sufficient to reproduce this deficit. Concurrent administration of memantine during the period of methotrexate exposure was protective, decreasing the incidence of methotrexate-induced spatial memory deficits from 56% to 20% (P < 0.05). Memantine neither altered expression of NMDA receptors within the hippocampus nor blunted the methotrexate-induced increases in glutamate or HCA. Conclusions Excitotoxic glutamate analogs including HCA contribute to cognitive deficits observed after intrathecal methotrexate. Memantine, an NMDA receptor antagonist, reduces the incidence of cognitive deficits in rats treated with intrathecal methotrexate, and may therefore benefit patients with cancer receiving similar treatment. PMID:23833301

Correlation between insight dimensions and cognitive functions in patients with deficit and nondeficit schizophrenia.

PubMed

Pegoraro, Luiz F L; Dantas, Clarissa R; Banzato, Claudio E M; Fuentes, Daniel

2013-06-01

Previous studies have shown correlations between poor insight and neurocognitive impairment in schizophrenia. Deficit schizophrenia has been associated with worse cognitive functioning and poorer insight. This study aimed at investigating the relationship between insight dimensions (measured by Schedule for the Assessment of Insight-Expanded Version and its factors) and specific neurocognitive functions (assessed through a battery of neuropsychological tests) considering separately patients with deficit (n=29) and nondeficit schizophrenia (n=44), categorized according to the Schedule for the Deficit Syndrome. We found that working memory correlated positively and significantly with awareness of mental illness in both groups. In nondeficit group, awareness of mental illness correlated additionally with verbal fluency and attention. If confirmed by further studies, these results may have important consequences, such as the need of tailoring differently cognitive rehabilitation for each group. Copyright © 2013 Elsevier B.V. All rights reserved.

Original nootropic drug noopept prevents memory deficit in rats with muscarinic and nicotinic receptor blockade.

PubMed

Radionova, K S; Belnik, A P; Ostrovskaya, R U

2008-07-01

Antiamnesic activity of Noopept was studied on the original three-way model of conditioned passive avoidance response, which allows studying spatial component of memory. Cholinoceptor antagonists of both types (scopolamine and mecamylamine) decreased entry latency and reduced the probability for selection of the safe compartment. Noopept abolished the antiamnesic effect of cholinoceptor antagonists and improved spatial preference.

Contextual Social Cognition Impairments in Schizophrenia and Bipolar Disorder

PubMed Central

Villarin, Lilian; Theil, Donna; Gonzalez-Gadea, María Luz; Gomez, Pedro; Mosquera, Marcela; Huepe, David; Strejilevich, Sergio; Vigliecca, Nora Silvana; Matthäus, Franziska; Decety, Jean; Manes, Facundo; Ibañez, Agustín M.

2013-01-01

Background The ability to integrate contextual information with social cues to generate social meaning is a key aspect of social cognition. It is widely accepted that patients with schizophrenia and bipolar disorders have deficits in social cognition; however, previous studies on these disorders did not use tasks that replicate everyday situations. Methodology/Principal Findings This study evaluates the performance of patients with schizophrenia and bipolar disorders on social cognition tasks (emotional processing, empathy, and social norms knowledge) that incorporate different levels of contextual dependence and involvement of real-life scenarios. Furthermore, we explored the association between social cognition measures, clinical symptoms and executive functions. Using a logistic regression analysis, we explored whether the involvement of more basic skills in emotional processing predicted performance on empathy tasks. The results showed that both patient groups exhibited deficits in social cognition tasks with greater context sensitivity and involvement of real-life scenarios. These deficits were more severe in schizophrenic than in bipolar patients. Patients did not differ from controls in tasks involving explicit knowledge. Moreover, schizophrenic patients’ depression levels were negatively correlated with performance on empathy tasks. Conclusions/Significance Overall performance on emotion recognition predicted performance on intentionality attribution during the more ambiguous situations of the empathy task. These results suggest that social cognition deficits could be related to a general impairment in the capacity to implicitly integrate contextual cues. Important implications for the assessment and treatment of individuals with schizophrenia and bipolar disorders, as well as for neurocognitive models of these pathologies are discussed. PMID:23520477

Cognitive Deficits in Problematic Drinkers with and without Mild to Borderline Intellectual Disability

ERIC Educational Resources Information Center

van Duijvenbode, Neomi; Didden, Robert; VanDerNagel, Joanne E. L.; Korzilius, Hubert P. L. M.; Engels, Rutger C. M. E.

2018-01-01

We examined cognitive deficits in problematic drinkers with and without mild to borderline intellectual disability (MBID). Problematic drinkers were expected to show a significantly lower estimated performance IQ (PIQ), but not a lower estimated verbal IQ (VIQ), compared to light drinkers. Participants (N = 474) were divided into four groups based…

Cognitive Impairments Are Different in Single-Incidence and Multi-Incidence ADHD Families

ERIC Educational Resources Information Center

Oerlemans, Anoek M.; Hartman, Catharina A.; Bruijn, Yvette G. E.; Franke, Barbara; Buitelaar, Jan K.; Rommelse, Nanda N. J.

2015-01-01

Background: We may improve our understanding of the role of common versus unique risk factors in attention-deficit/hyperactivity disorder (ADHD) by examining ADHD-related cognitive deficits in single- (SPX), and multi-incidence (MPX) families. Given that individuals from multiplex (MPX) families are likely to share genetic vulnerability for the…

Agnosia, apraxia, callosal disconnection and other specific cognitive disorders.

PubMed

Acciarresi, Monica

2012-01-01

Cortical function deficits have long been studied by anatomoclinic correlations. Recent functional imaging studies have allowed scientists to better understand which cerebral areas and which networks are involved in cognitive function deficit. This chapter will review the current knowledge on agnosia, apraxia and callosal disconnection syndromes. Copyright © 2012 S. Karger AG, Basel.

A Case Study of the Cognitive and Behavioral Deficits of Temporal Lobe Damage in Herpes Simplex Encephalitis.

ERIC Educational Resources Information Center

Greer, Margaret K.; And Others

1989-01-01

This case study illustrates the highly significant language difficulties, marked memory deficits, and propensity for physical aggression following temporal lobe damage brought about by herpes encephalitis, and presents the usefulness of a new diagnostic measure in delineating such a variable cognitive pattern. (Author)

Cognitive Flexibility and Its Relationship to Academic Achievement and Career Choice of College Students with and without Attention Deficit Hyperactivity Disorder

ERIC Educational Resources Information Center

Kercood, Suneeta; Lineweaver, Tara T.; Frank, Colleen C.; Fromm, Erik D.

2017-01-01

The purpose of this study was to investigate the relationship between cognitive flexibility, academic skills, educational trajectories, and career goals of college students with and without Attention Deficit Hyperactivity Disorder (ADHD). Participants completed a demographic questionnaire, objective and subjective measures of cognitive…

Cognitive Attributes, Attention, and Self-Efficacy of Adequate and Inadequate Responders in a Fourth Grade Reading Intervention

ERIC Educational Resources Information Center

Cho, Eunsoo; Roberts, Garrett J.; Capin, Philip; Roberts, Greg; Miciak, Jeremy; Vaughn, Sharon

2015-01-01

We examined cognitive attributes, attention, and self-efficacy of fourth grade struggling readers who were identified as adequate responders (n = 27), inadequate responders with comprehension only deficits (n = 46), and inadequate responders with comprehension and word reading deficits (n = 52) after receiving a multicomponent reading…

Dyslexia Heterogeneity: Cognitive Profiling of Portuguese Children with Dyslexia

ERIC Educational Resources Information Center

Pacheco, Andreia; Reis, Alexandra; Araújo, Susana; Inácio, Filomena; Petersson, Karl Magnus; Faísca, Luís

2014-01-01

Recent studies have emphasized that developmental dyslexia is a multiple-deficit disorder, in contrast to the traditional single-deficit view. In this context, cognitive profiling of children with dyslexia may be a relevant contribution to this unresolved discussion. The aim of this study was to profile 36 Portuguese children with dyslexia from…

Cognitive Deficits in Adults with ADHD Go beyond Comorbidity Effects

ERIC Educational Resources Information Center

Silva, Katiane L.; Guimaraes-da-Silva, Paula O.; Grevet, Eugenio H.; Victor, Marcelo M.; Salgado, Carlos A. I.; Vitola, Eduardo S.; Mota, Nina R.; Fischer, Aline G.; Contini, Veronica; Picon, Felipe A.; Karam, Rafael G.; Belmonte-de-Abreu, Paulo; Rohde, Luis A.; Bau, Claiton H. D.

2013-01-01

Objective: This study addresses if deficits in cognitive, attention, and inhibitory control performance in adults with ADHD are better explained by the disorder itself or by comorbid conditions. Method Adult patients with ADHD ("n" = 352) and controls ("n" = 94) were evaluated in the ADHD program of a tertiary hospital. The…

Idiosyncratic Genetic Specificity for Neurolinguistic Systems: A Cause of Atypical or Delayed Language Acquisition.

ERIC Educational Resources Information Center

Lamendella, John T.

The diagnostic problem presented by children without obvious neurological, cognitive, genetic, emotional or environmental basis for their atypical or delayed language development is discussed. One unresolved issue is whether the deficits of such dysphasic children are linguistic or are more fundamental cognitive or perceptuomotor deficits. A…

Teacher Beliefs and Responses toward Student Misbehavior: Influence of Cognitive Skill Deficits

ERIC Educational Resources Information Center

Hart, Susan Crandall; DiPerna, James Clyde

2017-01-01

This study aimed to examine whether having knowledge of student cognitive skill deficits changes teacher beliefs and responses in regard to classroom misbehavior. Teachers (N = 272) were randomly assigned to an experimental or control condition. Although teachers in both conditions read the same vignette describing a student's misbehavior, the…

Social cognition deficits and the 'ultra high risk' for psychosis population: a review of literature.

PubMed

Thompson, Andrew D; Bartholomeusz, Cali; Yung, Alison R

2011-08-01

A number of risk factors for developing a psychotic disorder have been investigated in the 'ultra high risk' (UHR) population, including neurocognitive abilities, social functioning and, more recently, social cognition. We aimed to review the literature on social cognition in the UHR population. Literature was restricted to English articles and identified using Pubmed, Medline, PsychINFO and CINAHLplus, as well as the reference lists of published studies and reviews. Search terms included social cognition, theory of mind, emotion recognition, attributional style, social knowledge, social perception, 'at risk mental state', psychosis prodrome 'clinical high risk' and 'ultra high risk'. Inclusion criteria were an outcome measure of a social cognition task and an UHR population defined by a structured validated instrument. Seven original research articles met the inclusion criteria, one of which was a conference abstract. One of the two studies that assessed theory of mind, two of the four studies that assessed emotion recognition and both the two studies that assessed social perception/knowledge found significant deficits in UHR patients. The single study that assessed attributional bias also reported differences in UHR patients compared with healthy controls. There is limited published literature on social cognitive performance in the UHR population. Despite this, deficits in certain social cognitive abilities do appear to be present, but further research with more reliable cross-cultural measures is needed. The characterization of social cognitive deficits in the UHR populations may aid in the identification of potential markers for development of a subsequent psychotic disorder, as well as targets for early intervention. © 2011 Blackwell Publishing Asia Pty Ltd.

A cognitive psychometric model for the psychodiagnostic assessment of memory-related deficits.

PubMed

Alexander, Gregory E; Satalich, Timothy A; Shankle, W Rodman; Batchelder, William H

2016-03-01

Clinical tests used for psychodiagnostic purposes, such as the well-known Alzheimer's Disease Assessment Scale: Cognitive subscale (ADAS-Cog), include a free-recall task. The free-recall task taps into latent cognitive processes associated with learning and memory components of human cognition, any of which might be impaired with the progression of Alzheimer's disease (AD). A Hidden Markov model of free recall is developed to measure latent cognitive processes used during the free-recall task. In return, these cognitive measurements give us insight into the degree to which normal cognitive functions are differentially impaired by medical conditions, such as AD and related disorders. The model is used to analyze the free-recall data obtained from healthy elderly participants, participants diagnosed as having mild cognitive impairment, and participants diagnosed with early AD. The model is specified hierarchically to handle item differences because of the serial position curve in free recall, as well as within-group individual differences in participants' recall abilities. Bayesian hierarchical inference is used to estimate the model. The model analysis suggests that the impaired patients have the following: (1) long-term memory encoding deficits, (2) short-term memory (STM) retrieval deficits for all but very short time intervals, (3) poorer transfer into long-term memory for items successfully retrieved from STM, and (4) poorer retention of items encoded into long-term memory after longer delays. Yet, impaired patients appear to have no deficit in immediate recall of encoded words in long-term memory or for very short time intervals in STM. (c) 2016 APA, all rights reserved).

Paradoxical effect of dopamine medication on cognition in Parkinson's disease: relationship to side of motor onset.

PubMed

Hanna-Pladdy, Brenda; Pahwa, Rajesh; Lyons, Kelly E

2015-04-01

Parkinson's disease (PD) is characterized by asymmetric motor symptom onset attributed to greater degeneration of dopamine neurons contralateral to the affected side. However, whether motor asymmetries predict cognitive profiles in PD, and to what extent dopamine influences cognition remains controversial. This study evaluated cognitive variability in PD by measuring differential response to dopamine replacement therapy (DRT) based on hemispheric asymmetries. The influence of DRT on cognition was evaluated in mild PD patients (n = 36) with left or right motor onset symptoms. All subjects were evaluated on neuropsychological measures on and off DRT and compared to controls (n = 42). PD patients were impaired in executive, memory and motor domains irrespective of side of motor onset, although patients with left hemisphere deficit displayed greater cognitive impairment. Patients with right hemisphere deficit responded to DRT with significant improvement in sensorimotor deficits, and with corresponding improvement in attention and verbal memory functions. Conversely, patients with greater left hemisphere dopamine deficiency did not improve in attentional functions and declined in verbal memory recall following DRT. These findings support the presence of extensive mild cognitive deficits in early PD not fully explained by dopamine depletion alone. The paradoxical effects of levodopa on verbal memory were predicted by extent of fine motor impairment and sensorimotor response to levodopa, which reflects extent of dopamine depletion. The findings are discussed with respect to factors influencing variable cognitive profiles in early PD, including hemispheric asymmetries and differential response to levodopa based on dopamine levels predicting amelioration or overdosing.

Inducing Autophagy by Rapamycin Before, but Not After, the Formation of Plaques and Tangles Ameliorates Cognitive Deficits

PubMed Central

Majumder, Smita; Richardson, Arlan; Strong, Randy; Oddo, Salvatore

2011-01-01

Previous studies have shown that inducing autophagy ameliorates early cognitive deficits associated with the build-up of soluble amyloid-β (Aβ). However, the effects of inducing autophagy on plaques and tangles are yet to be determined. While soluble Aβ and tau represent toxic species in Alzheimer's disease (AD) pathogenesis, there is well documented evidence that plaques and tangles also are detrimental to normal brain function. Thus, it is critical to assess the effects of inducing autophagy in an animal model with established plaques and tangles. Here we show that rapamycin, when given prophylactically to 2-month-old 3xTg-AD mice throughout their life, induces autophagy and significantly reduces plaques, tangles and cognitive deficits. In contrast, inducing autophagy in 15-month-old 3xTg-AD mice, which have established plaques and tangles, has no effects on AD-like pathology and cognitive deficits. In conclusion, we show that autophagy induction via rapamycin may represent a valid therapeutic strategy in AD when administered early in the disease progression. PMID:21980451

Cognitive measures in long-term cannabis users.

PubMed

Pope, Harrison G; Gruber, Amanda J; Hudson, James I; Huestis, Marilyn A; Yurgelun-Todd, Deborah

2002-11-01

The cognitive effects of long-term cannabis use are insufficiently understood. Most studies concur that cognitive deficits persist at least several days after stopping heavy cannabis use. But studies differ on whether such deficits persist long term or whether they are correlated with increasing duration of lifetime cannabis use. The authors administered neuropsychological tests to 77 current heavy cannabis users who had smoked cannabis at least 5000 times in their lives, and to 87 control subjects who had smoked no more than 50 times in their lives. The heavy smokers showed deficits on memory of word lists on Days 0, 1, and 7 of a supervised abstinence period. By Day 28, however, few significant differences were found between users and controls on the test measures, and there were few significant associations between total lifetime cannabis consumption and test performance. Although these findings may be affected by residual confounding, as in all retrospective studies, they suggest that cannabis-associated cognitive deficits are reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use.

ABT-089, but not ABT-107, ameliorates nicotine withdrawal-induced cognitive deficits in C57BL6/J mice

PubMed Central

Yildirim, Emre; Connor, David A.; Gould, Thomas J.

2015-01-01

Nicotine withdrawal produces cognitive deficits that can predict relapse. Amelioration of these cognitive deficits emerges as a target in current smoking cessation therapies. In rodents, withdrawal from chronic nicotine disrupts contextual fear conditioning (CFC), whereas acute nicotine enhances this hippocampus-specific learning and memory. These modifications are mediated by β2-subunit-containing (β2*) nicotinic acetylcholine receptors in the hippocampus. We aimed to test ABT-089, a partial agonist of α4β2*, and ABT-107, an α7 nicotinic acetylcholine receptor agonist, for amelioration of cognitive deficits induced by withdrawal from chronic nicotine in mice. Mice underwent chronic nicotine administration (12.6 mg/kg/day or saline for 12 days), followed by 24 h of withdrawal. At the end of withdrawal, mice received 0.3 or 0.6 mg/kg ABT-089 or 0.3 mg/kg ABT-107 (doses were determined through initial dose–response experiments and prior studies) and were trained and tested for CFC. Nicotine withdrawal produced deficits in CFC that were reversed by acute ABT-089, but not ABT-107. Cued conditioning was not affected. Taken together, our results suggest that modulation of hippocampal learning and memory using ABT-089 may be an effective component of novel therapeutic strategies for nicotine addiction. PMID:25426579

Hippocampal and Cognitive Function, Exercise, and Ovarian Cancer: A Pilot Study

DTIC Science & Technology

2016-08-01

with   schizophrenia  (SZ)  display  substantial  cognitive  deficits  across  multiple  domains.  These  deficits  have  been...Cognition  via  Exercise  in   Schizophrenia Stress  Reactivity  in  Mitochondrial  Disease:  Physiological,  Neural,  and...the hypothesis of hippocampal hyperfunction as a pathogenic driver in schizophrenia and related disorders. P50 AG08702 (Small) 09/29/89-05/31/20

Rutin protects against cognitive deficits and brain damage in rats with chronic cerebral hypoperfusion.

PubMed

Qu, Jie; Zhou, Qiong; Du, Ying; Zhang, Wei; Bai, Miao; Zhang, Zhuo; Xi, Ye; Li, Zhuyi; Miao, Jianting

2014-08-01

Chronic cerebral hypoperfusion is a critical causative factor for the development of cognitive decline and dementia in the elderly, which involves many pathophysiological processes. Consequently, inhibition of several pathophysiological pathways is an attractive therapeutic strategy for this disorder. Rutin, a biologically active flavonoid, protects the brain against several insults through its antioxidant and anti-inflammatory properties, but its effect on cognitive deficits and brain damage caused by chronic cerebral hypoperfusion remains unknown. Here, we investigated the neuroprotective effect of rutin on cognitive impairments and the potential mechanisms underlying its action in rats with chronic cerebral hypoperfusion. We used Sprague-Dawley rats with permanent bilateral common carotid artery occlusion (BCCAO), a well-established model of chronic cerebral hypoperfusion. After rutin treatment for 12 weeks, the neuroprotective effect of rutin in rats was evaluated by behavioural tests, biochemical and histopathological analyses. BCCAO rats showed marked cognitive deficits, which were improved by rutin treatment. Moreover, BCCAO rats exhibited central cholinergic dysfunction, oxidative damage, inflammatory responses and neuronal damage in the cerebral cortex and hippocampus, compared with sham-operated rats. All these effects were significantly alleviated by treatment with rutin. Our results provide new insights into the pharmacological actions of rutin and suggest that rutin has multi-targeted therapeutical potential on cognitive deficits associated with conditions with chronic cerebral hypoperfusion such as vascular dementia and Alzheimer's disease. © 2014 The British Pharmacological Society.

A systematic review of cognitive performance in patients with childhood craniopharyngioma.

PubMed

Özyurt, Jale; Müller, Hermann L; Thiel, Christiane M

2015-10-01

Craniopharyngiomas are rare brain tumors of the sellar/suprasellar region, often adversely affecting patients' physical and psychosocial functioning. Until a few years ago, knowledge on cognitive deficits in craniopharyngioma patients was based on little valid evidence, with considerable inconsistencies across studies. Findings from recent research, with partly larger sample sizes, add to existing evidence to provide a more clear and reliable picture. The current review aims to summarize and systemize current findings on cognitive deficits in childhood craniopharyngioma, taking account of patient- and treatment-related variables where possible. Those studies were included that reported results of childhood craniopharyngioma patients tested with formalized neuropsychological tests (irrespective of their age at study, group size ≥10). A systematic assignment of test results to subcomponents of broader cognitive domains (e.g. to specific memory systems and processes) allows for a first comprehensive overview of patterns of spared and impaired cognitive functions. We show that episodic memory recall in particular is impaired, largely sparing other memory components. In accordance with recent knowledge on mammillary function, patients with hypothalamic involvement appear to be at particular risk. Deficits in higher cognitive processes, relying on the integrity of the prefrontal cortex and its subcortical pathways, may also occur, but results are still inconsistent. To gain deeper insight into the pattern of deficits and their association with patient- and treatment-related variables, further multi-site research with larger cohorts is needed.

Interventions for the treatment of theory of mind deficits in schizophrenia: Systematic literature review.

PubMed

Vass, Edit; Fekete, Zita; Simon, Viktória; Simon, Lajos

2018-05-22

Theory of Mind (ToM) plays a central role in regulating social interactions and its impairment is consistently reported in schizophrenia. Regarding schizophrenia, ToM is usually discussed as a sub-domain of social cognition. Since social cognitive deficits have drawn the attention of researchers, a variety of novel treatment techniques and approaches targeting social cognitive deficits have been developed. Encouraging results have repeatedly been reported on the modifiability of social cognitive impairment through these techniques. However, emotional perception seems to be over-represented in these approaches at the expense of other areas, such as ToM. This article presents a systematic review on the social cognitive interventions of the last 10 years, which focused on the remediation of ToM or used techniques primarily focusing on one or more social cognitive domains other than ToM, but with hypothetical effects on it. The aim of our systematic review was to compare these intervention techniques in order to see how effective they are in the remediation of ToM, and to find the best techniques to ameliorate ToM deficits in schizophrenia. According to our findings targeted ToM intervention produced more improvement in ToM tasks, while data regarding non-ToM interventions showed contradictory results with limited effects on ToM. Copyright © 2018. Published by Elsevier B.V.

Curcumin Improves Amyloid β-Peptide (1-42) Induced Spatial Memory Deficits through BDNF-ERK Signaling Pathway.

PubMed

Zhang, Lu; Fang, Yu; Xu, Yuming; Lian, Yajun; Xie, Nanchang; Wu, Tianwen; Zhang, Haifeng; Sun, Limin; Zhang, Ruifang; Wang, Zhenhua

2015-01-01

Curcumin, the most active component of turmeric, has various beneficial properties, such as antioxidant, anti-inflammatory, and antitumor effects. Previous studies have suggested that curcumin reduces the levels of amyloid and oxidized proteins and prevents memory deficits and thus is beneficial to patients with Alzheimer's disease (AD). However, the molecular mechanisms underlying curcumin's effect on cognitive functions are not well-understood. In the present study, we examined the working memory and spatial reference memory in rats that received a ventricular injection of amyloid-β1-42 (Aβ1-42), representing a rodent model of Alzheimer's disease (AD). The rats treated with Aβ1-42 exhibited obvious cognitive deficits in behavioral tasks. Chronic (seven consecutive days, once per day) but not acute (once a day) curcumin treatments (50, 100, and 200 mg/kg) improved the cognitive functions in a dose-dependent manner. In addition, the beneficial effect of curcumin is accompanied by increased BDNF levels and elevated levels of phosphorylated ERK in the hippocampus. Furthermore, the cognition enhancement effect of curcumin could be mimicked by the overexpression of BDNF in the hippocampus and blocked by either bilateral hippocampal injections with lentiviruses that express BDNF shRNA or a microinjection of ERK inhibitor. These findings suggest that chronic curcumin ameliorates AD-related cognitive deficits and that upregulated BDNF-ERK signaling in the hippocampus may underlie the cognitive improvement produced by curcumin.

Drug-induced cerebral glucose metabolism resembling Alzheimer's Disease: a case study.

PubMed

Riepe, Matthias W; Walther, Britta; Vonend, Catharina; Beer, Ambros J

2015-07-11

With aging of society the absolute number and the proportion of patients with cognitive deficits increase. Multiple disorders and diseases can foster cognitive impairment, e.g., Alzheimer's disease (AD), depressive disorder, or polypharmacy. A 74 year old man presented to the Old Age Psychiatry Service with cognitive deficits while being treated for recurrent depressive episodes and essential tremor with Venlafaxine, Lithium, and Primidone. Neuropsychological testing revealed a medio-temporal pattern of deficits with pronounced impairment of episodic memory, particularly delayed recall. Likewise, cognitive flexibility, semantic fluency, and attention were impaired. Positron emission tomography (PET) with fluorodeoxyglucose was performed and revealed a pattern of glucose utilization deficit resembling AD. On cessation of treatment with Lithium and Primidone, cognitive performance improved, particularly episodic memory performance and cognitive flexibility. Likewise, glucose metabolism normalized. Despite normalization of both, clinical symptoms and glucose utilization, the patient remained worried about possible underlying Alzheimer's disease pathology. To rule this out, an amyloid-PET was performed. No cortical amyloid was observed. Pharmacological treatment of older subjects may mimic glucose metabolism and clinical symptoms of Alzheimer's disease. In the present case both, imaging and clinical findings, reversed to normal on change of treatment. Amyloid PET is a helpful tool to additionally rule out underlying Alzheimer's disease in situations of clinical doubt even if clinical or other imaging findings are suggestive of Alzheimer's disease.

Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice.

PubMed

Andrews-Zwilling, Yaisa; Bien-Ly, Nga; Xu, Qin; Li, Gang; Bernardo, Aubrey; Yoon, Seo Yeon; Zwilling, Daniel; Yan, Tonya Xue; Chen, Ligong; Huang, Yadong

2010-10-13

Apolipoprotein E4 (apoE4) is the major genetic risk factor for Alzheimer's disease. However, the underlying mechanisms are unclear. We found that female apoE4 knock-in (KI) mice had an age-dependent decrease in hilar GABAergic interneurons that correlated with the extent of learning and memory deficits, as determined in the Morris water maze, in aged mice. Treating apoE4-KI mice with daily peritoneal injections of the GABA(A) receptor potentiator pentobarbital at 20 mg/kg for 4 weeks rescued the learning and memory deficits. In neurotoxic apoE4 fragment transgenic mice, hilar GABAergic interneuron loss was even more pronounced and also correlated with the extent of learning and memory deficits. Neurodegeneration and tauopathy occurred earliest in hilar interneurons in apoE4 fragment transgenic mice; eliminating endogenous Tau prevented hilar GABAergic interneuron loss and the learning and memory deficits. The GABA(A) receptor antagonist picrotoxin abolished this rescue, while pentobarbital rescued learning deficits in the presence of endogenous Tau. Thus, apoE4 causes age- and Tau-dependent impairment of hilar GABAergic interneurons, leading to learning and memory deficits in mice. Consequently, reducing Tau and enhancing GABA signaling are potential strategies to treat or prevent apoE4-related Alzheimer's disease.

Adolescent social defeat decreases spatial working memory performance in adulthood.

PubMed

Novick, Andrew M; Miiller, Leah C; Forster, Gina L; Watt, Michael J

2013-10-17

Adolescent social stress is associated with increased incidence of mental illnesses in adulthood that are characterized by deficits in cognitive focus and flexibility. Such enhanced vulnerability may be due to psychosocial stress-induced disruption of the developing mesocortical dopamine system, which plays a fundamental role in facilitating complex cognitive processes such as spatial working memory. Adolescent rats exposed to repeated social defeat as a model of social stress develop dopaminergic hypofunction in the medial prefrontal cortex as adults. To evaluate a direct link between adolescent social stress and later deficits in cognitive function, the present study tested the effects of adolescent social defeat on two separate tests of spatial working memory performance. Adult rats exposed to adolescent social defeat and their controls were trained on either the delayed win-shift task or the delayed alternating T-Maze task and then challenged with various delay periods. To evaluate potential differences in motivation for the food reward used in memory tasks, consumption and conditioned place preference for sweetened condensed milk were tested in a separate cohort of previously defeated rats and controls. Compared to controls, adult rats defeated in adolescence showed a delay-dependent deficit in spatial working memory performance, committing more errors at a 90 s and 5 min delay period on the T-maze and win-shift tasks, respectively. Observed memory deficits were likely independent of differences in reward motivation, as conditioned place preference for the palatable food used on both tasks was similar between the adolescent social defeat group and control. The results demonstrate that severe social stressors during adolescence can produce long term deficits in aspects of cognitive function. Given the dependence of spatial working memory on prefrontal dopamine, pharmacologically reversing dopaminergic deficiencies caused by adolescent social stress has the potential to treat such cognitive deficits.

Consequences, Characteristics, and Causes of Mathematical Learning Disabilities and Persistent Low Achievement in Mathematics

PubMed Central

Geary, David C.

2011-01-01

Objective The goals of the review are threefold; a) to highlight the educational and employment consequences of poorly developed mathematical competencies; b) overview the characteristics of the children with persistently low achievement in mathematics; and c) provide a primer on cognitive science research that is aimed at identifying the cognitive mechanisms underlying these learning disabilities and associated cognitive interventions. Method Literatures on the educational and economic consequences of poor mathematics achievement were reviewed and integrated with reviews of epidemiological, behavioral genetic, and cognitive science studies of poor mathematics achievement. Results Poor mathematical competencies are common among adults and result in employment difficulties and difficulties in many common day-to-day activities. Among students, about 7% of children and adolescents have a mathematical learning disability (MLD) and another 10% show persistent low achievement (LA) in mathematics despite average abilities in most other areas. Children with MLD and their LA peers have deficits in understanding and representing numerical magnitude, difficulties retrieving basic arithmetic facts from long-term memory, and delays in learning mathematical procedures. These deficits and delays cannot be attributed to intelligence, but are related to working memory deficits for children with MLD, but not LA children. Interventions that target these cognitive deficits are in development and preliminary results are promising. Conclusion Mathematical learning disabilities and learning difficulties associated with persistent low achievement in mathematics are common and not attributable to intelligence. These individuals have identifiable number and memory delays and deficits that appear to be specific to mathematics learning. The most promising interventions are those that target these specific deficits and, in addition, for children with MLD interventions that target their low working memory capacity. PMID:21285895

Evidence for distinct cognitive deficits after focal cerebellar lesions.

PubMed

Gottwald, B; Wilde, B; Mihajlovic, Z; Mehdorn, H M

2004-11-01

Anatomical evidence and lesion studies, as well as functional magnetic resonance imaging (fMRI) studies, indicate that the cerebellum contributes to higher cognitive functions. Cerebellar posterior lateral regions seem to be relevant for cognition, while vermal lesions seem to be associated with changes in affect. However, the results remain controversial. Deficits of patients are sometimes still attributed to motor impairment. We present data from a detailed neuropsychological examination of 21 patients with cerebellar lesions due to tumour or haematoma, and 21 controls matched for age, sex, and years of education. Patients showed deficits in executive function, and in attentional processes such as working memory and divided attention. Further analysis revealed that patients with right-sided lesions were in general more impaired than those with left-sided lesions. Those hypotheses that suggest that lesions of the right cerebellar hemisphere lead to verbal deficits, while those of the left lead to non-verbal deficits, have in part been confirmed. The generally greater impairment of those patients with a right-sided lesion has been interpreted as resulting from the connection of the right cerebellum to the left cerebral hemisphere, which is dominant for language functions and crucial for right hand movements. Motor impairment was correlated with less than half of the cognitive measures, with no stronger tendency for correlation with cognitive tests that require motor responses discernible. The results are discussed on the basis of an assumption that the cerebellum has a predicting and preparing function, indicating that cerebellar lesions lead to a "dysmetria of thought."

Are malnutrition and stress risk factors for accelerated cognitive decline? A prisoner of war study.

PubMed

Sulway, M R; Broe, G A; Creasey, H; Dent, O F; Jorm, A F; Kos, S C; Tennant, C C

1996-03-01

We set out to test the hypothesis that severe malnutrition and stress experienced by prisoners of war (POWs) are associated with cognitive deficits later in life. We assessed 101 former Australian POWs of the Japanese and 108 veteran control subjects using a battery of neuropsychological tests, a depression scale, a clinical examination for dementia, and CT. We divided the POWs into high weight loss (>35%) and low weight loss groups (<35%). We found no significant differences in cognitive performance between the POWs and control subjects or between high and low weight loss groups on any of the tests or in the prevalence of dementia. Scores on the depression scale showed that the former POWs had more depressive symptoms than the control subjects a decade previous, but the difference had diminished over time. This study does not support the hypothesis that malnutrition is a risk factor for accelerated cognitive decline nor the theory that severe stress can lead to hippocampal neuronal loss and cognitive deficits. Cognitive deficits in earlier studies of former POWs may have been associated with concurrent depression.

Cognitive functioning following traumatic brain injury: A five-year follow-up.

PubMed

Marsh, Nigel V; Ludbrook, Maria R; Gaffaney, Lauren C

2016-01-01

To describe the long-term prevalence and severity of cognitive deficits following significant (i.e., ventilation required for >24 hours) traumatic brain injury. To assess a comprehensive range of cognitive functions using psychometric measures with established normative, reliability, and validity data. A group of 71 adults was assessed at approximately five years (mean = 66 months) following injury. Assessment of cognitive functioning covered the domains of intelligence, attention, verbal and visual memory, visual-spatial construction, and executive functions. Impairment was evident across all domains but prevalence varied both within and between domains. Across aspects of intelligence clinical impairment ranged from 8-25% , attention 39-62% , verbal memory 16-46% , visual memory 23-51% , visual-spatial construction 38% , and executive functions (verbal fluency) 13% . In addition, 3-23% of performances across the measures were in the borderline range, suggesting a high prevalence of subclinical deficit. Although the prevalence of impairment may vary across cognitive domains, long-term follow-up documented deficits in all six domains. These findings provide further evidence that while improvement of cognitive functioning following significant traumatic brain injury may be possible, recovery of function is unlikely.

Decrease of SYNGAP1 in GABAergic cells impairs inhibitory synapse connectivity, synaptic inhibition and cognitive function

PubMed Central

Berryer, Martin H.; Chattopadhyaya, Bidisha; Xing, Paul; Riebe, Ilse; Bosoi, Ciprian; Sanon, Nathalie; Antoine-Bertrand, Judith; Lévesque, Maxime; Avoli, Massimo; Hamdan, Fadi F.; Carmant, Lionel; Lamarche-Vane, Nathalie; Lacaille, Jean-Claude; Michaud, Jacques L.; Di Cristo, Graziella

2016-01-01

Haploinsufficiency of the SYNGAP1 gene, which codes for a Ras GTPase-activating protein, impairs cognition both in humans and in mice. Decrease of Syngap1 in mice has been previously shown to cause cognitive deficits at least in part by inducing alterations in glutamatergic neurotransmission and premature maturation of excitatory connections. Whether Syngap1 plays a role in the development of cortical GABAergic connectivity and function remains unclear. Here, we show that Syngap1 haploinsufficiency significantly reduces the formation of perisomatic innervations by parvalbumin-positive basket cells, a major population of GABAergic neurons, in a cell-autonomous manner. We further show that Syngap1 haploinsufficiency in GABAergic cells derived from the medial ganglionic eminence impairs their connectivity, reduces inhibitory synaptic activity and cortical gamma oscillation power, and causes cognitive deficits. Our results indicate that Syngap1 plays a critical role in GABAergic circuit function and further suggest that Syngap1 haploinsufficiency in GABAergic circuits may contribute to cognitive deficits. PMID:27827368

Cognitive Functioning and Driving Simulator Performance in Middle-aged and Older Adults with HIV

PubMed Central

Vance, David E.; Fazeli, Pariya L.; Ball, David A.; Slater, Larry Z.; Ross, Lesley A.

2014-01-01

Nearly half of people living with HIV experience cognitive deficits that may impact instrumental activities of daily living. As the number of people aging with HIV increases, concerns mount that disease-related cognitive deficits may be compounded by age-related deficits, which may further compromise everyday functions such as driving. In this cross-sectional pilot study, during a 2.5-hour visit, 26 middle-aged and older adults (40+ years) were administered demographic, health, psychosocial, and driving habits questionnaires; cognitive assessments; and driving simulator tests. Although CD4+T lymphocyte count and viral load were unrelated to driving performance, older age was related to poorer driving. Furthermore, poorer visual speed of processing performance (i.e., Useful Field of View) was related to poorer driving performance (e.g., average gross reaction time). Mixed findings were observed between driving performance and cognitive function on self-reported driving habits of participants. Implications for these findings on nursing practice and research are posited. PMID:24513104

Rescue of Impaired mGluR5-Driven Endocannabinoid Signaling Restores Prefrontal Cortical Output to Inhibit Pain in Arthritic Rats.

PubMed

Kiritoshi, Takaki; Ji, Guangchen; Neugebauer, Volker

2016-01-20

The medial prefrontal cortex (mPFC) serves executive functions that are impaired in neuropsychiatric disorders and pain. Underlying mechanisms remain to be determined. Here we advance the novel concept that metabotropic glutamate receptor 5 (mGluR5) fails to engage endocannabinoid (2-AG) signaling to overcome abnormal synaptic inhibition in pain, but restoring endocannabinoid signaling allows mGluR5 to increase mPFC output hence inhibit pain behaviors and mitigate cognitive deficits. Whole-cell patch-clamp recordings were made from layer V pyramidal cells in the infralimbic mPFC in rat brain slices. Electrical and optogenetic stimulations were used to analyze amygdala-driven mPFC activity. A selective mGluR5 activator (VU0360172) increased pyramidal output through an endocannabinoid-dependent mechanism because intracellular inhibition of the major 2-AG synthesizing enzyme diacylglycerol lipase or blockade of CB1 receptors abolished the facilitatory effect of VU0360172. In an arthritis pain model mGluR5 activation failed to overcome abnormal synaptic inhibition and increase pyramidal output. mGluR5 function was rescued by restoring 2-AG-CB1 signaling with a CB1 agonist (ACEA) or inhibitors of postsynaptic 2-AG hydrolyzing enzyme ABHD6 (intracellular WWL70) and monoacylglycerol lipase MGL (JZL184) or by blocking GABAergic inhibition with intracellular picrotoxin. CB1-mediated depolarization-induced suppression of synaptic inhibition (DSI) was also impaired in the pain model but could be restored by coapplication of VU0360172 and ACEA. Stereotaxic coadministration of VU0360172 and ACEA into the infralimbic, but not anterior cingulate, cortex mitigated decision-making deficits and pain behaviors of arthritic animals. The results suggest that rescue of impaired endocannabinoid-dependent mGluR5 function in the mPFC can restore mPFC output and cognitive functions and inhibit pain. Significance statement: Dysfunctions in prefrontal cortical interactions with subcortical brain regions, such as the amygdala, are emerging as important players in neuropsychiatric disorders and pain. This study identifies a novel mechanism and rescue strategy for impaired medial prefrontal cortical function in an animal model of arthritis pain. Specifically, an integrative approach of optogenetics, pharmacology, electrophysiology, and behavior is used to advance the novel concept that a breakdown of metabotropic glutamate receptor subtype mGluR5 and endocannabinoid signaling in infralimbic pyramidal cells fails to control abnormal amygdala-driven synaptic inhibition in the arthritis pain model. Restoring endocannabinoid signaling allows mGluR5 activation to increase infralimbic output hence inhibit pain behaviors and mitigate pain-related cognitive deficits. Copyright © 2016 the authors 0270-6474/16/360837-14$15.00/0.

Optimizing treatments for nicotine dependence by increasing cognitive performance during withdrawal.

PubMed

Ashare, Rebecca L; Schmidt, Heath D

2014-06-01

Current FDA-approved smoking cessation pharmacotherapies have limited efficacy and are associated with high rates of relapse. Therefore, there is a clear need to develop novel antismoking medications. Nicotine withdrawal is associated with cognitive impairments that predict smoking relapse. It has been proposed that these cognitive deficits are a hallmark of nicotine withdrawal that could be targeted in order to prevent smoking relapse. Thus, pharmacotherapies that increase cognitive performance during nicotine withdrawal may represent potential smoking cessation agents. The authors review the clinical literature demonstrating that nicotine withdrawal is associated with deficits in working memory, attention and response inhibition. They then briefly summarize different classes of compounds and strategies to increase cognitive performance during nicotine withdrawal. Particular emphasis has been placed on translational research in order to highlight areas for which there is strong rationale for pilot clinical trials of potential smoking cessation medications. There is emerging evidence that supports deficits in cognitive function as a plausible nicotine withdrawal phenotype. The authors furthermore believe that the translational paradigms presented here may represent efficient and valid means for the evaluation of cognitive-enhancing medications as possible treatments for nicotine dependence.

Thalamic and hippocampal volume associated with memory functions in multiple sclerosis.

PubMed

Tremblay, Alexandra; Jobin, Céline; Demers, Mélanie; Dagenais, Emmanuelle; Narayanan, Sridar; Araújo, David; Douglas, Arnold L; Roger, Elaine; Chamelian, Laury; Duquette, Pierre; Rouleau, Isabelle

2018-06-08

Although multiple sclerosis (MS) has long been considered to primarily affect white matter, it is now recognized that cognitive deficits in MS are also related to neocortical, thalamic and hippocampal damage. However, the association between damage to these structures and memory deficits in MS is unclear. This study examines whether MS patients with cognitive impairment have a reduction of hippocampal and/or thalamic volumes compared to cognitively intact patients, and whether these volume reductions correlate with various aspects of memory function. Volumetric MRI measures of thalamus and hippocampus of forty-one patients with MS were performed. The patients were divided in two groups depending on the presence or absence of cognitive impairment, based on their neuropsychological tests scores. Right hippocampal volume was found to be associated with learning, and the left thalamic volume was found to predict performance in verbal memory. Cognitively impaired patients had a tendency to have a reduced left thalamic volume compared to cognitively intact patients. This study does not support a direct relationship between hippocampal atrophy and verbal memory. These results add to the growing evidence of the involvement of thalamus in cognitive impairment in MS and its association with verbal memory deficits. Copyright © 2018. Published by Elsevier Inc.

Optimizing treatments for nicotine dependence by increasing cognitive performance during withdrawal

PubMed Central

Ashare, Rebecca L; Schmidt, Heath D

2014-01-01

Introduction Current FDA-approved smoking cessation pharmacotherapies have limited efficacy and are associated with high rates of relapse. Therefore, there is a clear need to develop novel antismoking medications. Nicotine withdrawal is associated with cognitive impairments that predict smoking relapse. It has been proposed that these cognitive deficits are a hallmark of nicotine withdrawal that could be targeted in order to prevent smoking relapse. Thus, pharmacotherapies that increase cognitive performance during nicotine withdrawal may represent potential smoking cessation agents. Areas covered The authors review the clinical literature demonstrating that nicotine withdrawal is associated with deficits in working memory, attention and response inhibition. They then briefly summarize different classes of compounds and strategies to increase cognitive performance during nicotine withdrawal. Particular emphasis has been placed on translational research in order to highlight areas for which there is strong rationale for pilot clinical trials of potential smoking cessation medications. Expert opinion There is emerging evidence that supports deficits in cognitive function as a plausible nicotine withdrawal phenotype. The authors furthermore believe that the translational paradigms presented here may represent efficient and valid means for the evaluation of cognitive-enhancing medications as possible treatments for nicotine dependence. PMID:24707983

Chronic 5-HT4 receptor agonist treatment restores learning and memory deficits in a neuroendocrine mouse model of anxiety/depression.

PubMed

Darcet, Flavie; Gardier, Alain M; David, Denis J; Guilloux, Jean-Philippe

2016-03-11

Cognitive disturbances are often reported as serious invalidating symptoms in patients suffering from major depression disorders (MDD) and are not fully corrected by classical monoaminergic antidepressant drugs. If the role of 5-HT4 receptor agonists as cognitive enhancers is well established in naïve animals or in animal models of cognitive impairment, their cognitive effects in the context of stress need to be examined. Using a mouse model of anxiety/depression (CORT model), we reported that a chronic 5-HT4 agonist treatment (RS67333, 1.5mg/kg/day) restored chronic corticosterone-induced cognitive deficits, including episodic-like, associative and spatial learning and memory impairments. On the contrary, a chronic monoaminergic antidepressant drug treatment with fluoxetine (18mg/kg/day) only partially restored spatial learning and memory deficits and had no effect in the associative/contextual task. These results suggest differential mechanisms underlying cognitive effects of these drugs. Finally, the present study highlights 5-HT4 receptor stimulation as a promising therapeutic mechanism to alleviate cognitive symptoms related to MDD. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Improving Temporal Cognition by Enhancing Motivation

PubMed Central

Avlar, Billur; Kahn, Julia B.; Jensen, Greg; Kandel, Eric R.; Simpson, Eleanor H.; Balsam, Peter D.

2015-01-01

Increasing motivation can positively impact cognitive performance. Here we employed a cognitive timing task that allows us to detect changes in cognitive performance that are not influenced by general activity or arousal factors such as the speed or persistence of responding. This approach allowed us to manipulate motivation using three different methods; molecular/genetic, behavioral and pharmacological. Increased striatal D2Rs resulted in deficits in temporal discrimination. Switching off the transgene improved motivation in earlier studies, and here partially rescued the temporal discrimination deficit. To manipulate motivation behaviorally, we altered reward magnitude and found that increasing reward magnitude improved timing in control mice and partially rescued timing in the transgenic mice. Lastly, we manipulated motivation pharmacologically using a functionally selective 5-HT2C receptor ligand, SB242084, which we previously found to increase incentive motivation. SB242084 improved temporal discrimination in both control and transgenic mice. Thus, while there is a general intuitive belief that motivation can affect cognition, we here provide a direct demonstration that enhancing motivation, in a variety of ways, can be an effective strategy for enhancing temporal cognition. Understanding the interaction of motivation and cognition is of clinical significance since many psychiatric disorders are characterized by deficits in both domains. PMID:26371378

Hoping for more: How cognitive science has and hasn't been helpful to the OCD clinician.

PubMed

Ouimet, Allison J; Ashbaugh, Andrea R; Radomsky, Adam S

2018-04-12

Cognitive-behavioural models of obsessive-compulsive disorder (OCD) stemmed from knowledge acquired from cognitive science. Researchers continue to apply basic cognitive-affective science methods to understanding OCD, with the overarching goal of improving and refining evidence-based treatments. However, the degree to which such research has contributed to this goal is unclear. We reviewed OCD research in the general areas that comprise basic cognitive science, and evaluated the degree to which it has contributed to our understanding of the development, maintenance, and treatment of OCD. We focused on studies that either compared people with and without OCD and/or used experimental psychopathology methods with human participants, and attempted to resolve some of the conflicting theories related to the importance of cognitive deficits vs. cognitive biases. Overall, we observed equivocal findings for deficits in perception, attention, memory, and executive functioning. Moreover, many so-called deficits were moderated and/or explained by OCD-relevant beliefs, highlighting the role of confidence in cognitive processes as integral to our understanding of OCD. We discussed these findings in terms of cognitive measurement, cognitive-behavioural models, and clinical applicability, and made recommendations for future research that may offer innovation and insight helpful to clinicians working to improve the symptoms and lives of people with OCD. Copyright © 2018 Elsevier Ltd. All rights reserved.

The role of genes, intelligence, personality, and social engagement in cognitive performance in Klinefelter syndrome.

PubMed

Skakkebæk, Anne; Moore, Philip J; Pedersen, Anders Degn; Bojesen, Anders; Kristensen, Maria Krarup; Fedder, Jens; Laurberg, Peter; Hertz, Jens Michael; Østergaard, John Rosendahl; Wallentin, Mikkel; Gravholt, Claus Højbjerg

2017-03-01

The determinants of cognitive deficits among individuals with Klinefelter syndrome (KS) are not well understood. This study was conducted to assess the impact of general intelligence, personality, and social engagement on cognitive performance among patients with KS and a group of controls matched for age and years of education. Sixty-nine patients with KS and 69 controls were assessed in terms of IQ, NEO personality inventory, the Autism Spectrum Quotient (AQ) scale, and measures of cognitive performance reflecting working memory and executive function. Patients with KS performed more poorly on memory and executive-function tasks. Patients with KS also exhibited greater neuroticism and less extraversion, openness, and conscientiousness than controls. Memory deficits among patients with KS were associated with lower intelligence, while diminished executive functioning was mediated by both lower intelligence and less social engagement. Our results suggest that among patients with KS, memory deficits are principally a function of lower general intelligence, while executive-function deficits are associated with both lower intelligence and poorer social skills. This suggests a potential influence of social engagement on executive cognitive functioning (and/or vice-versa) among individuals with KS, and perhaps those with other genetic disorders. Future longitudinal research would be important to further clarify this and other issues discussed in this research.

Working memory load affects repetitive behaviour but not cognitive flexibility in adolescent autism spectrum disorder.

PubMed

Wolff, Nicole; Chmielewski, Witold X; Beste, Christian; Roessner, Veit

2017-03-16

Autism spectrum disorder (ASD) is associated with repetitive and stereotyped behaviour, suggesting that cognitive flexibility may be deficient in ASD. A central, yet not examined aspect to understand possible deficits in flexible behaviour in ASD relates (i) to the role of working memory and (ii) to neurophysiological mechanisms underlying behavioural modulations. We analysed behavioural and neurophysiological (EEG) correlates of cognitive flexibility using a task-switching paradigm with and without working memory load in adolescents with ASD and typically developing controls (TD). Adolescents with ASD versus TD show similar performance in task switching with no memory load, indicating that 'pure' cognitive flexibility is not in deficit in adolescent ASD. However performance during task repetition decreases with increasing memory load. Neurophysiological data reflect the pattern of behavioural effects, showing modulations in P2 and P3 event-related potentials. Working memory demands affect repetitive behaviour while processes of cognitive flexibility are unaffected. Effects emerge due to deficits in preparatory attentional processes and deficits in task rule activation, organisation and implementation of task sets when repetitive behaviour is concerned. It may be speculated that the habitual response mode in ASD (i.e. repetitive behaviour) is particularly vulnerable to additional demands on executive control processes.

Lack of association between mutation size and cognitive/behavior deficits in fragile X males: A brief report

DOE Office of Scientific and Technical Information (OSTI.GOV)

Fisch, G.S.; Carpenter, N.; Simensen, R.

1996-08-09

Previously, researchers reported molecular-neurobehavioral or molecular-cognitive associations in individuals with fra(X) (fragile X) mutation. However, not all investigators have noted molecular-behavioral relationships. Consequently, we examined prospectively 30 fra(X) males age 3-15 years from four testing sites to determine whether there was a relationship between mutation size and degree of either cognitive or adaptive behavior deficit. To measure cognitive abilities, all individuals were administered the Stanford-Binet (4th edition) IQ test. To evaluate adaptive behavior (DQ) skills, all individuals were assessed using the Vineland Adaptive Behavior Scale. To determine fra(X) status, genomic DNA from all individuals was extracted and digested with EcoRImore » and EagI restriction enzymes. Southern blots were prepared and hybridized with the pE5.1 probe. The Pearson correlation coefficient between full mutation size and composite IQ score revealed a non-significant, near-zero association (r = 0.06; P > .76). The Pearson coefficient between mutation size and DQ also showed a non-significant, near-zero association (r = 0.06; P >.73). We conclude that while fra(X) mutation produces cognitive and behavior deficits in males who inherit the defective gene, there is no relationship between mutation size and degree of deficit. 14 refs., 2 figs.« less

Social Cognition Deficits: The Key to Discriminate Behavioral Variant Frontotemporal Dementia from Alzheimer's Disease Regardless of Amnesia?

PubMed

Bertoux, Maxime; de Souza, Leonardo Cruz; O'Callaghan, Claire; Greve, Andrea; Sarazin, Marie; Dubois, Bruno; Hornberger, Michael

2016-01-01

Relative sparing of episodic memory is a diagnostic criterion of behavioral variant frontotemporal dementia (bvFTD). However, increasing evidence suggests that bvFTD patients can show episodic memory deficits at a similar level as Alzheimer's disease (AD). Social cognition tasks have been proposed to distinguish bvFTD, but no study to date has explored the utility of such tasks for the diagnosis of amnestic bvFTD. Here, we contrasted social cognition performance of amnestic and non-amnestic bvFTD from AD, with a subgroup having confirmed in vivo pathology markers. Ninety-six participants (38 bvFTD and 28 AD patients as well as 30 controls) performed the short Social-cognition and Emotional Assessment (mini-SEA). BvFTD patients were divided into amnestic versus non-amnestic presentation using the validated Free and Cued Selective Reminding Test (FCSRT) assessing episodic memory. As expected, the accuracy of the FCSRT to distinguish the overall bvFTD group from AD was low (69.7% ) with ∼50% of bvFTD patients being amnestic. By contrast, the diagnostic accuracy of the mini-SEA was high (87.9% ). When bvFTD patients were split on the level of amnesia, mini-SEA diagnostic accuracy remained high (85.1% ) for amnestic bvFTD versus AD and increased to very high (93.9% ) for non-amnestic bvFTD versus AD. Social cognition deficits can distinguish bvFTD and AD regardless of amnesia to a high degree and provide a simple way to distinguish both diseases at presentation. These findings have clear implications for the diagnostic criteria of bvFTD. They suggest that the emphasis should be on social cognition deficits with episodic memory deficits not being a helpful diagnostic criterion in bvFTD.

The location discrimination reversal task in mice is sensitive to deficits in performance caused by aging, pharmacological and other challenges.

PubMed

Graf, Radka; Longo, Jami L; Hughes, Zoë A

2018-06-01

Deficits in hippocampal-mediated pattern separation are one aspect of cognitive function affected in schizophrenia (SZ) or Alzheimer's disease (AD). To develop novel therapies, it is beneficial to explore this specific aspect of cognition preclinically. The location discrimination reversal (LDR) task is a hippocampal-dependent operant paradigm that evaluates spatial learning and cognitive flexibility using touchscreens. Here we assessed baseline performance as well as multimodal disease-relevant manipulations in mice. Mice were trained to discriminate between the locations of two images where the degree of separation impacted performance. Administration of putative pro-cognitive agents was unable to improve performance at narrow separation. Furthermore, a range of disease-relevant manipulations were characterized to assess whether performance could be impaired and restored. Pertinent to the cholinergic loss in AD, scopolamine (0.1 mg/kg) produced a disruption in LDR, which was attenuated by donepezil (1 mg/kg). Consistent with NMDA hypofunction in cognitive impairment associated with SZ, MK-801 (0.1 mg/kg) also disrupted performance; however, this deficit was not modified by rolipram. Microdeletion of genes associated with SZ (22q11) resulted in impaired performance, which was restored by rolipram (0.032 mg/kg). Since aging and inflammation affect cognition and are risk factors for AD, these aspects were also evaluated. Aged mice were slower to acquire the task than young mice and did not reach the same level of performance. A systemic inflammatory challenge (lipopolysaccharide (LPS), 1 mg/kg) produced prolonged (7 days) deficits in the LDR task. These data suggest that LDR task is a valuable platform for evaluating disease-relevant deficits in pattern separation and offers potential for identifying novel therapies.

Improved Social Interaction, Recognition and Working Memory with Cannabidiol Treatment in a Prenatal Infection (poly I:C) Rat Model

PubMed Central

Osborne, Ashleigh L; Solowij, Nadia; Babic, Ilijana; Huang, Xu-Feng; Weston-Green, Katrina

2017-01-01

Neuropsychiatric disorders such as schizophrenia are associated with cognitive impairment, including learning, memory and attention deficits. Antipsychotic drugs are limited in their efficacy to improve cognition; therefore, new therapeutic agents are required. Cannabidiol (CBD), the non-intoxicating component of cannabis, has anti-inflammatory, neuroprotective and antipsychotic-like properties; however, its ability to improve the cognitive deficits of schizophrenia remains unclear. Using a prenatal infection model, we examined the effect of chronic CBD treatment on cognition and social interaction. Time-mated pregnant Sprague-Dawley rats (n=16) were administered polyinosinic-polycytidilic acid (poly I:C) (POLY; 4 mg/kg) or saline (CONT) at gestation day 15. Male offspring (PN56) were injected twice daily with 10 mg/kg CBD (CONT+CBD, POLY+CBD; n=12 per group) or vehicle (VEH; CONT+VEH, POLY+VEH; n=12 per group) for 3 weeks. Body weight, food and water intake was measured weekly. The Novel Object Recognition and rewarded T-maze alternation tests assessed recognition and working memory, respectively, and the social interaction test assessed sociability. POLY+VEH offspring exhibited impaired recognition and working memory, and reduced social interaction compared to CONT+VEH offspring (p<0.01). CBD treatment significantly improved recognition, working memory and social interaction deficits in the poly I:C model (p<0.01 vs POLY+VEH), did not affect total body weight gain, food or water intake, and had no effect in control animals (all p>0.05). In conclusion, chronic CBD administration can attenuate the social interaction and cognitive deficits induced by prenatal poly I:C infection. These novel findings present interesting implications for potential use of CBD in treating the cognitive deficits and social withdrawal of schizophrenia. PMID:28230072

Improved Social Interaction, Recognition and Working Memory with Cannabidiol Treatment in a Prenatal Infection (poly I:C) Rat Model.

PubMed

Osborne, Ashleigh L; Solowij, Nadia; Babic, Ilijana; Huang, Xu-Feng; Weston-Green, Katrina

2017-06-01

Neuropsychiatric disorders such as schizophrenia are associated with cognitive impairment, including learning, memory and attention deficits. Antipsychotic drugs are limited in their efficacy to improve cognition; therefore, new therapeutic agents are required. Cannabidiol (CBD), the non-intoxicating component of cannabis, has anti-inflammatory, neuroprotective and antipsychotic-like properties; however, its ability to improve the cognitive deficits of schizophrenia remains unclear. Using a prenatal infection model, we examined the effect of chronic CBD treatment on cognition and social interaction. Time-mated pregnant Sprague-Dawley rats (n=16) were administered polyinosinic-polycytidilic acid (poly I:C) (POLY; 4 mg/kg) or saline (CONT) at gestation day 15. Male offspring (PN56) were injected twice daily with 10 mg/kg CBD (CONT+CBD, POLY+CBD; n=12 per group) or vehicle (VEH; CONT+VEH, POLY+VEH; n=12 per group) for 3 weeks. Body weight, food and water intake was measured weekly. The Novel Object Recognition and rewarded T-maze alternation tests assessed recognition and working memory, respectively, and the social interaction test assessed sociability. POLY+VEH offspring exhibited impaired recognition and working memory, and reduced social interaction compared to CONT+VEH offspring (p<0.01). CBD treatment significantly improved recognition, working memory and social interaction deficits in the poly I:C model (p<0.01 vs POLY+VEH), did not affect total body weight gain, food or water intake, and had no effect in control animals (all p>0.05). In conclusion, chronic CBD administration can attenuate the social interaction and cognitive deficits induced by prenatal poly I:C infection. These novel findings present interesting implications for potential use of CBD in treating the cognitive deficits and social withdrawal of schizophrenia.

Applications of the Morris water maze in translational traumatic brain injury research.

PubMed

Tucker, Laura B; Velosky, Alexander G; McCabe, Joseph T

2018-05-01

Acquired traumatic brain injury (TBI) is frequently accompanied by persistent cognitive symptoms, including executive function disruptions and memory deficits. The Morris Water Maze (MWM) is the most widely-employed laboratory behavioral test for assessing cognitive deficits in rodents after experimental TBI. Numerous protocols exist for performing the test, which has shown great robustness in detecting learning and memory deficits in rodents after infliction of TBI. We review applications of the MWM for the study of cognitive deficits following TBI in pre-clinical studies, describing multiple ways in which the test can be employed to examine specific aspects of learning and memory. Emphasis is placed on dependent measures that are available and important controls that must be considered in the context of TBI. Finally, caution is given regarding interpretation of deficits as being indicative of dysfunction of a single brain region (hippocampus), as experimental models of TBI most often result in more diffuse damage that disrupts multiple neural pathways and larger functional networks that participate in complex behaviors required in MWM performance. Published by Elsevier Ltd.

Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer's and Parkinson's Diseases.

PubMed

Scharre, Douglas W; Chang, Shu-Ing; Nagaraja, Haikady N; Park, Ariane; Adeli, Anahita; Agrawal, Punit; Kloos, Anne; Kegelmeyer, Deb; Linder, Shannon; Fritz, Nora; Kostyk, Sandra K; Kataki, Maria

2016-10-04

Limited data compares clinical profiles of Lewy Body Dementia (LBD) with Alzheimer's disease (AD) and Parkinson's disease (PD). Twenty-one mildly demented ambulatory LBD subjects were individually matched by MMSE score with 21 AD subjects and by UPDRS motor score with 21 PD subjects. Matched by age, gender, education, and race, pairs were compared using cognitive, functional, behavioral, and motor measures. LBD group performed worse than PD on axial motor, gait, and balance measures. AD had more amnesia and orientation impairments, but less executive and visuospatial deficits than LBD subjects. LBD group had more sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea than AD or PD. Axial motor, gait, and balance disturbances correlated with executive, visuospatial, and global cognition deficits. LBD is differentiated from AD and PD by retrieval memory, visuospatial, and executive deficits; axial motor, gait and balance impairments; sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea.

Neuroimaging of cognitive dysfunction and depression in aging retired National Football League players: a cross-sectional study.

PubMed

Hart, John; Kraut, Michael A; Womack, Kyle B; Strain, Jeremy; Didehbani, Nyaz; Bartz, Elizabeth; Conover, Heather; Mansinghani, Sethesh; Lu, Hanzhang; Cullum, C Munro

2013-03-01

OBJECTIVES To assess cognitive impairment and depression in aging former professional football (National Football League [NFL]) players and to identify neuroimaging correlates of these dysfunctions. DESIGN We compared former NFL players with cognitive impairment and depression, cognitively normal retired players who were not depressed, and matched healthy control subjects. SETTING Research center in the North Texas region of the United States. PATIENTS Cross-sectional sample of former NFL players with and without a history of concussion recruited from the North Texas region and age-, education-, and IQ-matched controls. Thirty-four retired NFL players (mean age, 61.8 years) underwent neurological and neuropsychological assessment. A subset of 26 players also underwent detailed neuroimaging; imaging data in this subset were compared with imaging data acquired in 26 healthy matched controls. MAIN OUTCOME MEASURES Neuropsychological measures, clinical diagnoses of depression, neuroimaging mea-sures of white matter pathology, and a measure of cerebral blood flow. RESULTS Of the 34 former NFL players, 20 were cognitively normal. Four were diagnosed as having a fixed cognitive deficit; 8, mild cognitive impairment; 2, dementia; and 8, depression. Of the subgroup in whom neuroimaging data were acquired, cognitively impaired participants showed the greatest deficits on tests of naming, word finding, and visual/verbal episodic memory. We found significant differences in white matter abnormalities in cognitively impaired and depressed retired players compared with their respective controls. Regional blood flow differences in the cognitively impaired group (left temporal pole, inferior parietal lobule, and superior temporal gyrus) corresponded to regions associated with impaired neurocognitive performance (problems with memory, naming, and word finding). CONCLUSIONS Cognitive deficits and depression appear to be more common in aging former NFL players compared with healthy controls. These deficits are correlated with white matter abnormalities and changes in regional cerebral blood flow.

Neuropsychological Impairments in Schizophrenia and Psychotic Bipolar Disorder: Findings from the Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) Study

PubMed Central

Hill, S. Kristian; Reilly, James L.; Keefe, Richard S.E.; Gold, James M.; Bishop, Jeffrey R.; Gershon, Elliot S.; Tamminga, Carol A.; Pearlson, Godfrey D.; Keshavan, Matcheri S.; Sweeney, John A.

2017-01-01

Objective Familial neuropsychological deficits are well established in schizophrenia but remain less well characterized in other psychotic disorders. This study from the Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) consortium 1) compares cognitive impairment in schizophrenia and bipolar disorder with psychosis, 2) tests a continuum model of cognitive dysfunction in psychotic disorders, 3) reports familiality of cognitive impairments across psychotic disorders, and 4) evaluates cognitive impairment among nonpsychotic relatives with and without cluster A personality traits. Method Participants included probands with schizophrenia (N=293), psychotic bipolar disorder (N=227), schizoaffective disorder (manic, N=110; depressed, N=55), their first-degree relatives (N=316, N=259, N=133, and N=64, respectively), and healthy comparison subjects (N=295). All participants completed the Brief Assessment of Cognition in Schizophrenia (BACS) neuropsychological battery. Results Cognitive impairments among psychotic probands, compared to healthy comparison subjects, were progressively greater from bipolar disorder (z=−0.77) to schizoaffective disorder (manic z=−1.08; depressed z=−1.25) to schizophrenia (z=−1.42). Profiles across subtests of the BACS were similar across disorders. Familiality of deficits was significant and comparable in schizophrenia and bipolar disorder. Of particular interest were similar levels of neuropsychological deficits in relatives with elevated cluster A personality traits across proband diagnoses. Nonpsychotic relatives of schizophrenia probands without these personality traits exhibited significant cognitive impairments, while relatives of bipolar probands did not. Conclusions Robust cognitive deficits are present and familial in schizophrenia and psychotic bipolar disorder. Severity of cognitive impairments across psychotic disorders was consistent with a continuum model, in which more prominent affective features and less enduring psychosis were associated with less cognitive impairment. Cognitive dysfunction in first-degree relatives is more closely related to psychosis-spectrum personality disorder traits in psychotic bipolar disorder than in schizophrenia. PMID:23771174

Cognitive deficits caused by prefrontal cortical and hippocampal neural disinhibition.

PubMed

Bast, Tobias; Pezze, Marie; McGarrity, Stephanie

2017-10-01

We review recent evidence concerning the significance of inhibitory GABA transmission and of neural disinhibition, that is, deficient GABA transmission, within the prefrontal cortex and the hippocampus, for clinically relevant cognitive functions. Both regions support important cognitive functions, including attention and memory, and their dysfunction has been implicated in cognitive deficits characterizing neuropsychiatric disorders. GABAergic inhibition shapes cortico-hippocampal neural activity, and, recently, prefrontal and hippocampal neural disinhibition has emerged as a pathophysiological feature of major neuropsychiatric disorders, especially schizophrenia and age-related cognitive decline. Regional neural disinhibition, disrupting spatio-temporal control of neural activity and causing aberrant drive of projections, may disrupt processing within the disinhibited region and efferent regions. Recent studies in rats showed that prefrontal and hippocampal neural disinhibition (by local GABA antagonist microinfusion) dysregulates burst firing, which has been associated with important aspects of neural information processing. Using translational tests of clinically relevant cognitive functions, these studies showed that prefrontal and hippocampal neural disinhibition disrupts regional cognitive functions (including prefrontal attention and hippocampal memory function). Moreover, hippocampal neural disinhibition disrupted attentional performance, which does not require the hippocampus but requires prefrontal-striatal circuits modulated by the hippocampus. However, some prefrontal and hippocampal functions (including inhibitory response control) are spared by regional disinhibition. We consider conceptual implications of these findings, regarding the distinct relationships of distinct cognitive functions to prefrontal and hippocampal GABA tone and neural activity. Moreover, the findings support the proposition that prefrontal and hippocampal neural disinhibition contributes to clinically relevant cognitive deficits, and we consider pharmacological strategies for ameliorating cognitive deficits by rebalancing disinhibition-induced aberrant neural activity. Linked Articles This article is part of a themed section on Pharmacology of Cognition: a Panacea for Neuropsychiatric Disease? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.19/issuetoc. © 2017 The British Pharmacological Society.

The influence of medical burden severity and cognition on functional competence in older community-dwelling individuals with schizophrenia.

PubMed

Tsoutsoulas, Christopher; Mulsant, Benoit H; Kalache, Sawsan M; Kumar, Sanjeev; Ghazala, Zaid; Voineskos, Aristotle N; Butters, Meryl A; Menon, Mahesh; Rajji, Tarek K

2016-02-01

Cognition predicts functional competence among individuals with schizophrenia across the lifespan. However, as these individuals age, increasing levels of medical burden may also contribute to functional deficits both directly and indirectly through cognition. Thus, we assessed the relationship among, cognition, medical burden, and functional competence in older individuals with schizophrenia. We analyzed data obtained from 60 community-dwelling participants with schizophrenia and 30 control participants aged 50 or above. Cognition was assessed using the MATRICS Consensus Cognitive Battery (MCCB), functional competence was assessed using the USCD Performance-Based Skills Assessment (UPSA), and medical burden was assessed using the Cumulative Illness Rating Scale for Geriatrics (CIRS-G). Group differences were assessed using independent samples t-tests or chi-square tests. Mediation analyses using bootstrapping techniques were used to assess whether cognition mediated the effects of medical burden on functional competence. Participants with schizophrenia had higher levels of medical burden, cognitive deficits, and functional impairments. In participants with schizophrenia, cognition, but not medical burden, predicted functional competence after adjusting for age, education, gender, clinical symptoms, and anticholinergic burden of medications. In control participants, cognition and medical burden both predicted functional competence after adjusting for age, education, and gender. Further, cognition was found to fully mediate the association between medical burden and functional competence in control participants. Cognition is a robust predictor of functional competence among older individuals with schizophrenia, regardless of medical burden. Cognitive deficits associated with schizophrenia may mask any further cognitive impairment associated with medical burden and its impact on function. Copyright © 2015 Elsevier B.V. All rights reserved.

Impairments in social cognition following severe traumatic brain injury.

PubMed

McDonald, Skye

2013-03-01

Severe traumatic brain injury (TBI) leads to physical, neuropsychological, and emotional deficits that interfere with the individual’s capacity to return to his or her former lifestyle. This review focuses on social cognition, that is, the capacity to attend to, recognize and interpret interpersonal cues that guide social behavior. Social cognition entails ‘‘hot’’ processes, that is, emotion perception and emotional empathy and ‘‘cold’’ processes, that is, the ability to infer the beliefs, feelings, and intentions of others (theory of mind: ToM) to see their point of view (cognitive empathy) and what they mean when communicating (pragmatic inference). This review critically examines research attesting to deficits in each of these domains and also examines evidence for theorized mechanisms including specific neural networks, the role of simulation, and non-social cognition. Current research is hampered by small, heterogeneous samples and the inherent complexity of TBI pathology. Nevertheless, there is evidence that facets of social cognition are impaired in this population. New assessment tools to measure social cognition following TBI are required that predict everyday social functioning. In addition, research into remediation needs to be guided by the growing empirical base for understanding social cognition that may yet reveal how deficits dissociate following TBI.

Diagnostic Utility of WISC-IV General Abilities Index and Cognitive Proficiency Index Difference Scores among Children with ADHD

ERIC Educational Resources Information Center

Devena, Sarah E.; Watkins, Marley W.

2012-01-01

The Wechsler Intelligence Scale for Children-Fourth Edition General Abilities Index and Cognitive Proficiency Index have been advanced as possible diagnostic markers of attention deficit hyperactivity disorder. This hypothesis was tested with a hospital sample with attention deficit hyperactivity disorder (n = 78), a referred but nondiagnosed…

Short-Term Memory of Children with Mental Retardation: Structural Defects or Control Deficits.

ERIC Educational Resources Information Center

Katims, David S.

The short-term memory of 24 retarded and 24 nonretarded individuals, aged 10 to 14, under conditions of restricted cognitive strategy use was investigated. An attempt was made to determine whether short-term memory difficulties of persons with mental retardation are caused by deficits in voluntary cognitive strategies, such as the organization and…

"SLC2A3" Single-Nucleotide Polymorphism and Duplication Influence Cognitive Processing and Population-Specific Risk for Attention-Deficit/Hyperactivity Disorder

ERIC Educational Resources Information Center

Merker, Sören; Reif, Andreas; Ziegler, Georg C.; Weber, Heike; Mayer, Ute; Ehlis, Ann-Christine; Conzelmann, Annette; Johansson, Stefan; Müller-Reible, Clemens; Nanda, Indrajit; Haaf, Thomas; Ullmann, Reinhard; Romanos, Marcel; Fallgatter, Andreas J.; Pauli, Paul; Strekalova, Tatyana; Jansch, Charline; Vasquez, Alejandro Arias; Haavik, Jan; Ribasés, Marta; Ramos-Quiroga, Josep Antoni; Buitelaar, Jan K.; Franke, Barbara; Lesch, Klaus-Peter

2017-01-01

Background: Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder with profound cognitive, behavioral, and psychosocial impairments with persistence across the life cycle. Our initial genome-wide screening approach for copy number variants (CNVs) in ADHD implicated a duplication of…

A Cognitive and Affective Pattern in Posterior Fossa Strokes in Children: A Case Series

ERIC Educational Resources Information Center

Kossorotoff, Manoelle; Gonin-Flambois, Coralie; Gitiaux, Cyril; Quijano, Susana; Boddaert, Nathalie; Bahi-Buisson, Nadia; Barnerias, Christine; Dulac, Olivier; Brunelle, Francis; Desguerre, Isabelle

2010-01-01

Aim: Posterior fossa strokes account for about 10% of ischaemic strokes in children. Although motor and dysautonomic symptoms are common, to our knowledge cognitive and affective deficits have not been described in the paediatric literature. Our aim, therefore, was to describe these symptoms and deficits. Method: In a retrospective study, we…

Spelling Difficulties in School-Aged Girls with Attention-Deficit/Hyperactivity Disorder: Behavioral, Psycholinguistic, Cognitive, and Graphomotor Correlates

ERIC Educational Resources Information Center

Åsberg Johnels, Jakob; Kopp, Svenny; Gillberg, Christopher

2014-01-01

Writing difficulties are common among children with attention-deficit/hyperactivity disorder (ADHD), but the nature of these difficulties has not been well studied. Here we relate behavioral, psycholinguistic, cognitive (memory/executive), and graphomotor measures to spelling skills in school-age girls with ADHD (n = 30) and an age-matched group…

Cognitive deficits and educational loss in children with schistosome infection-A systematic review and meta-analysis.

PubMed

Ezeamama, Amara E; Bustinduy, Amaya L; Nkwata, Allan K; Martinez, Leonardo; Pabalan, Noel; Boivin, Michael J; King, Charles H

2018-01-01

By means of meta-analysis of information from all relevant epidemiologic studies, we examined the hypothesis that Schistosoma infection in school-aged children (SAC) is associated with educational loss and cognitive deficits. This review was prospectively registered in the PROSPERO database (CRD42016040052). Medline, Biosis, and Web of Science were searched for studies published before August 2016 that evaluated associations between Schistosoma infection and cognitive or educational outcomes. Cognitive function was defined in four domains-learning, memory, reaction time, and innate intelligence. Educational outcome measures were defined as attendance and scholastic achievement. Risk of bias (ROB) was evaluated using the Newcastle-Ottawa quality assessment scale. Standardized mean differences (SMD) and 95% confidence intervals (CI) were calculated to compare cognitive and educational measures for Schistosoma infected /not dewormed vs. uninfected/dewormed children. Sensitivity analyses by study design, ROB, and sequential exclusion of individual studies were implemented. Thirty studies from 14 countries, including 38,992 SAC between 5-19 years old, were identified. Compared to uninfected children and children dewormed with praziquantel, the presence of Schistosoma infection and/or non-dewormed status was associated with deficits in school attendance (SMD = -0.36, 95%CI: -0.60, -0.12), scholastic achievement (SMD = -0.58, 95%CI: -0.96, -0.20), learning (SMD = -0.39, 95%CI: -0.70, -0.09) and memory (SMD = -0.28, 95%CI: -0.52, -0.04) tests. By contrast, Schistosoma-infected/non-dewormed and uninfected/dewormed children were similar with respect to performance in tests of reaction time (SMD = -0.06, 95%CI: -0.42, 0.30) and intelligence (SMD = -0.25, 95%CI: -0.57, 0.06). Schistosoma infection-associated deficits in educational measures were robust among observational studies, but not among interventional studies. The significance of infection-associated deficits in scholastic achievement was sensitive to ROB. Schistosoma infection-related deficits in learning and memory tests were invariant by ROB and study design. Schistosoma infection/non-treatment was significantly associated with educational, learning, and memory deficits in SAC. Early treatment of children in Schistosoma-endemic regions could potentially mitigate these deficits. ClinicalTrials.gov CRD42016040052.

Repeated exposure to delta 9-tetrahydrocannabinol reduces prefrontal cortical dopamine metabolism in the rat.

PubMed

Jentsch, J D; Verrico, C D; Le, D; Roth, R H

1998-05-01

Long-term abuse of marijuana by humans can induce profound behavioral deficits characterized by cognitive and memory impairments. In particular, deficits on tasks dependent on frontal lobe function have been reported in cannabis abusers. In the current study, we examined whether long-term exposure to delta9-tetrahydrocannabinol, the active ingredient in marijuana, altered the neurochemistry of the frontal cortex in rats. Two weeks administration of delta9-tetrahydrocannabinol reduced dopamine transmission in the medial prefrontal cortex, while dopamine metabolism in striatal regions was unaffected. These data are consistent with earlier findings of dopaminergic regulation of frontal cortical cognition. Thus, cognitive deficits in heavy abusers of cannabis may be subserved by drug-induced alterations in frontal cortical dopamine transmission.

The multiple deficit model of dyslexia: what does it mean for identification and intervention?

PubMed

Ring, Jeremiah; Black, Jeffrey L

2018-04-24

Research demonstrates that phonological skills provide the basis of reading acquisition and are a primary processing deficit in dyslexia. This consensus has led to the development of effective methods of reading intervention. However, a single phonological deficit is not sufficient to account for the heterogeneity of individuals with dyslexia, and recent research provides evidence that supports a multiple-deficit model of reading disorders. Two studies are presented that investigate (1) the prevalence of phonological and cognitive processing deficit profiles in children with significant reading disability and (2) the effects of those same phonological and cognitive processing skills on reading development in a sample of children that received treatment for dyslexia. The results are discussed in the context of implications for identification and an intervention approach that accommodates multiple deficits within a comprehensive skills-based reading program.

[Mathematical abilities and executive function in children with attention deficit hyperactivity disorder and learning disabilities in mathematics].

PubMed

Miranda Casas, Ana; Meliá de Alba, Amanda; Marco Taverner, Rafaela

2009-02-01

Mathematical abilities and executive function in children with attention deficit hyperactivity disorder and learning disabilities in mathematics. Even though 26% of children with attention deficit hyperactivity disorder (ADHD) show a specific mathematic learning difficulty (MLD), the studies have been scarce. The present study had the following goals: 1) to study the profile related to cognitive and metacognitive skills implied in calculation and problem-solving in children with ADHD+MLD, and to compare them in children with ADHD, children with MLD, and children without problems; 2) to study the severity of the deficit in executive function (EF) in children with ADHD+MLD. Comparing the groups MLD, ADHD, ADHD+MLD, and children without problems, the results highlighted that children with ADHD+MLD showed a cognitive and metacognitive deficit in mathematic achievement. Furthermore, results showed a more severe deficit in the EF in children with ADHD+MLD.

Nicotine withdrawal-induced inattention is absent in alpha7 nAChR knockout mice

PubMed Central

Higa, K. K.; Grim, A.; Kamenski, M. E.; van Enkhuizen, J.; Zhou, X.; Li, K.; Naviaux, J. C.; Wang, L.; Naviaux, R. K.; Geyer, M. A.; Markou, A.; Young, J. W.

2017-01-01

Rationale Smoking is the leading cause of preventable death in the U.S., but quit attempts result in withdrawal-induced cognitive dysfunction and predicts relapse. Greater understanding of the neural mechanism(s) underlying these cognitive deficits is required to develop targeted treatments to aid quit attempts. Objectives We examined nicotine withdrawal-induced inattention in mice lacking the α7 nicotinic acetylcholine receptor (nAChR) using the 5-choice continuous performance test (5C-CPT). Methods Mice were trained in the 5C-CPT prior to osmotic minipump implantation containing saline or nicotine. Experiment 1 used 40 mg/kg/day nicotine treatment and tested C57BL/6 mice 4, 28, and 52 h after pump removal. Experiment 2 used 14 and 40 mg/kg/day nicotine treatment in α7 nAChR knockout (KO) and wildtype (WT) littermates tested 4 h after pump removal. Subsets of WT mice were sacrificed before and after pump removal to assess changes in receptor expression associated with nicotine administration and withdrawal. Results Nicotine withdrawal impaired attention in the 5C-CPT, driven by response inhibition and target detection deficits. The overall attentional deficit was absent in α7 nAChR KO mice despite response disinhibition in these mice. Synaptosomal glutamate mGluR5 and dopamine D4 receptor expression were reduced during chronic nicotine but increased during withdrawal, potentially contributing to cognitive deficits. Conclusions The α7 nAChR may underlie nicotine withdrawal-induced deficits in target detection but is not required for response disinhibition deficits. Alterations to the glutamatergic and dopaminergic pathways may also contribute to withdrawal-induced attentional deficits, providing novel targets to alleviate the cognitive symptoms of withdrawal during quit attempts. PMID:28243714

Mechanism and treatment for the learning and memory deficits associated with mouse models of Noonan syndrome

PubMed Central

Lee, Yong-Seok; Ehninger, Dan; Zhou, Miou; Oh, Jun-Young; Kang, Minkyung; Kwak, Chuljung; Ryu, Hyun-Hee; Butz, Delana; Araki, Toshiyuki; Cai, Ying; Balaji, J.; Sano, Yoshitake; Nam, Christine I.; Kim, Hyong Kyu; Kaang, Bong-Kiun; Burger, Corinna; Neel, Benjamin G.; Silva, Alcino J.

2015-01-01

In Noonan Syndrome (NS) 30% to 50% of subjects show cognitive deficits of unknown etiology and with no known treatment. Here, we report that knock-in mice expressing either of two NS-associated Ptpn11 mutations show hippocampal-dependent spatial learning impairments and deficits in hippocampal long-term potentiation (LTP). In addition, viral overexpression of the PTPN11D61G in adult hippocampus results in increased baseline excitatory synaptic function, deficits in LTP and spatial learning, which can all be reversed by a MEK inhibitor. Furthermore, brief treatment with lovastatin reduces Ras-Erk activation in the brain, and normalizes the LTP and learning deficits in adult Ptpn11D61G/+ mice. Our results demonstrate that increased basal Erk activity and corresponding baseline increases in excitatory synaptic function are responsible for the LTP impairments and, consequently, the learning deficits in mouse models of NS. These data also suggest that lovastatin or MEK inhibitors may be useful for treating the cognitive deficits in NS. PMID:25383899

Preliminary cognitive scale of basic and instrumental activities of daily living for dementia and mild cognitive impairment.

PubMed

Rodríguez-Bailón, María; Montoro-Membila, Nuria; Garcia-Morán, Tamara; Arnedo-Montoro, María Luisa; Funes Molina, María Jesús

2015-01-01

In the present study we explored cognitive and functional deficits in patients with multidomain mild cognitive impairment (MCI), patients with dementia, and healthy age-matched control participants using the Cognitive Scale for Basic and Instrumental Activities of Daily Living, a new preliminary informant-based assessment tool. This tool allowed us to evaluate four key cognitive abilities-task memory schema, error detection, problem solving, and task self-initiation-in a range of basic and instrumental activities of daily living (BADL and IADL, respectively). The first part of the present study was devoted to testing the psychometric adequateness of this new informant-based tool and its convergent validity with other global functioning and neuropsychological measures. The second part of the study was aimed at finding the patterns of everyday cognitive factors that best discriminate between the three groups. We found that patients with dementia exhibited impairment in all cognitive abilities in both basic and instrumental activities. By contrast, patients with MCI were found to have preserved task memory schema in both types of ADL; however, such patients exhibited deficits in error detection and task self-initiation but only in IADL. Finally, patients with MCI also showed a generalized problem solving deficit that affected even BADL. Studying various cognitive processes instantiated in specific ADL differing in complexity seems a promising strategy to further understand the specific relationships between cognition and function in these and other cognitively impaired populations.

Cognition in schizophrenia and schizo-affective disorder: impairments that are more similar than different

PubMed Central

Owoso, A.; Carter, C. S.; Gold, J.M.; MacDonald, A.W.; Ragland, J.D.; Silverstein, S.M.; Strauss, M. E.; Barch, D. M.

2014-01-01

Background Cognition is increasingly being recognized as an important aspect of psychotic disorders and a key contributor to functional outcome. In the past, comparative studies have been performed in schizophrenia and schizo-affective disorder with regard to cognitive performance, but the results have been mixed and the cognitive measures used have not always assessed the cognitive deficits found to be specific to psychosis. A set of optimized cognitive paradigms designed by the Cognitive Neuroscience Test Reliability and Clinical Applications for Schizophrenia (CNTRACS) Consortium to assess deficits specific to schizophrenia was used to measure cognition in a large group of individuals with schizophrenia and schizo-affective disorder. Method A total of 519 participants (188 with schizophrenia, 63 with schizo-affective disorder and 268 controls) were administered three cognitive paradigms assessing the domains of goal maintenance in working memory, relational encoding and retrieval in episodic memory and visual integration. Results Across the three domains, the results showed no major quantitative differences between patient groups, with both groups uniformly performing worse than healthy subjects. Conclusions The findings of this study suggests that, with regard to deficits in cognition, considered a major aspect of psychotic disorder, schizophrenia and schizo-affective disorder do not demonstrate major significant distinctions. These results have important implications for our understanding of the nosological structure of major psychopathology, providing evidence consistent with the hypothesis that there is no natural distinction between cognitive functioning in schizophrenia and schizo-affective disorder. PMID:23522057

Beyond Emotional and Spatial Processes: Cognitive Dysfunction in a Depressive Phenotype Produced by Long Photoperiod Exposure.

PubMed

Barnes, Abigail K; Smith, Summer B; Datta, Subimal

2017-01-01

Cognitive dysfunction in depression has recently been given more attention and legitimacy as a core symptom of the disorder. However, animal investigations of depression-related cognitive deficits have generally focused on emotional or spatial memory processing. Additionally, the relationship between the cognitive and affective disturbances that are present in depression remains obscure. Interestingly, sleep disruption is one aspect of depression that can be related both to cognition and affect, and may serve as a link between the two. Previous studies have correlated sleep disruption with negative mood and impaired cognition. The present study investigated whether a long photoperiod-induced depressive phenotype showed cognitive deficits, as measured by novel object recognition, and displayed a cognitive vulnerability to an acute period of total sleep deprivation. Adult male Wistar rats were subjected to a long photoperiod (21L:3D) or a normal photoperiod (12L:12D) condition. Our results indicate that our long photoperiod exposed animals showed behaviors in the forced swim test consistent with a depressive phenotype, and showed significant deficits in novel object recognition. Three hours of total sleep deprivation, however, did not significantly change novel object recognition in either group, but the trends suggest that the long photoperiod and normal photoperiod groups had different cognitive responses to total sleep deprivation. Collectively, these results underline the extent of cognitive dysfunction present in depression, and suggest that altered sleep plays a role in generating both the affective and cognitive symptoms of depression.

Dietary Intake of Sulforaphane-Rich Broccoli Sprout Extracts during Juvenile and Adolescence Can Prevent Phencyclidine-Induced Cognitive Deficits at Adulthood.

PubMed

Shirai, Yumi; Fujita, Yuko; Hashimoto, Ryota; Ohi, Kazutaka; Yamamori, Hidenaga; Yasuda, Yuka; Ishima, Tamaki; Suganuma, Hiroyuki; Ushida, Yusuke; Takeda, Masatoshi; Hashimoto, Kenji

2015-01-01

Oxidative stress and inflammation play a role in cognitive impairment, which is a core symptom of schizophrenia. Furthermore, a hallmark of the pathophysiology of this disease is the dysfunction of cortical inhibitory γ-aminobutyric acid (GABA) neurons expressing parvalbumin (PV), which is also involved in cognitive impairment. Sulforaphane (SFN), an isothiocyanate derived from broccoli, is a potent activator of the transcription factor Nrf2, which plays a central role in the inducible expressions of many cytoprotective genes in response to oxidative stress. Keap1 is a cytoplasmic protein that is essential for the regulation of Nrf2 activity. Here, we found that pretreatment with SFN attenuated cognitive deficits, the increase in 8-oxo-dG-positive cells, and the decrease in PV-positive cells in the medial prefrontal cortex and hippocampus after repeated administration of phencyclidine (PCP). Furthermore, PCP-induced cognitive deficits were improved by the subsequent subchronic administration of SFN. Interestingly, the dietary intake of glucoraphanin (a glucosinolate precursor of SFN) during the juvenile and adolescence prevented the onset of PCP-induced cognitive deficits as well as the increase in 8-oxo-dG-positive cells and the decrease in PV-positive cells in the brain at adulthood. Moreover, the NRF2 gene and the KEAP1 gene had an epistatic effect on cognitive impairment (e.g., working memory and processing speed) in patients with schizophrenia. These findings suggest that SFN may have prophylactic and therapeutic effects on cognitive impairment in schizophrenia. Therefore, the dietary intake of SFN-rich broccoli sprouts during the juvenile and adolescence may prevent the onset of psychosis at adulthood.

Cognitive Effects of Stimulant, Guanfacine, and Combined Treatment in Child and Adolescent Attention-Deficit/Hyperactivity Disorder

PubMed Central

Bilder, Robert M.; Loo, Sandra; McGough, James J.; Whelan, Fiona; Hellemann, Gerhard; Sugar, Catherine; Del’Homme, Melissa; Sturm, Alexandra; Cowen, Jennifer; Hanada, Grant; McCracken, James T.

2016-01-01

Objective Psychostimulants are partially effective in reducing cognitive dysfunction associated with attention-deficit/hyperactivity disorder (ADHD). Cognitive effects of guanfacine, an alternative treatment, are poorly understood. Given its distinct action on α2A receptors, guanfacine may have different or complementary effects relative to stimulants. This study tested stimulant and guanfacine monotherapies relative to combined treatment on cognitive functions important in ADHD. Method Children with ADHD (n = 182; age 7–14 years) completed an eight-week double blind randomized controlled trial with three arms: d-methylphenidate (DMPH), guanfacine (GUAN), or combination treatment with DMPH and GUAN (COMB). A non-clinical comparison group (n = 93) had baseline testing, and a subset was re-tested 8 weeks later (n = 38). Analyses examined treatment effects in four cognitive domains (working memory, response inhibition, reaction time, and reaction time variability) constructed from 20 variables. Results The ADHD group showed impaired working memory relative to the non-clinical comparison group (effect size = −0.53 SD units). The treatments differed in effects on working memory but not other cognitive domains. Combination treatment improved working memory more than GUAN, but was not significantly better than DMPH alone. Treatment did not fully normalize the initial deficit in ADHD relative to the comparison group. Conclusion Combined treatment with DMPH and GUAN yielded greater improvements in working memory than placebo or GUAN alone, but the combined treatment was not superior to DMPH alone, and did not extend to other cognitive domains. Although GUAN may be a useful add-on treatment to psychostimulants, additional strategies appear necessary to achieve normalization of cognitive function in ADHD. Clinical trial registration information Single Versus Combination Medication Treatment for Children With Attention Deficit Hyperactivity Disorder; http://clinicaltrials.gov/; NCT00429273 PMID:27453080

Uncovering the Neural Bases of Cognitive and Affective Empathy Deficits in Alzheimer's Disease and the Behavioral-Variant of Frontotemporal Dementia.

PubMed

Dermody, Nadene; Wong, Stephanie; Ahmed, Rebekah; Piguet, Olivier; Hodges, John R; Irish, Muireann

2016-05-30

Loss of empathy is a core presenting feature of the behavioral-variant of frontotemporal dementia (bvFTD), resulting in socioemotional difficulties and behavioral transgressions. In contrast, interpersonal functioning remains relatively intact in Alzheimer's disease (AD), despite marked cognitive decline. The neural substrates mediating these patterns of loss and sparing in social functioning remain unclear, yet are relevant for our understanding of the social brain. We investigated cognitive versus affective aspects of empathy using the Interpersonal Reactivity Index (IRI) in 25 AD and 24 bvFTD patients and contrasted their performance with 22 age- and education-matched controls. Cognitive empathy was comparably compromised in AD and bvFTD, whereas affective empathy was impaired exclusively in bvFTD. While controlling for overall cognitive dysfunction ameliorated perspective-taking deficits in AD, empathy loss persisted across cognitive and affective domains in bvFTD. Voxel-based morphometry analyses revealed divergent neural substrates of empathy loss in each patient group. Perspective-taking deficits correlated with predominantly left-sided temporoparietal atrophy in AD, whereas widespread bilateral frontoinsular, temporal, parietal, and occipital atrophy was implicated in bvFTD. Reduced empathic concern in bvFTD was associated with atrophy in the left orbitofrontal, inferior frontal, and insular cortices, and the bilateral mid-cingulate gyrus. Our findings suggest that social cognitive deficits in AD arise largely as a consequence of global cognitive dysfunction, rather than a loss of empathy per se. In contrast, loss of empathy in bvFTD reflects the deterioration of a distributed network of frontoinsular and temporal structures that appear crucial for monitoring and processing social information.

Meta-Analysis of Cognitive Functioning in Breast Cancer Survivors Previously Treated With Standard-Dose Chemotherapy

PubMed Central

Jim, Heather S.L.; Phillips, Kristin M.; Chait, Sari; Anne Faul, Leigh; Popa, Mihaela A.; Lee, Yun-Hsiang; Hussin, Mallory G.; Jacobsen, Paul B.; Small, Brent J.

2012-01-01

Purpose Evidence is mixed regarding long-term cognitive deficits in patients treated with chemotherapy. Previous meta-analyses have not focused specifically on the postchemotherapy period and have not incorporated several recent studies. The goal of the current study was to conduct a meta-analysis of cognitive functioning in breast cancer survivors who were treated with chemotherapy ≥ 6 months previously. Methods A search of PubMed, PsycInfo, Cumulative Index to Nursing and Allied Health Literature, and Cochrane Library yielded 2,751 abstracts, which were independently evaluated by pairs of raters. Meta-analysis was conducted on 17 studies of 807 patients previously treated with standard-dose chemotherapy for breast cancer. Neuropsychological tests were categorized according to eight cognitive domains: attention, executive functioning, information processing, motor speed, verbal ability, verbal memory, visual memory, and visuospatial ability. Results Deficits in cognitive functioning were observed in patients treated with chemotherapy relative to controls or prechemotherapy baseline in the domains of verbal ability (g = −0.19; P < .01) and visuospatial ability (g = −0.27; P < .01). Patients treated with chemotherapy performed worse than noncancer controls in verbal ability and worse than patients treated without chemotherapy in visuospatial ability (both P < .01). Age, education, time since treatment, and endocrine therapy did not moderate observed cognitive deficits in verbal ability or visuospatial ability (all P ≥ .51). Conclusion Results indicate that, on average, observed cognitive deficits in patients with breast cancer previously treated with chemotherapy are small in magnitude and limited to the domains of verbal ability and visuospatial ability. This information can be used to inform interventions to educate patients with breast cancer regarding the long-term impact of chemotherapy on cognitive functioning. PMID:22927526

Dietary Intake of Sulforaphane-Rich Broccoli Sprout Extracts during Juvenile and Adolescence Can Prevent Phencyclidine-Induced Cognitive Deficits at Adulthood

PubMed Central

Shirai, Yumi; Fujita, Yuko; Hashimoto, Ryota; Ohi, Kazutaka; Yamamori, Hidenaga; Yasuda, Yuka; Ishima, Tamaki; Suganuma, Hiroyuki; Ushida, Yusuke; Takeda, Masatoshi; Hashimoto, Kenji

2015-01-01

Oxidative stress and inflammation play a role in cognitive impairment, which is a core symptom of schizophrenia. Furthermore, a hallmark of the pathophysiology of this disease is the dysfunction of cortical inhibitory γ-aminobutyric acid (GABA) neurons expressing parvalbumin (PV), which is also involved in cognitive impairment. Sulforaphane (SFN), an isothiocyanate derived from broccoli, is a potent activator of the transcription factor Nrf2, which plays a central role in the inducible expressions of many cytoprotective genes in response to oxidative stress. Keap1 is a cytoplasmic protein that is essential for the regulation of Nrf2 activity. Here, we found that pretreatment with SFN attenuated cognitive deficits, the increase in 8-oxo-dG-positive cells, and the decrease in PV-positive cells in the medial prefrontal cortex and hippocampus after repeated administration of phencyclidine (PCP). Furthermore, PCP-induced cognitive deficits were improved by the subsequent subchronic administration of SFN. Interestingly, the dietary intake of glucoraphanin (a glucosinolate precursor of SFN) during the juvenile and adolescence prevented the onset of PCP-induced cognitive deficits as well as the increase in 8-oxo-dG-positive cells and the decrease in PV-positive cells in the brain at adulthood. Moreover, the NRF2 gene and the KEAP1 gene had an epistatic effect on cognitive impairment (e.g., working memory and processing speed) in patients with schizophrenia. These findings suggest that SFN may have prophylactic and therapeutic effects on cognitive impairment in schizophrenia. Therefore, the dietary intake of SFN-rich broccoli sprouts during the juvenile and adolescence may prevent the onset of psychosis at adulthood. PMID:26107664

Investigation of left and right lateral fluid percussion injury in C57BL6/J mice: In vivo functional consequences

PubMed Central

Schurman, Lesley D.; Smith, Terry L.; Morales, Anthony J.; Lee, Nancy N.; Reeves, Thomas M.; Phillips, Linda L.; Lichtman, Aron H.

2017-01-01

Although rodent models of traumatic brain injury (TBI) reliably produce cognitive and motor disturbances, behavioral characterization resulting from left and right hemisphere injuries remains unexplored. Here we examined the functional consequences of targeting the left versus right parietal cortex in lateral fluid percussion injury, on Morris water maze (MWM) spatial memory tasks (fixed platform and reversal) and neurological motor deficits (neurological severity score and rotarod). In the MWM fixed platform task, right lateral injury produced a small delay in acquisition rate compared to left. However, injury to either hemisphere resulted in probe trial deficits. In the MWM reversal task, left-right performance deficits were not evident, though left lateral injury produced mild acquisition and probe trial deficits compared to sham controls. Additionally, left and right injury produced similar neurological motor task deficits, impaired righting times, and lesion volumes. Injury to either hemisphere also produced robust ipsilateral, and modest contralateral, morphological changes in reactive microglia and astrocytes. In conclusion, left and right lateral TBI impaired MWM performance, with mild fixed platform acquisition rate differences, despite similar motor deficits, histological damage, and glial cell reactivity. Thus, while both left and right lateral TBI produce cognitive deficits, laterality in mouse MWM learning and memory merits consideration in the investigation of TBI-induced cognitive consequences. PMID:28527714

Investigation of left and right lateral fluid percussion injury in C57BL6/J mice: In vivo functional consequences.

PubMed

Schurman, Lesley D; Smith, Terry L; Morales, Anthony J; Lee, Nancy N; Reeves, Thomas M; Phillips, Linda L; Lichtman, Aron H

2017-07-13

Although rodent models of traumatic brain injury (TBI) reliably produce cognitive and motor disturbances, behavioral characterization resulting from left and right hemisphere injuries remains unexplored. Here we examined the functional consequences of targeting the left versus right parietal cortex in lateral fluid percussion injury, on Morris water maze (MWM) spatial memory tasks (fixed platform and reversal) and neurological motor deficits (neurological severity score and rotarod). In the MWM fixed platform task, right lateral injury produced a small delay in acquisition rate compared to left. However, injury to either hemisphere resulted in probe trial deficits. In the MWM reversal task, left-right performance deficits were not evident, though left lateral injury produced mild acquisition and probe trial deficits compared to sham controls. Additionally, left and right injury produced similar neurological motor task deficits, impaired righting times, and lesion volumes. Injury to either hemisphere also produced robust ipsilateral, and modest contralateral, morphological changes in reactive microglia and astrocytes. In conclusion, left and right lateral TBI impaired MWM performance, with mild fixed platform acquisition rate differences, despite similar motor deficits, histological damage, and glial cell reactivity. Thus, while both left and right lateral TBI produce cognitive deficits, laterality in mouse MWM learning and memory merits consideration in the investigation of TBI-induced cognitive consequences. Copyright © 2017. Published by Elsevier B.V.

Episodic memory impairment in Addison's disease: results from a telephonic cognitive assessment.

PubMed

Henry, Michelle; Thomas, Kevin G F; Ross, Ian L

2014-06-01

Patients with Addison's disease frequently self-report memory and attention difficulties, even when on standard replacement therapy. However, few published studies examine, using objective measures and assessing across multiple domains, the cognitive functioning of Addison's disease patients relative to healthy controls. The primary aim of this study was to investigate whether the previously reported subjective cognitive deficits in Addison's disease are confirmed by objective measures. Conducting comprehensive neuropsychological assessments of patients with relatively rare clinical disorders, such as Addison's disease, is challenging because access to those patients is often limited, and because their medical condition might prevent extended testing sessions. Brief telephonic cognitive assessments are a useful tool in such circumstances. Hence, we administered the Brief Test of Adult Cognition by Telephone to 27 Addison's disease patients and 27 matched healthy controls. The instrument provides objective assessment of episodic memory, working memory, executive functioning, reasoning, and speed of processing. Statistical analyses confirmed that, as expected, patients performed significantly more poorly than controls on the episodic memory subtest. There were, however, no significant between-group differences on the attention, executive functioning, reasoning, and speed of processing subtests. Furthermore, patients with a longer duration of illness performed more poorly across all domains of cognition. We conclude that, for Addison's disease patients, previously reported subjective cognitive deficits are matched by objective impairment, but only in the domain of episodic memory. Future research might investigate (a) whether these memory deficits are material-specific (i.e., whether non-verbal memory is also affected), and (b) the neurobiological mechanisms underlying these deficits.

Modafinil Reverses Phencyclidine-Induced Deficits in Cognitive Flexibility, Cerebral Metabolism, and Functional Brain Connectivity

PubMed Central

Dawson, Neil; Thompson, Rhiannon J.; McVie, Allan; Thomson, David M.; Morris, Brian J.; Pratt, Judith A.

2012-01-01

Objective: In the present study, we employ mathematical modeling (partial least squares regression, PLSR) to elucidate the functional connectivity signatures of discrete brain regions in order to identify the functional networks subserving PCP-induced disruption of distinct cognitive functions and their restoration by the procognitive drug modafinil. Methods: We examine the functional connectivity signatures of discrete brain regions that show overt alterations in metabolism, as measured by semiquantitative 2-deoxyglucose autoradiography, in an animal model (subchronic phencyclidine [PCP] treatment), which shows cognitive inflexibility with relevance to the cognitive deficits seen in schizophrenia. Results: We identify the specific components of functional connectivity that contribute to the rescue of this cognitive inflexibility and to the restoration of overt cerebral metabolism by modafinil. We demonstrate that modafinil reversed both the PCP-induced deficit in the ability to switch attentional set and the PCP-induced hypometabolism in the prefrontal (anterior prelimbic) and retrosplenial cortices. Furthermore, modafinil selectively enhanced metabolism in the medial prelimbic cortex. The functional connectivity signatures of these regions identified a unifying functional subsystem underlying the influence of modafinil on cerebral metabolism and cognitive flexibility that included the nucleus accumbens core and locus coeruleus. In addition, these functional connectivity signatures identified coupling events specific to each brain region, which relate to known anatomical connectivity. Conclusions: These data support clinical evidence that modafinil may alleviate cognitive deficits in schizophrenia and also demonstrate the benefit of applying PLSR modeling to characterize functional brain networks in translational models relevant to central nervous system dysfunction. PMID:20810469

Detection of Subtle Cognitive Changes after mTBI Using a Novel Tablet-Based Task.

PubMed

Fischer, Tara D; Red, Stuart D; Chuang, Alice Z; Jones, Elizabeth B; McCarthy, James J; Patel, Saumil S; Sereno, Anne B

2016-07-01

This study examined the potential for novel tablet-based tasks, modeled after eye tracking techniques, to detect subtle sensorimotor and cognitive deficits after mild traumatic brain injury (mTBI). Specifically, we examined whether performance on these tablet-based tasks (Pro-point and Anti-point) was able to correctly categorize concussed versus non-concussed participants, compared with performance on other standardized tests for concussion. Patients admitted to the emergency department with mTBI were tested on the Pro-point and Anti-point tasks, a current standard cognitive screening test (i.e., the Standard Assessment of Concussion [SAC]), and another eye movement-based tablet test, the King-Devick(®) (KD). Within hours after injury, mTBI patients showed significant slowing in response times, compared with both orthopedic and age-matched control groups, in the Pro-point task, demonstrating deficits in sensorimotor function. Mild TBI patients also showed significant slowing, compared with both control groups, on the Anti-point task, even when controlling for sensorimotor slowing, indicating deficits in cognitive function. Performance on the SAC test revealed similar deficits of cognitive function in the mTBI group, compared with the age-matched control group; however, the KD test showed no evidence of cognitive slowing in mTBI patients, compared with either control group. Further, measuring the sensitivity and specificity of these tasks to accurately predict mTBI with receiver operating characteristic analysis indicated that the Anti-point and Pro-point tasks reached excellent levels of accuracy and fared better than current standardized tools for assessment of concussion. Our findings suggest that these rapid tablet-based tasks are able to reliably detect and measure functional impairment in cognitive and sensorimotor control within hours after mTBI. These tasks may provide a more sensitive diagnostic measure for functional deficits that could prove key to earlier detection of concussion, evaluation of interventions, or even prediction of persistent symptoms.

Detection of Subtle Cognitive Changes after mTBI Using a Novel Tablet-Based Task

PubMed Central

Red, Stuart D.; Chuang, Alice Z.; Jones, Elizabeth B.; McCarthy, James J.; Patel, Saumil S.; Sereno, Anne B.

2016-01-01

Abstract This study examined the potential for novel tablet-based tasks, modeled after eye tracking techniques, to detect subtle sensorimotor and cognitive deficits after mild traumatic brain injury (mTBI). Specifically, we examined whether performance on these tablet-based tasks (Pro-point and Anti-point) was able to correctly categorize concussed versus non-concussed participants, compared with performance on other standardized tests for concussion. Patients admitted to the emergency department with mTBI were tested on the Pro-point and Anti-point tasks, a current standard cognitive screening test (i.e., the Standard Assessment of Concussion [SAC]), and another eye movement–based tablet test, the King-Devick® (KD). Within hours after injury, mTBI patients showed significant slowing in response times, compared with both orthopedic and age-matched control groups, in the Pro-point task, demonstrating deficits in sensorimotor function. Mild TBI patients also showed significant slowing, compared with both control groups, on the Anti-point task, even when controlling for sensorimotor slowing, indicating deficits in cognitive function. Performance on the SAC test revealed similar deficits of cognitive function in the mTBI group, compared with the age-matched control group; however, the KD test showed no evidence of cognitive slowing in mTBI patients, compared with either control group. Further, measuring the sensitivity and specificity of these tasks to accurately predict mTBI with receiver operating characteristic analysis indicated that the Anti-point and Pro-point tasks reached excellent levels of accuracy and fared better than current standardized tools for assessment of concussion. Our findings suggest that these rapid tablet-based tasks are able to reliably detect and measure functional impairment in cognitive and sensorimotor control within hours after mTBI. These tasks may provide a more sensitive diagnostic measure for functional deficits that could prove key to earlier detection of concussion, evaluation of interventions, or even prediction of persistent symptoms. PMID:26398492

Neuro-cognition and social cognition elements of social functioning and social quality of life.

PubMed

Hasson-Ohayon, Ilanit; Mashiach-Eizenberg, Michal; Arnon-Ribenfeld, Nitzan; Kravetz, Shlomo; Roe, David

2017-12-01

Previous studies have shown that deficits in social cognition mediate the association between neuro-cognition and functional outcome. Based on these findings, the current study presents an examination of the mediating role of social cognition and includes two different outcomes: social functioning assessed by objective observer and social quality of life assessed by subjective self-report. Instruments measuring different aspects of social cognition, cognitive ability, social functioning and social quality of life were administered to 131 participants who had a diagnosis of a serious mental illness. Results showed that emotion recognition and attributional bias were significant mediators such that cognitive assessment was positively related to both, which in turn, were negatively related to SQoL. While one interpretation of the data suggests that deficits in emotion recognition may serve as a possible defense mechanism, future studies should re-assess this idea. Copyright © 2017 Elsevier B.V. All rights reserved.

Beyond Utterances: Distributed Cognition as a Framework for Studying Discourse in Adults with Acquired Brain Injury

PubMed Central

Duff, Melissa C.; Mutlu, Bilge; Byom, Lindsey; Turkstra, Lyn S.

2014-01-01

Considerable effort has been directed at understanding the nature of the communicative deficits observed in individuals with acquired brain injuries. Yet several theoretical, methodological, and clinical challenges remain. In this article, we examine distributed cognition as a framework for understanding interaction among communication partners, interaction of communication and cognition, and interaction with the environments and contexts of everyday language use. We review the basic principles of distributed cognition and the implications for applying this approach to the study of discourse in individuals with cognitive-communication disorders. We also review a range of protocols and findings from our research that highlight how the distributed cognition approach might offer a deeper understanding of communicative mechanisms and deficits in individuals with cognitive communication impairments. The advantages and implications of distributed cognition as a framework for studying discourse in adults with acquired brain injury are discussed. PMID:22362323

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice

PubMed Central

Rogers, Justin T.; Liu, Chia-Chen; Zhao, Na; Wang, Jian; Putzke, Travis; Yang, Longyu; Shinohara, Mitsuru; Fryer, John D.; Kanekiyo, Takahisa; Bu, Guojun

2017-01-01

Aging is accompanied by increased neuroinflammation, synaptic dysfunction and cognitive deficits both in rodents and humans, yet the onset and progression of these deficits throughout the life span remain unknown. These aging-related deficits affect the quality of life and present challenges to our aging society. Here, we defined age-dependent and progressive impairments of synaptic and cognitive functions and showed that reducing astrocyte-related neuroinflammation through anti-inflammatory drug treatment in aged mice reverses these events. By comparing young (3 months), middle-aged (18 months), aged (24 months) and advanced-aged wild-type mice (30 months), we found that the levels of an astrocytic marker, GFAP, progressively increased after 18 months of age, which preceded the decreases of the synaptic marker PSD-95. Hippocampal long-term potentiation (LTP) was also suppressed in an age-dependent manner, where significant deficits were observed after 24 months of age. Fear conditioning tests demonstrated that associative memory in the context and cued conditions was decreased starting at the ages of 18 and 30 months, respectively. When the mice were tested on hidden platform water maze, spatial learning memory was significantly impaired after 24 months of age. Importantly, subacute treatment with the anti-inflammatory drug ibuprofen suppressed astrocyte activation, and restored synaptic plasticity and memory function in advanced-aged mice. These results support the critical contribution of aging-related inflammatory responses to hippocampal-dependent cognitive function and synaptic plasticity, in particular during advanced aging. Our findings provide strong evidence that suppression of neuroinflammation could be a promising treatment strategy to preserve cognition during aging. PMID:28254590

Consuming a Diet Supplemented with Resveratrol Reduced Infection-Related Neuroinflammation and Deficits in Working Memory in Aged Mice

PubMed Central

Abraham, Jayne

2009-01-01

Abstract Aged mice treated peripherally with lipopolysaccharide (LPS) show an exaggerated neuroinflammatory response and cognitive deficits compared to adults. Considerable evidence suggests resveratrol, a polyphenol found in red grapes, has potent antiinflammatory effects in the periphery, but its effects on the central inflammatory response and cognitive behavior are unknown. Therefore, the current study investigated if resveratrol dietary supplementation would inhibit neuroinflammation as well as behavioral and cognitive deficits in aged mice given LPS to mimic a peripheral infection. In initial studies, adult (3–6 months) and aged (22–24 months) mice were provided control or resveratrol-supplemented diet for 4 weeks and then injected intraperitoneally (i.p.) with saline or LPS, and locomotor activity and spatial working memory were assessed. As anticipated, deficits in locomotor activity and spatial working memory indicated aged mice are more sensitive to LPS compared to adults. More importantly, the LPS-induced deficits in aged animals were mitigated by dietary supplementation of resveratrol. In addition, resveratrol consumption reduced LPS-induced interleukin-1β (IL-1β) in plasma and the IL-1β mRNA in the hippocampus of aged mice. Finally, pretreatment of BV-2 microglial cells with resveratrol potently inhibited LPS-induced IL-1β production. These data show that aged mice are more sensitive than adult mice to both the inflammatory and cognitive effects of peripheral immune stimulation and suggest that resveratrol may be useful for attenuating acute cognitive disorders in elderly individuals with an infection. PMID:20041738

Aniracetam reversed learning and memory deficits following prenatal ethanol exposure by modulating functions of synaptic AMPA receptors.

PubMed

Vaglenova, Julia; Pandiella, Noemi; Wijayawardhane, Nayana; Vaithianathan, Tiru; Birru, Sandjay; Breese, Charles; Suppiramaniam, Vishnu; Randal, Clark

2008-04-01

Specific pharmacological treatments are currently not available to address problems resulting from fetal ethanol exposure, described as Fetal Alcohol Syndrome or Fetal Alcohol Spectrum Disorders (FASD). The present study evaluated the therapeutic effects of aniracetam against cognitive deficits in a well-characterized and sensitive FASD Sprague-Dawley rat model. Ethanol, administered orally at a moderate dose (4 g/kg/24 h; 38% v/v) during the entire course of pregnancy, caused severe cognitive deficits in offspring. Furthermore, both progeny genders were affected by a spectrum of behavioral abnormalities, such as a delay in the development of the righting reflex, poor novelty seeking behavior, and high anxiety levels in female rats. Cognitive disabilities, monitored in adult rats by a two-way active avoidance task, correlated well with a significant reduction of AMPA (alpha-amino-3 hydro-5 methyl-isoxazole propionic acid) receptor-mediated miniature excitatory postsynaptic responses (mEPSCs) in the hippocampus. Administration of aniracetam for 10 days (post-natal days (PND) 18-27), at a dose of 50 mg/kg reversed cognitive deficits in both rat genders, indicated by a significant increase in the number of avoidances and the number of 'good learners'. After the termination of the nootropic treatment, a significant increase in both amplitude and frequency of AMPA receptor-mediated mEPSCs in hippocampal CA-1 pyramidal cells was observed. Significant anxiolytic effects on PND 40 also preceded acquisition improvements in the avoidance task. This study provides evidence for the therapeutic potential of aniracetam in reversing cognitive deficits associated with FASD through positive post-natal modulation of AMPA receptors.

Deficits in visual working-memory capacity and general cognition in African Americans with psychosis.

PubMed

Mathias, Samuel R; Knowles, Emma E M; Barrett, Jennifer; Beetham, Tamara; Leach, Olivia; Buccheri, Sebastiano; Aberizk, Katrina; Blangero, John; Poldrack, Russell A; Glahn, David C

2018-03-01

On average, patients with psychosis perform worse than controls on visual change-detection tasks, implying that psychosis is associated with reduced capacity of visual working memory (WM). In the present study, 79 patients diagnosed with various psychotic disorders and 166 controls, all African Americans, completed a change-detection task and several other neurocognitive measures. The aims of the study were to (1) determine whether we could observe a between-group difference in performance on the change-detection task in this sample; (2) establish whether such a difference could be specifically attributed to reduced WM capacity (k); and (3) estimate k in the context of the general cognitive deficit in psychosis. Consistent with previous studies, patients performed worse than controls on the change-detection task, on average. Bayesian hierarchical cognitive modeling of the data suggested that this between-group difference was driven by reduced k in patients, rather than differences in other psychologically meaningful model parameters (guessing behavior and lapse rate). Using the same modeling framework, we estimated the effect of psychosis on k while controlling for general intellectual ability (g, obtained from the other neurocognitive measures). The results suggested that reduced k in patients was stronger than predicted by the between-group difference in g. Moreover, a mediation analysis suggested that the relationship between psychosis and g (i.e., the general cognitive deficit) was mediated by k. The results were consistent with the idea that reduced k is a specific deficit in psychosis, which contributes to the general cognitive deficit. Copyright © 2017 Elsevier B.V. All rights reserved.

Randomised multicentre trial on safety and efficacy of rivastigmine in cognitively impaired multiple sclerosis patients.

PubMed

Mäurer, M; Ortler, S; Baier, M; Meergans, M; Scherer, P; Hofmann, We; Tracik, F

2013-04-01

Cognitive decline has been recognised as a frequent symptom in multiple sclerosis (MS). Cholinesterase inhibitors (ChEIs) are employed for the treatment of Alzheimer's disease, but there is some evidence that ChEIs might also be effective in MS patients with cognitive deficits, particularly deficits of memory function. The aim of this study was to evaluate efficacy on memory function and safety of the ChEI rivastigmine in MS patients with cognitive deficits as measured by the change from baseline of the total recall score of the selective reminding test (SRT) after 16 weeks of treatment. Efficacy and safety of rivastigmine were analysed in a 16-week, multicentre, double-blind, randomised, placebo-controlled study, followed by an optional one-year open-label treatment phase. Effects of rivastigmine and placebo were compared by an analysis of covariance. In total, 86 patients were enrolled. Patients who received rivastigmine (n = 43) showed a non-significant increase in total recall score (sum of all words immediately recalled over all six trials) over placebo (n = 38) after 16 weeks of treatment (p = 0.2576). Other outcome measures provided no evidence supporting benefits of rivastigmine. Treatment with rivastigmine was well tolerated. With the results of this study, the need for an effective therapy in cognitively impaired MS patients is still required. Thus, intensive and continued clinical research is required to explore therapeutic options for cognitive deficits in MS patients.

A longitudinal study of neuropsychological functioning and academic achievement in children with and without signs of attention-deficit/hyperactivity disorder.

PubMed

Rennie, Brandon; Beebe-Frankenberger, Margaret; Swanson, H Lee

2014-01-01

Attention-deficit/hyperactivity disorder (ADHD) in childhood is associated with poor academic functioning. Deficits in academic functioning have proven to be less responsive to intervention than behavioral deficits in this population, yet the causes of this academic underperformance are not well understood. The purpose of this study is to examine the relationship between ADHD and academic performance in elementary-aged children in a developmental context. To do this, we study important cognitive variables and academic achievement over a three-year timeframe. Based on teacher ratings of ADHD, children were divided into a high symptom group (n = 17) and a low symptom group (n = 34). A thorough battery of cognitive and academic tests was administered at Time 1 and again 2 years later. Cognitive measures focused specifically on working memory and response inhibition. RESULTS indicate that children who have high levels of ADHD signs differ from their low-sign peers in academic achievement and in several cognitive domains. Differences in cognitive functioning show a developmental trend consistent with earlier developmental delays in response inhibition and later delays in working memory. Working memory appears to be particularly important in several academic domains. Importantly, in a longitudinal model, working memory was more predictive of math achievement for students demonstrating signs of ADHD than for those who did not. The relationship between these cognitive variables and academic functioning are explicated in the domains of reading, math, and problem solving.

Attention and memory deficits in crack-cocaine users persist over four weeks of abstinence.

PubMed

Almeida, Priscila P; de Araujo Filho, Gerardo M; Malta, Stella M; Laranjeira, Ronaldo R; Marques, Ana Cecilia R P; Bressan, Rodrigo A; Lacerda, Acioly L T

2017-10-01

Crack-cocaine addiction is an important public health problem worldwide. Although there is not a consensus, preliminary evidence has suggested that cognitive impairments in patients with crack-cocaine dependence persist during abstinence, affecting different neuropsychological domains. However, few studies have prospectively evaluated those deficits in different phases of abstinence. The main aim of present study was to examine neuropsychological performance of patients with crack-cocaine dependence during early abstinence and after four weeks, comparing with matched controls. Thirty-five males with crack-cocaine dependence, aged 18 to 50years, who met DSM-IV criteria for cocaine dependence and a control group of 33 healthy men were enrolled. They were assessed through Block Design, Digit Span and Vocabulary of Wechsler Adult Intelligence Scale (WAIS-III), the Rey Auditory Learning Test (RAVLT) and the Verbal Fluency (FAS) between 3 and 10days (mean of 6.1±2.0days) and after 4weeks of abstinence. Compared to controls, the crack-cocaine dependent group exhibited deficits in cognitive performance affecting attention, verbal memory and learning tasks in early withdrawal. Most of the cognitive deficits persisted after four weeks of abstinence. Present results observed that the group of patients with crack-cocaine dependence presented persistent deficits affecting memory and attention even after four weeks of abstinence, confirming previous studies that had disclosed such cognitive impairments. Copyright © 2017 Elsevier Inc. All rights reserved.

Pain and major depressive disorder: Associations with cognitive impairment as measured by the THINC-integrated tool (THINC-it).

PubMed

Cha, Danielle S; Carmona, Nicole E; Mansur, Rodrigo B; Lee, Yena; Park, Hyun Jung; Rodrigues, Nelson B; Subramaniapillai, Mehala; Rosenblat, Joshua D; Pan, Zihang; Lee, Jae Hon; Lee, JungGoo; Almatham, Fahad; Alageel, Asem; Shekotikhina, Margarita; Zhou, Aileen J; Rong, Carola; Harrison, John; McIntyre, Roger S

2017-04-01

To examine the role of pain on cognitive function in adults with major depressive disorder (MDD). Adults (18-65) with a Diagnostic and Statistical Manual - Fifth Edition (DSM-5)-defined diagnosis of MDD experiencing a current major depressive episode (MDE) were enrolled (n MDD =100). All subjects with MDD were matched in age, sex, and years of education to healthy controls (HC) (n HC =100) for comparison. Cognitive function was assessed using the recently validated THINC-integrated tool (THINC-it), which comprises variants of the choice reaction time (i.e., THINC-it: Spotter), One-Back (i.e., THINC-it: Symbol Check), Digit Symbol Substitution Test (i.e., THINC-it: Codebreaker), Trail Making Test - Part B (i.e., THINC-it: Trails), as well as the Perceived Deficits Questionnaire for Depression - 5-item (i.e., THINC-it: PDQ-5-D). A global index of objective cognitive function was computed using objective measures from the THINC-it, while self-rated cognitive deficits were measured using the PDQ-5-D. Pain was measured using a Visual Analogue Scale (VAS). Regression analyses evaluated the role of pain in predicting objective and subjective cognitive function. A significant between-group differences on the VAS was observed (p<0.001), with individuals with MDD reporting higher pain severity as evidenced by higher scores on the VAS than HC. Significant interaction effects were observed between self -rated cognitive deficits and pain ratings (p<0.001) on objective cognitive performance (after adjusting for MADRS total score), suggesting that pain moderates the association between self-rated and objective cognitive function. Results indicated that pain is associated with increased self-rated and objective cognitive deficits in adults with MDD. The study herein provides preliminary evidence demonstrating that adults with MDD reporting pain symptomatology and poorer subjective cognitive function is predictive of poorer objective cognitive performance. THINC-it is capable of detecting cognitive dysfunction amongst adults with MDD and pain. Copyright © 2017 Scandinavian Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Bacopa monnieri (Brahmi) improved novel object recognition task and increased cerebral vesicular glutamate transporter type 3 in sub-chronic phencyclidine rat model of schizophrenia.

PubMed

Piyabhan, Pritsana; Wannasiri, Supaporn; Naowaboot, Jarinyaporn

2016-12-01

Reduced vesicular glutamate transporter 1 (VGLUT1) and 2 (VGLUT2) indicate glutamatergic hypofunction leading to cognitive impairment in schizophrenia. However, VGLUT3 involvement in cognitive dysfunction has not been reported in schizophrenia. Brahmi (Bacopa monnieri) might be a new treatment and prevention for cognitive deficits in schizophrenia by acting on cerebral VGLUT3 density. We aimed to study cognitive enhancement- and neuroprotective-effects of Brahmi on novel object recognition and cerebral VGLUT3 immunodensity in sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia. Rats were assigned to three groups for cognitive enhancement effect study: Group 1, Control; Group 2, PCP administration; Group 3, PCP+Brahmi. A neuroprotective-effect study was also carried out. Rats were again assigned to three groups: Group 1, Control; Group 2, PCP administration; Group 3, Brahmi+PCP. Discrimination ratio (DR) representing cognitive ability was obtained from a novel object recognition task. VGLUT3 immunodensity was measured in the prefrontal cortex, striatum and cornu ammonis fields 1-3 (CA1-3) using immunohistochemistry. We found reduced DR in the PCP group, which occurred alongside VGLUT3 reduction in all brain areas. PCP+Brahmi showed higher DR score with increased VGLUT3 immunodensity in the prefrontal cortex and striatum. Brahmi+PCP group showed a higher DR score with increased VGLUT3 immunodensity in the prefrontal cortex, striatum and CA1-3. We concluded that reduced cerebral VGLUT3 was involved in cognitive deficit in PCP-administrated rats. Receiving Brahmi after PCP restored cognitive deficit by increasing VGLUT3 in the prefrontal cortex and striatum. Receiving Brahmi before PCP prevented cognitive impairment by elevating VGLUT3 in prefrontal cortex, striatum and CA1-3. Therefore, Brahmi could be a new frontier of restoration and prevention of cognitive deficit in schizophrenia. © 2016 John Wiley & Sons Australia, Ltd.

[Learning potential and cognitive remediation in schizophrenia].

PubMed

Raffard, S; Gely-Nargeot, M-C; Capdevielle, D; Bayard, S; Boulenger, J-P

2009-09-01

Many studies have stressed the importance of neurocognitive deficits in schizophrenia that represent a core feature of the pathology. Cognitive dysfunctions are present in 80% of schizophrenic patients, including deficits in attention, memory, speed processing and executive functioning, with well-known functional consequences on daily life, social functioning and rehabilitation outcome. Recent studies have stressed that cognitive deficits, rather than the positive or negative symptoms of schizophrenia, predict poor performance in basic activities of daily living. If it is possible to reduce psychotic symptoms and to prevent relapses with antipsychotic medication, it is not yet possible to have the same convincing impact on cognitive or functional impairments. Cognitive remediation is a new psychological treatment which has proved its efficacy in reducing cognitive deficits. A growing literature on cognitive rehabilitation suggests possibilities that in schizophrenia, specific techniques are able to enhance an individual's cognitive functioning. Presently, two distinct and complementary cognitive remediation methods have been developed: the compensatory and the restorative approaches: (A) restorative approaches attempt to improve function by recruiting relatively intact cognitive processes to fill the role of those impaired, or by using prosthetic aids to compensate for the loss of function; (B) in contrast, in the restorative approach cognitive deficits are targeted directly through repeated practice training. However, results concerning cognitive remediation remain inconsistent. It is clear that not all individuals with schizophrenia display cognitive impairment, and even among those who do, the specific pattern of cognitive functioning varies. Moreover, traditional neurocognitive assessment, with a single or static administration of cognitive measures, provides moderately good prediction of skills acquisition in schizophrenia. Among other factors such as motivation, awareness of having a disease and acuteness of symptomatology, some studies have exposed that a cognitive variable, learning potential could mediate in part the effectiveness of cognitive remediation. The concept of learning potential is used to explain some of the observed variability in cognitive functioning. Learning potential is the ability to attain and utilize cognitive skills after cognitive training: it is assessed by individual variation in performance across three consecutive administrations of the Wisconsin Card Sorting Test (WCST): a pretest with standard instruction procedures, a training phase with expanded instruction and a post test with only standard instruction. Three learner subtypes can be identified: "learners" who perform poorly at the pretest but improve performance during the post-test, "non-retainers" who perform poorly at pre-test and do not improve at post-testing and "high achievers" who perform well in the initial pretest and maintain their good performance across the other two administrations. The assessment of learning potential could predict, with other psychological measures such as insight and motivation, the most effective neurocognitive rehabilitation program for an individual patient, and could help the clinician to optimize patient outcome through appropriate individual management. Indeed, learning potential could represent a good cognitive predictor and indicator for rehabilitation in schizophrenia for clinicians and should be used in cognitive assessment practice. However, the individuals most likely to benefit from cognitive remediation, and whether changes in cognitive function translate into functional improvements, are as yet unclear.

"Gadd45b" Knockout Mice Exhibit Selective Deficits in Hippocampus-Dependent Long-Term Memory

ERIC Educational Resources Information Center

Leach, Prescott T.; Poplawski, Shane G.; Kenney, Justin W.; Hoffman, Barbara; Liebermann, Dan A.; Abel, Ted; Gould, Thomas J.

2012-01-01

Growth arrest and DNA damage-inducible [beta] ("Gadd45b") has been shown to be involved in DNA demethylation and may be important for cognitive processes. "Gadd45b" is abnormally expressed in subjects with autism and psychosis, two disorders associated with cognitive deficits. Furthermore, several high-throughput screens have identified "Gadd45b"…

Randomized Controlled Trial of Osmotic-Release Methylphenidate with Cognitive-Behavioral Therapy in Adolescents with Attention-Deficit/Hyperactivity Disorder and Substance Use Disorders

ERIC Educational Resources Information Center

Riggs, Paula D.; Winhusen, Theresa; Davies, Robert D.; Leimberger, Jeffrey D.; Mikulich-Gilbertson, Susan; Klein, Constance; Macdonald, Marilyn; Lohman, Michelle; Bailey, Genie L.; Haynes, Louise; Jaffee, William B.; Haminton, Nancy; Hodgkins, Candace; Whitmore, Elizabeth; Trello-Rishel, Kathlene; Tamm, Leanne; Acosta, Michelle C.; Royer-Malvestuto, Charlotte; Subramaniam, Geetha; Fishman, Marc; Holmes, Beverly W.; Kaye, Mary Elyse; Vargo, Mark A.; Woody, George E.; Nunes, Edward V.; Liu, David

2011-01-01

Objective: To evaluate the efficacy and safety of osmotic-release methylphenidate (OROS-MPH) compared with placebo for attention-deficit/hyperactivity disorder (ADHD), and the impact on substance treatment outcomes in adolescents concurrently receiving cognitive-behavioral therapy (CBT) for substance use disorders (SUD). Method: This was a…

Cognitive Ability and Continuous Measures of Relative Hand Skill: A Note

ERIC Educational Resources Information Center

Denny, Kevin

2008-01-01

This note re-examines a finding by Crow et al. [Crow, T. J., Crow, L. R., Done, D. J., & Leask, S. (1998). Relative hand skill predicts academic ability: Global deficits at the point of hemispheric indecision. "Neuropsychologia", 36(12), 1275-1281] that equal skill of right and left hands is associated with deficits in cognitive ability. This is…

Attention-Deficit/Hyperactivity Disorder and Sluggish Cognitive Tempo throughout Childhood: Temporal Invariance and Stability from Preschool through Ninth Grade

ERIC Educational Resources Information Center

Leopold, Daniel R.; Christopher, Micaela E.; Burns, G. Leonard; Becker, Stephen P.; Olson, Richard K.; Willcutt, Erik G.

2016-01-01

Background: Although multiple cross-sectional studies have shown symptoms of sluggish cognitive tempo (SCT) and attention-deficit/hyperactivity disorder (ADHD) to be statistically distinct, studies have yet to examine the temporal stability and measurement invariance of SCT in a longitudinal sample. To date, only six studies have assessed SCT…

An Investigation of an Evaluation Method and Retraining Procedures for Emotionally Handicapped Children with Cognitive-Motor Deficits. Final Report.

ERIC Educational Resources Information Center

Rubin, Eli Z.; And Others

To assess the effects of specialized retraining of cognitive, perceptual, and motor (CPM) deficits, a battery of tests was prepared and used with 200 behaviorally maladjusted and 200 problem-free children. The composite score indicated that 40% of the maladjusted group manifested major dysfunction whereas none of the problem-free group…

Determining Differences in Social Cognition between High-Functioning Autistic Disorder and Other Pervasive Developmental Disorders Using New Advanced "Mind-Reading" Tasks

ERIC Educational Resources Information Center

Kuroda, Miho; Wakabayashi, Akio; Uchiyama, Tokio; Yoshida, Yuko; Koyama, Tomonori; Kamio, Yoko

2011-01-01

Deficits in understanding the mental state of others ("mind-reading") have been well documented in individuals with pervasive developmental disorders (PDD). However, it is unclear whether this deficit in social cognition differs between the subgroups of PDD defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text…

The Relationship between Prenatal and Postnatal Exposure to Polychlorinated Biphenyls (PCBs) and Cognitive, Neuropsychological, and Behavioral Deficits: A Critical Appraisal

ERIC Educational Resources Information Center

Cicchetti, Domenic V.; Kaufman, Alan S.; Sparrow, Sara S.

2004-01-01

Our purpose in this report is to evaluate scientifically that body of literature relating the effects of prenatal and postnatal exposure to polychlorinated biphenyls (PCBs) upon neurobehavioral, health-related, and cognitive deficits in neonates, developing infants, children, and adults. The data derive from seven cohorts: six cohorts of mothers…

Divergent Patterns of Social Cognition Performance in Autism and 22q11.2 Deletion Syndrome (22q11DS)

ERIC Educational Resources Information Center

McCabe, Kathryn L.; Melville, Jessica L.; Rich, Dominique; Strutt, Paul A.; Cooper, Gavin; Loughland, Carmel M.; Schall, Ulrich; Campbell, Linda E.

2013-01-01

Individuals with developmental disorders frequently report a range of social cognition deficits including difficulties identifying facial displays of emotion. This study examined the specificity of face emotion processing deficits in adolescents with either autism or 22q11DS compared to typically developing (TD) controls. Two tasks (face emotion…

High Suicide Risk after the Development of Cognitive and Working Memory Deficits Caused by Cannabis, Cocaine and Ecstasy Use

ERIC Educational Resources Information Center

Pompili, Maurizio; Lester, David; Girardi, Paolo; Tatarelli, Roberto

2007-01-01

We report the case of attempted suicide by a 30-year-old man who had significant cognitive deficits that developed after at least three years of polysubstance use with cannabis, methylenedioxymethamphetamine (MDMA, "ecstasy") and cocaine. The patient reported increasing difficulties in his professional and interpersonal life which may have been…

16p11.2 Deletion Mice Display Cognitive Deficits in Touchscreen Learning and Novelty Recognition Tasks

ERIC Educational Resources Information Center

Yang, Mu; Lewis, Freeman C.; Sarvi, Michael S.; Foley, Gillian M.; Crawley, Jacqueline N.

2015-01-01

Chromosomal 16p11.2 deletion syndrome frequently presents with intellectual disabilities, speech delays, and autism. Here we investigated the Dolmetsch line of 16p11.2 heterozygous (+/-) mice on a range of cognitive tasks with different neuroanatomical substrates. Robust novel object recognition deficits were replicated in two cohorts of 16p11.2…

A neurocomputational account of cognitive deficits in Parkinson’s disease

PubMed Central

Hélie, Sébastien; Paul, Erick J.; Ashby, F. Gregory

2014-01-01

Parkinson’s disease (PD) is caused by the accelerated death of dopamine (DA) producing neurons. Numerous studies documenting cognitive deficits of PD patients have revealed impairments in a variety of tasks related to memory, learning, visuospatial skills, and attention. While there have been several studies documenting cognitive deficits of PD patients, very few computational models have been proposed. In this article, we use the COVIS model of category learning to simulate DA depletion and show that the model suffers from cognitive symptoms similar to those of human participants affected by PD. Specifically, DA depletion in COVIS produced deficits in rule-based categorization, non-linear information-integration categorization, probabilistic classification, rule maintenance, and rule switching. These were observed by simulating results from younger controls, older controls, PD patients, and severe PD patients in five well-known tasks. Differential performance among the different age groups and clinical populations was modeled simply by changing the amount of DA available in the model. This suggests that COVIS may not only be an adequate model of the simulated tasks and phenomena but also more generally of the role of DA in these tasks and phenomena. PMID:22683450

Stimulants improve theory of mind in children with attention deficit/hyperactivity disorder.

PubMed

Maoz, Hagai; Tsviban, Lior; Gvirts, Hila Z; Shamay-Tsoory, Simone G; Levkovitz, Yechiel; Watemberg, Nathan; Bloch, Yuval

2014-03-01

Impairments in 'theory of mind' (ToM) were linked to social cognition and reciprocal relationships deficits in children with attention deficit/hyperactivity disorder (ADHD). Twenty-four children with ADHD (13 with inattentive type and 11 with combined type, mean age 10.2 years) completed the Interpersonal Reactivity Index (IRI), a self-reported empathy questionnaire. All children performed the 'faux pas' task and a computerized ToM task in two different sessions either with or without administration of methylphenidate (MPH). Administration of MPH was associated with an improvement in cognitive and affective ToM. Children with ADHD-combined type had significantly lower scores in total IRI and the fantasy scale compared to children with ADHD-inattentive type. We conclude that deficits in empathy and ToM may play an important role in the impairments in social cognition and peer relationship in children with ADHD, especially children a hyperactive component. Stimulants may improve ToM and empathic functions. Future studies including larger samples and additional cognitive tasks are warranted in order to generalize these results and to identify possible underlying mechanisms for improvement in ToM following the administration of MPH.

Glioma surgery with intraoperative mapping-balancing the onco-functional choice.

PubMed

Brennum, Jannick; Engelmann, Christina M; Thomsen, Johanne Asperud; Skjøth-Rasmussen, Jane

2018-05-01

Balancing survival versus risk of inducing functional deficits is a challenge when resecting gliomas in or near eloquent areas. Our objectives were to assess deficits prior to and at 6 and 12 months after awake craniotomies with cortical and subcortical mapping in patients with suspected grade 2 gliomas in eloquent areas. We analyzed whether pre- and intraoperative factors were linked to an increased risk of postoperative deficits. Retrospective study of 92 consecutive patients operated between January 2010 and June 2014. All deficits reported by any healthcare professional and KPS-score preoperatively, immediately postoperatively (day 1-10), at 6 months and 12 months, were analyzed. A decrease in neurological and or cognitive function was common in the first days after surgery, with a significant improvement at 6 months after surgery and further improvement at 12 months. Immediately after surgery, 33% of the patients had severe deficits compared to 2% prior to surgery; this improved to 9% at 6 months and 3% at 12 months. However, at 12 months, 18% of the patients had new or worsened minor or moderate deficits and only 10% had no deficits compared to 39% prior to surgery. There were only minor changes in KPS. None of the recorded pre/intraoperative factors were found significantly to influence the risk of moderate/severe late postoperative deficits. A significant amount of the patients in this study experienced new or worsened neurological and or cognitive deficits during follow-up. We found a higher frequency of deficits than normally reported. This is due to the inclusion of mild deficits, the use of patient-reported data, and our focus on cognitive deficits. Our study indicates that the impact of awake craniotomy with mapping on patient outcome is larger than expected. This in no way negates the use of the technique.

Effectiveness of interventions to improve occupational performance of people with cognitive impairments after stroke: an evidence-based review.

PubMed

Gillen, Glen; Nilsen, Dawn M; Attridge, Jessica; Banakos, Erasmia; Morgan, Marie; Winterbottom, Lauren; York, Wesley

2015-01-01

This evidence-based review was conducted to determine which interventions are effective in improving occupational performance after stroke. Forty-six articles met the inclusion criteria and were examined. Interventions for the following impairments were reviewed: general cognitive deficits, executive dysfunction, apraxia, memory loss, attention deficits, visual field deficits (included because of their close relationship with neglect), and unilateral neglect. Evidence is available from a variety of clinical trials to guide interventions regarding general cognition, apraxia, and neglect. The evidence regarding interventions for executive dysfunction and memory loss is limited. There is insufficient evidence regarding impairments of attention and mixed evidence regarding interventions for visual field deficits. The effective interventions have some commonalities, including being performance focused, involving strategy training, and using a compensatory as opposed to a remediation approach. The implications of the findings for practice, research, and education are discussed. Copyright © 2015 by the American Occupational Therapy Association, Inc.

A meta-analysis and scoping review of social cognition performance in social phobia, posttraumatic stress disorder and other anxiety disorders.

PubMed

Plana, India; Lavoie, Marie-Audrey; Battaglia, Marco; Achim, Amélie M

2014-03-01

Social cognition deficits are observed in a variety of psychiatric illnesses. However, data concerning anxiety disorders are sparse and difficult to interpret. This meta-analysis aims at determining if social cognition is affected in social phobia (SP) or posttraumatic stress disorder (PTSD) compared to non-clinical controls and the specificity of such deficits relatively to other anxiety disorders. The scoping review aims to identify research gaps in the field. Forty studies assessing mentalizing, emotion recognition, social perception/knowledge or attributional style in anxiety disorders were included, totalizing 1417 anxious patients and 1321 non-clinical controls. Results indicate distinct patterns of social cognition impairments: people with PTSD show deficits in mentalizing (effect size d = -1.13) and emotion recognition (d = -1.6) while other anxiety disorders including SP showed attributional biases (d = -0.53 to d = -1.15). The scoping review identified several under investigated domains of social cognition in anxiety disorders. Some recommendations are expressed for future studies to explore the full range of social cognition in anxiety disorders and allow direct comparisons between different disorders. Copyright © 2013 Elsevier Ltd. All rights reserved.

[Contemporary cognitive theories about developmental dyscalculia].

PubMed

Castro-Cañizares, D; Estévez-Pérez, N; Reigosa-Crespo, V

To analyze the current theories describing the cognitive mechanisms underlying developmental dyscalculia. The four most researched hypotheses concerning the cognitive deficits related to developmental dyscalculia, as well as experimental evidences supporting or refusing them are presented. The first hypothesis states that developmental dyscalculia is consequence of domain general cognitive deficits. The second hypothesis suggests that it is due to a failure in the development of specialized brain systems dedicated to numerosity processing. The third hypothesis asserts the disorder is caused by a deficit in accessing quantity representation through numerical symbols. The last hypothesis states developmental dyscalculia appears as a consequence of impairments in a generalized magnitude system dedicated to the processing of continuous and discrete magnitudes. None of the hypotheses has been proven more plausible than the rest. Relevant issues rose by them need to be revisited and answered in the light of new experimental designs. In the last years the understanding of cognitive disorders involved in developmental dyscalculia has remarkably increased, but it is nonetheless insufficient. Additional research is required in order to achieve a comprehensive cognitive model of numerical processing development and its disorders. This will improve the diagnostic precision and the effectiveness of developmental dyscalculia intervention strategies.

Rivastigmine reverses cognitive deficit and acetylcholinesterase activity induced by ketamine in an animal model of schizophrenia.

PubMed

Zugno, Alexandra I; Julião, Ricardo Filipe; Budni, Josiane; Volpato, Ana Maria; Fraga, Daiane B; Pacheco, Felipe D; Deroza, Pedro F; Luca, Renata D; de Oliveira, Mariana B; Heylmann, Alexandra S; Quevedo, João

2013-09-01

Schizophrenia is one of the most disabling mental disorders that affects up to 1 % of the population worldwide. Although the causes of this disorder remain unknown, it has been extensively characterized by a broad range of emotional, ideational and cognitive impairments. Studies indicate that schizophrenia affects neurotransmitters such as dopamine, glutamate and acetylcholine. Recent studies suggest that rivastigmine (an acetylcholinesterase inhibitor) is important to improve the cognitive symptoms of schizophrenia. Therefore, the present study evaluated the protective effect of rivastigmine against the ketamine-induced behavioral (hyperlocomotion and cognitive deficit) and biochemical (increase of acetylcholinesterase activity) changes which characterize an animal model of schizophrenia in rats. Our results indicated that rivastigmine was effective to improve the cognitive deficit in different task (immediate memory, long term memory and short term memory) induced by ketamine in rats. Moreover, we observed that rivastigmina reversed the increase of acetylcholinesterase activity induced by ketamine in the cerebral cortex, hippocampus and striatum. However, rivastigmine was not able to prevent the ketamine-induced hyperlocomotion. In conslusion, ours results indicate that cholinergic system might be an important therapeutic target in the physiopathology of schizophrenia, mainly in the cognition, but additional studies should be carried.

Response-Conflict Moderates the Cognitive Control of Episodic and Contextual Load in Older Adults.

PubMed

Eich, Teal S; Rakitin, Brian C; Stern, Yaakov

2016-11-01

Decline in cognitive control is one of the primary cognitive changes in normal aging. Reaching a consensus regarding the nature of these age-related changes, however, is complicated by the complexity of cognitive control as a construct. Healthy older and younger adults participated in a multifactorial test of cognitive control. Within participants, the procedure varied as a function of the amount contextual load, episodic load, and response-conflict load present. We found that older adults showed impaired performance relative to younger adults. We also found, however, that the response selection process underlying the response-conflict manipulation was a major moderator of age-related differences in both the contextual and episodic load conditions-suggesting a hierarchical organization. These findings are consistent with previous findings, suggesting that deficits in cognitive control in older adults are directly related to the resolution of response-conflict and that other apparent deficits may be derivative upon the more basic response-conflict related deficit. © The Author 2015. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Relationship between cognitive and non-cognitive symptoms of delirium.

PubMed

Rajlakshmi, Aarya Krishnan; Mattoo, Surendra Kumar; Grover, Sandeep

2013-04-01

To study relationship between the cognitive and the non-cognitive symptoms of delirium. Eighty-four patients referred to psychiatry liaison services and met DSM-IVTR criteria of delirium were assessed using the Delirium Rating Scale Revised-1998 (DRSR-98) and Cognitive Test for Delirium (CTD). The mean DRS-R-98 severity score was 17.19 and DRS-R-98 total score was 23.36. The mean total score on CTD was 11.75. The mean scores on CTD were highest for comprehension (3.47) and lowest for vigilance (1.71). Poor attention was associated with significantly higher motor retardation and higher DRS-R-98 severity scores minus the attention scores. There were no significant differences between those with and without poor attention. Higher attention deficits were associated with higher dysfunction on all other domains of cognition on CTD. There was significant correlation between cognitive functions as assessed on CTD and total DRS-R-98 score, DRS-R-98 severity score and DRS-R-98 severity score without the attention item score. However, few correlations emerged between CTD domains and CTD total scores with cognitive symptom total score of DRS-R-98 (items 9-13) and non-cognitive symptom total score of DRS-R-98 (items 1-8). Our study suggests that in delirium, cognitive deficits are quite prevalent and correlate with overall severity of delirium. Attention deficit is a core symptom of delirium. Copyright © 2012 Elsevier B.V. All rights reserved.

Converging on a core cognitive deficit: the impact of various neurodevelopmental insults on cognitive control

PubMed Central

O'Reilly, Kally C.; Kao, Hsin-Yi; Lee, Heekyung; Fenton, André A.

2014-01-01

Despite substantial effort and immense need, the treatment options for major neuropsychiatric illnesses like schizophrenia are limited and largely ineffective at improving the most debilitating cognitive symptoms that are central to mental illness. These symptoms include cognitive control deficits, the inability to selectively use information that is currently relevant and ignore what is currently irrelevant. Contemporary attempts to accelerate progress are in part founded on an effort to reconceptualize neuropsychiatric illness as a disorder of neural development. This neuro-developmental framework emphasizes abnormal neural circuits on the one hand, and on the other, it suggests there are therapeutic opportunities to exploit the developmental processes of excitatory neuron pruning, inhibitory neuron proliferation, elaboration of myelination, and other circuit refinements that extend through adolescence and into early adulthood. We have crafted a preclinical research program aimed at cognition failures that may be relevant to mental illness. By working with a variety of neurodevelopmental rodent models, we strive to identify a common pathophysiology that underlies cognitive control failure as well as a common strategy for improving cognition in the face of neural circuit abnormalities. Here we review our work to characterize cognitive control deficits in rats with a neonatal ventral hippocampus lesion and rats that were exposed to Methylazoxymethanol acetate (MAM) in utero. We review our findings as they pertain to early developmental processes, including neurogenesis, as well as the power of cognitive experience to refine neural circuit function within the mature and maturing brain's cognitive circuitry. PMID:24966811

Evaluating the Specificity of Cognitive Control Deficits in Schizophrenia Using Antisaccades, Functional Magnetic Resonance Imaging, and Healthy Individuals With Poor Cognitive Control.

PubMed

Rodrigue, Amanda L; Schaeffer, David J; Pierce, Jordan E; Clementz, Brett A; McDowell, Jennifer E

2018-01-01

Cognitive control impairments in schizophrenia (SZ) can be evaluated using antisaccade tasks and functional magnetic resonance imaging (fMRI). Studies, however, often compare people with SZ to high performing healthy people, making it unclear if antisaccade-related disruptions are specific to the disease or due to generalized deficits in cognitive control. We included two healthy comparison groups in addition to people with SZ: healthy people with high cognitive control (HCC), who represent a more typical comparison group, and healthy people with low cognitive control (LCC), who perform similarly on antisaccade measures as people with SZ. Using two healthy comparison groups may help determine which antisaccade-related deficits are specific to SZ (distinguish SZ from LCC and HCC groups) and which are due to poor cognitive control (distinguish the LCC and SZ groups from the HCC group). People with SZ and healthy people with HCC or LCC performed an antisaccade task during fMRI acquisition. LCC and SZ groups showed under-activation of saccade circuitry. SZ-specific disruptions were observed in the left superior temporal gyrus and insula during error trials (suppression of activation in the SZ group compared to the LCC and HCC group). Differences related to antisaccade errors may distinguish people with SZ from healthy people with LCC.

A continuum of executive function deficits in early subcortical vascular cognitive impairment: A systematic review and meta-analysis.

PubMed

Sudo, Felipe Kenji; Amado, Patricia; Alves, Gilberto Sousa; Laks, Jerson; Engelhardt, Eliasz

2017-01-01

Subcortical Vascular Cognitive Impairment (SVCI) is a clinical continuum of vascular-related cognitive impairment, including Vascular Mild Cognitive Impairment (VaMCI) and Vascular Dementia. Deficits in Executive Function (EF) are hallmarks of the disorder, but the best methods to assess this function have yet to be determined. The insidious and almost predictable course of SVCI and the multidimensional concept of EF suggest that a temporal dissociation of impairments in EF domains exists early in the disorder. This study aims to review and analyze data from the literature about performance of VaMCI patients on the most used EF tests through a meta-analytic approach. Medline, Web of Knowledge and PsycINFO were searched, using the terms: "vascular mild cognitive impairment" OR "vascular cognitive impairment no dementia" OR "vascular mild neurocognitive disorder" AND "dysexecutive" OR "executive function". Meta-analyses were conducted for each of the selected tests, using random-effect models. Systematic review showed major discrepancies among the results of the studies included. Meta-analyses evidenced poorer performance on the Trail-Making Test part B and the Stroop color test by VaMCI patients compared to controls. A continuum of EF impairments has been proposed in SVCI. Early deficits appear to occur in cognitive flexibility and inhibitory control.

Going up in Smoke? A Review of nAChRs-based Treatment Strategies for Improving Cognition in Schizophrenia

PubMed Central

Boggs, Douglas L.; Carlson, Jon; Cortes-Briones, Jose; Krystal, John H.; D’Souza, D. Cyril

2015-01-01

Cognitive impairment is known to be a core deficit in schizophrenia. Existing treatments for schizophrenia have limited efficacy against cognitive impairment. The ubiquitous use of nicotine in this population is thought to reflect an attempt by patients to self-medicate certain symptoms associated with the illness. Concurrently there is evidence that nicotinic receptors that have lower affinity for nicotine are more important in cognition. Therefore, a number of medications that target nicotinic acetylcholine receptors (nAChRs) have been tested or are in development. In this article we summarize the clinical evidence of nAChRs dysfunction in schizophrenia and review clinical studies testing either nicotine or nicotinic medications for the treatment of cognitive impairment in schizophrenia. Some evidence suggests beneficial effects of nAChRs based treatments for the attentional deficits associated with schizophrenia. Standardized cognitive test batteries have failed to capture consistent improvements from drugs acting at nAChRs. However, more proximal measures of brain function, such as ERPs relevant to information processing impairments in schizophrenia, have shown some benefit. Further work is necessary to conclude that nAChRs based treatments are of clinical utility in the treatment of cognitive deficits of schizophrenia. PMID:24345265

Link between cognitive neuroscience and education: the case of clinical assessment of developmental dyscalculia.

PubMed

Rubinsten, Orly

2015-01-01

In recent years, cognitive neuroscience research has identified several biological and cognitive features of number processing deficits that may now make it possible to diagnose mental or educational impairments in arithmetic, even earlier and more precisely than is possible using traditional assessment tools. We provide two sets of recommendations for improving cognitive assessment tools, using the important case of mathematics as an example. (1) neurocognitive tests would benefit substantially from incorporating assessments (based on findings from cognitive neuroscience) that entail systematic manipulation of fundamental aspects of number processing. Tests that focus on evaluating networks of core neurocognitive deficits have considerable potential to lead to more precise diagnosis and to provide the basis for designing specific intervention programs tailored to the deficits exhibited by the individual child. (2) implicit knowledge, derived from inspection of variables that are irrelevant to the task at hand, can also provide a useful assessment tool. Implicit knowledge is powerful and plays an important role in human development, especially in cases of psychiatric or neurological deficiencies (such as math learning disabilities or math anxiety).

[Sensory functions and Alzheimer's disease: a multi-disciplinary approach].

PubMed

Kenigsberg, Paul-Ariel; Aquino, Jean-Pierre; Berard, Alain; Boucart, Muriel; Bouccara, Didier; Brand, Gérard; Charras, Kevin; Garcia-Larrea, Luis; Gzil, Fabrice; Krolak-Salmon, Pierre; Madjlessi, Arach; Malaquin-Pavan, Évelyne; Penicaud, Luc; Platel, Hervé; Pozzo, Thierry; Reintjens, Christophe; Salmon, Éric; Vergnon, Laurent; Robert, Philippe

2015-09-01

Relations between sensory functions and Alzheimer's disease are still under-explored. To understand them better, the Fondation Médéric Alzheimer has brought together a multi-disciplinary expert group. Aristote's five senses must be enhanced by today's knowledge of proprioception, motor cognition and pain perception. When cognition breaks down, the person with dementia perceives the world around her with her sensory experience, yet is unable to integrate all this information to understand the context. The treatment of multiple sensory inputs by the brain is closely linked to cognitive processes. Sensory deficits reduce considerably the autonomy of people with dementia in their daily life and their relations with others, increase their social isolation and the risk of accidents. Professionals involved with neurodegenerative diseases remain poorly aware of sensory deficits, which can bias the results of cognitive tests. However, there are simple tools to detect these deficits, notably for vision, hearing and balance disorders, which can be corrected. Many interventions for cognitive rehabilitation or quality of life improvement are based on sensory functions. The environment of people with dementia must be adapted to become understandable, comfortable, safe and eventually therapeutic.

The effects of oxytocin on social cognition in borderline personality disorder.

PubMed

Servan, A; Brunelin, J; Poulet, E

2018-02-01

Deficits in social cognition and interpersonal difficulties are key features in borderline personality disorder. Social cognition refers to the function of perceiving and adequately dealing with social signals, leading to the establishment and maintenance of healthy and positive social relationships. Evidence suggests that oxytocin (OT) may improve social cognition and human social behavior. Recently, several studies have highlighted the beneficial effects of oxytocin in several psychiatric conditions involving social cognition deficits such as schizophrenia, autism or social phobia. However, despite growing interest, the effects of oxytocin in patients with borderline personality disorder are far from being clearly demonstrated. The objective of this work was to review and discuss studies investigating the interest of oxytocin in alleviating social cognition deficits in patients with borderline personality disorder (recognition of emotion, trust and cooperation, affective and cognitive empathy, emotional expression and social problem-solving). A systematic review of the literature was conducted up to September 31, 2016 on the Pubmed, Science direct, Medline and Scopus databases using "borderline personality disorder" and "oxytocin" as keywords. To be included, studies were to include patients with borderline personality disorder; to investigate social cognition and to investigate the effect of oxytocin on social cognition in patients with TPB. The initial search yielded 52 articles. Among them, 11 studies were selected according to the PRISMA criteria. The effect of oxytocin on social cognition in patients with borderline personality disorder was mainly investigated in relation to recognition of emotions and trust and cooperation. We did not find any studies investigating the effect of oxytocin on affective and cognitive empathy, emotional expression or social problem-solving abilities. In patients with borderline personality disorder, oxytocin had a beneficial impact on recognition and discrimination of emotions and on hypervigilance towards social threats. However, oxytocin could hinder trust and cooperation. These data lead us to consider oxytocin as a treatment for emotion recognition deficit and hypervigilance towards social threats in borderline personality disorder. A beneficial effect of oxytocin of this nature may be obtained only in patients without deficits in trust and cooperation because of a risk of aggravating relational instability. There was no current evidence for the interest of oxytocin in enhancing affective and cognitive empathy in borderline personality disorder. Further studies are needed to evaluate the clinical interest of combining oxytocin with psychotherapeutic approaches such as dialectical behavioral therapy or mentalisation-based treatment. Copyright © 2017. Published by Elsevier Masson SAS.

Chotosan ameliorates cognitive and emotional deficits in an animal model of type 2 diabetes: possible involvement of cholinergic and VEGF/PDGF mechanisms in the brain

PubMed Central

2012-01-01

Background Diabetes is one of the risk factors for cognitive deficits such as Alzheimer’s disease. To obtain a better understanding of the anti-dementia effect of chotosan (CTS), a Kampo formula, we investigated its effects on cognitive and emotional deficits of type 2 diabetic db/db mice and putative mechanism(s) underlying the effects. Methods Seven-week-old db/db mice received daily administration of CTS (375 – 750 mg/kg, p.o.) and the reference drug tacrine (THA: 2.5 mg/kg, i.p.) during an experimental period of 7 weeks. From the age of 9-week-old, the animals underwent the novel object recognition test, the modified Y-maze test, and the water maze test to elucidate cognitive performance and the elevated plus maze test to elucidate anxiety-related behavior. After completing behavioral studies, Western blotting and immunohistochemical studies were conducted. Results Compared with age-matched non-diabetic control strain (m/m) mice, db/db mice exhibited impaired cognitive performance and an increased level of anxiety. CTS ameliorated cognitive and emotional deficits of db/db mice, whereas THA improved only cognitive performance. The phosphorylated levels of Akt and PKCα in the hippocampus were significantly lower and higher, respectively, in db/db mice than in m/m mice. Expression levels of the hippocampal cholinergic marker proteins and the number of the septal cholinergic neurons were also reduced in db/db mice compared with those in m/m mice. Moreover, the db/db mice had significantly reduced levels of vasculogenesis/angiogenesis factors, vascular endothelial growth factor (VEGF), VEGF receptor type 2, platelet-derived growth factor-B, and PDGF receptor β, in the hippocampus. CTS and THA treatment reversed these neurochemical and histological alterations caused by diabetes. Conclusion These results suggest that CTS ameliorates diabetes-induced cognitive deficits by protecting central cholinergic and VEGF/PDGF systems via Akt signaling pathway and that CTS exhibits the anxiolytic effect via neuronal mechanism(s) independent of cholinergic or VEGF/PDGF systems in db/db mice. PMID:23082896

Chotosan ameliorates cognitive and emotional deficits in an animal model of type 2 diabetes: possible involvement of cholinergic and VEGF/PDGF mechanisms in the brain.

PubMed

Zhao, Qi; Niu, Yimin; Matsumoto, Kinzo; Tsuneyama, Koichi; Tanaka, Ken; Miyata, Takeshi; Yokozawa, Takako

2012-10-20

Diabetes is one of the risk factors for cognitive deficits such as Alzheimer's disease. To obtain a better understanding of the anti-dementia effect of chotosan (CTS), a Kampo formula, we investigated its effects on cognitive and emotional deficits of type 2 diabetic db/db mice and putative mechanism(s) underlying the effects. Seven-week-old db/db mice received daily administration of CTS (375 - 750 mg/kg, p.o.) and the reference drug tacrine (THA: 2.5 mg/kg, i.p.) during an experimental period of 7 weeks. From the age of 9-week-old, the animals underwent the novel object recognition test, the modified Y-maze test, and the water maze test to elucidate cognitive performance and the elevated plus maze test to elucidate anxiety-related behavior. After completing behavioral studies, Western blotting and immunohistochemical studies were conducted. Compared with age-matched non-diabetic control strain (m/m) mice, db/db mice exhibited impaired cognitive performance and an increased level of anxiety. CTS ameliorated cognitive and emotional deficits of db/db mice, whereas THA improved only cognitive performance. The phosphorylated levels of Akt and PKCα in the hippocampus were significantly lower and higher, respectively, in db/db mice than in m/m mice. Expression levels of the hippocampal cholinergic marker proteins and the number of the septal cholinergic neurons were also reduced in db/db mice compared with those in m/m mice. Moreover, the db/db mice had significantly reduced levels of vasculogenesis/angiogenesis factors, vascular endothelial growth factor (VEGF), VEGF receptor type 2, platelet-derived growth factor-B, and PDGF receptor β, in the hippocampus. CTS and THA treatment reversed these neurochemical and histological alterations caused by diabetes. These results suggest that CTS ameliorates diabetes-induced cognitive deficits by protecting central cholinergic and VEGF/PDGF systems via Akt signaling pathway and that CTS exhibits the anxiolytic effect via neuronal mechanism(s) independent of cholinergic or VEGF/PDGF systems in db/db mice.

Inhibitory deficits for negative information in persons with major depressive disorder.

PubMed

Lau, Mark A; Christensen, Bruce K; Hawley, Lance L; Gemar, Michael S; Segal, Zindel V

2007-09-01

Within Beck's cognitive model of depression, little is known about the mechanism(s) by which activated self-schemas result in the production of negative thoughts. Recent research has demonstrated that inhibitory dysfunction is present in depression, and this deficit is likely valence-specific. However, whether valence-specific inhibitory deficits are associated with increased negative cognition and whether such deficits are specific to depression per se remains unexamined. The authors posit the theory that inhibitory dysfunction may influence the degree to which activated self-schemas result in the production of depressive cognition. Individuals with major depressive disorder (MDD, n=43) versus healthy (n=36) and non-depressed anxious (n=32) controls were assessed on the Prose Distraction Task (PDT), a measure of cognitive inhibition, and the Stop-Signal Task (SST), a measure of motor response inhibition. These two tasks were modified in order to present emotionally valenced semantic stimuli (i.e. negative, neutral, positive). Participants with MDD demonstrated performance impairments on the PDT, which were most pronounced for negatively valenced adjectives, relative to both control groups. Moreover, these impairments correlated with self-report measures of negative thinking and rumination. Conversely, the performance of the MDD participants did not differ from either control group on the SST. Implications of these findings for understanding the mechanisms underlying the development and maintenance of depressive cognition are discussed.

Cognitive reserve in multiple sclerosis: Protective effects of education.

PubMed

Martins Da Silva, Ana; Cavaco, Sara; Moreira, Inês; Bettencourt, Andreia; Santos, Ernestina; Pinto, Cláudia; Gonçalves, Alexandra; Coutinho, Ester; Samões, Raquel; Dias, Cláudia C; Teixeira-Pinto, Armando; Da Silva, Berta Martins; Montalban, Xavier

2015-09-01

Recent data suggest that cognitive reserve modulates the adverse effects of multiple sclerosis (MS) pathology on cognitive functioning; however, the protective effects of education in MS are still unclear. To explore education as an indicator of cognitive reserve, while controlling for demographic, clinical and genetic features. A total of 419 MS patients and 159 healthy comparison (HC) subjects underwent a comprehensive neuropsychological (NP) assessment, and answered the Hospital Anxiety and Depression Scale. Based on the HC data, MS patients' NP scores were adjusted for sex, age and education; and the estimated 5(th) percentile (or 95(th) percentile, when appropriate) was used to identify any deficits. Patients also performed the Mini-Mental State Examination (MMSE); and their human leucocyte antigen HLA-DRB1 and apolipoprotein E (ApoE) genotypes were investigated. Patients with higher education were less likely (p < 0.05) to have cognitive deficits than those with lower education, even when controlling for other covariates. Other significant predictors of cognitive deficit were: age, Expanded Disability Status Scale (EDSS), Multiple Sclerosis Severity Scale (MSSS), and a progressive course. No significant association was found with the HLA-DRB1*15:01 or ApoE ε4 alleles. These results provide support to the use of education as a proxy of cognitive reserve in MS and stress the need to take into account education when approaching cognition in MS. © The Author(s), 2015.

Impaired social cognition processes in Asperger syndrome and anorexia nervosa. In search for endophenotypes of social cognition.

PubMed

Kasperek-Zimowska, Beata Joanna; Zimowski, Janusz Grzegorz; Biernacka, Katarzyna; Kucharska-Pietura, Katarzyna; Rybakowski, Filip

2016-01-01

A growing number of publications indicates presence of significant deficits in social cognition in patients with anorexia nervosa (AN). These deficits appear to be comparable in qualitative and quantitative dimension with impairment of the same functions among people with Asperger syndrome (AS). The aim of this study is to identify subject areas in the field of impairment of social cognition processes among people with Asperger syndrome and anorexia nervosa taking into consideration the potential contribution of genetic pathways of oxytocin and vasopressin in the pathogenesis of these diseases. In the first part of the paper a systematic analysis of studies aimed at the evaluation of the processes of social cognition among patients with AN and AS has been carried out. The results of a significant number of studies confirm the presence of deficits in social cognition in AN and AS. In addition, among patients with AN and AS there exists a similar structure and distribution of the brain functions in regions responsible for social cognition. The second part of the paper describes the role of the oxytocin-vasopressin system (OT-AVP) in the processes of social cognition in AN and AS. Its genetic basis and the possible importance of single nucleotide polymorphisms within the genes: OXT, AVP, CD38, OXTR, AVPR1A and LNPEP have also been presented.

Does risk for bipolar disorder heighten the disconnect between objective and subjective appraisals of cognition?

PubMed

Rodriguez, Crystal; Ruggero, Camilo J; Callahan, Jennifer L; Kilmer, Jared N; Boals, Adriel; Banks, Jonathan B

2013-06-01

Deficits in cognitive functioning have been associated with bipolar disorder during episodes of depression and mania, as well as during periods of symptomatic remission. Separate evidence suggests that patients may lack awareness of these deficits and may even be overly confident with self-appraisals. The extent to which these separately or together represent prodromes of the disorder versus a consequence of the disorder remains unclear. The present study sought to test whether risk for bipolar disorder in a younger, college-aged cohort of individuals would be associated with lower performance in cognitive ability yet higher self-appraisal of cognitive functioning. Participants (N=128) completed an objective measure of working memory, a self-report measure of everyday cognitive deficits, and a measure associated with risk for bipolar disorder. Contrary to expectation, risk for bipolar disorder did not significantly predict poorer working memory. However, a person's risk for bipolar disorder was associated with higher self-appraisal of cognitive functioning relative to those with lower risk despite there being no indication of a difference in ability on the working memory task. Participant recruitment relied on an analog sample; moreover, assessment of cognitive functioning was limited to working memory. Results add to a growing body of evidence indicating that overconfidence may be part of the cognitive profile of individuals at risk for bipolar disorder. Copyright © 2012 Elsevier B.V. All rights reserved.

Correlates of self-reported, autobiographical, and mini-mental status examination defined memory deficits following electroconvulsive therapy in South India.

PubMed

Rajkumar, Anto P; Petit, Cheryl P; Rachana, Arun; Deinde, Funmi; Shyamsundar, G; Thangadurai, P; Jacob, Kuruthukulangara S

2018-04-01

Cognitive deficits, self-reported or found following electroconvulsive therapy (ECT), and their correlates are diverse. Despite the characteristics of people receiving ECT in Asia differ widely from the west, pertinent research from Asia remains sparse. We investigated the correlates of self-reported, mini-mental status examination (MMSE) defined, and autobiographical memory deficits in a cohort that received ECT in a south Indian tertiary-care setting. 76 consecutive consenting people were recruited within seven days of completing their ECT course. Memory was assessed by a subjective Likert scale, MMSE, and an autobiographical memory scale (AMS). Psychopathology was assessed by brief psychiatric rating scale, and serum cortisol levels were estimated by chemi-luminescence immunoassays. Relevant sociodemographic and clinical data were collected from the participants, and their medical records. The correlates were analysed using generalised linear models after adjusting for the effects of potential confounders. Self-reported, MMSE-defined, and autobiographical memory deficits were present in 27.6% (95%CI 17.6-37.7%), 42.1% (95%CI 31.0-53.2%), and 36.8% (95%CI 26.0-47.7%) of participants, respectively. Agreement between the memory deficits was poor. Age, less education, duration of illness, hypothyroidism, and past history of another ECT course were significantly associated with MMSE-defined deficits. Age, anaemia, past ECT course, and pre-ECT blood pressure were significantly associated with autobiographical memory deficits, while residual psychopathology and cortisol levels were significantly associated with self-reported memory deficits. Self-reported, MMSE-defined, and autobiographical memory deficits are common at the completion of ECT course, and their correlates differ. All service users receiving ECT need periodic cognitive assessments evaluating multiple cognitive domains. Copyright © 2018 Elsevier B.V. All rights reserved.

Major depressive disorder, cognitive symptoms, and neuropsychological performance among ethnically diverse HIV+ men and women.

PubMed

Fellows, Robert P; Byrd, Desiree A; Morgello, Susan

2013-02-01

Major depressive disorder (MDD), cognitive symptoms, and mild cognitive deficits commonly occur in HIV-infected individuals, despite highly active antiretroviral therapies. In this study, we compared neuropsychological performance and cognitive symptoms of 191 HIV-infected participants. Results indicated that participants with a formal diagnosis of current MDD performed significantly worse than participants without MDD in all seven neuropsychological domains evaluated, with the largest effect sizes in information processing speed, learning, and memory. In addition, a brief assessment of cognitive symptoms, derived from a comprehensive neuromedical interview, correlated significantly with neurocognitive functioning. Participants with MDD reported more cognitive symptoms and showed greater neurocognitive deficits than participants without MDD. These findings indicate that HIV-infected adults with MDD have more cognitive symptoms and worse neuropsychological performance than HIV-infected individuals without MDD. The results of this study have important implications for the diagnosis of HIV-associated neurocognitive disorders (HAND).

Facial emotion recognition deficits: The new face of schizophrenia

PubMed Central

Behere, Rishikesh V.

2015-01-01

Schizophrenia has been classically described to have positive, negative, and cognitive symptom dimension. Emerging evidence strongly supports a fourth dimension of social cognitive symptoms with facial emotion recognition deficits (FERD) representing a new face in our understanding of this complex disorder. FERD have been described to be one among the important deficits in schizophrenia and could be trait markers for the disorder. FERD are associated with socio-occupational dysfunction and hence are of important clinical relevance. This review discusses FERD in schizophrenia, challenges in its assessment in our cultural context, its implications in understanding neurobiological mechanisms and clinical applications. PMID:26600574

Cognitive Remediation Strategies

PubMed Central

WEINSTEIN, CHERYL S.

1994-01-01

Evidence continues to emerge that childhood symptoms of attention-deficit hyperactivity disorder (ADHD) persist into adulthood. These symptoms include motoric hyperactivity, restlessness, attention deficits, poor organizational skills, impulsivity, and memory impairment. Poor academic and work performance, frustration, humiliation, and shame are also components of adult ADHD. Psychotherapists are challenged to understand the meaning of the disorder and its ramifications in all aspects of life. An active multimodal approach, including somatic treatment and psychotherapy, is needed. In addition, cognitive remediation strategies to enhance attention, organization, memory, and problem-solving skills are an important adjunct to treatment. These strategies serve as psychological tools to circumvent deficits. PMID:22700173

Learning to Read Against All Odds: Using Precision Reading to Enhance Literacy in Students with Cognitive Impairments, Extreme Academic Deficits, and Severe Social, Emotional, and Psychiatric Problems

ERIC Educational Resources Information Center

Freeze, Rick; Cook, Paula

2005-01-01

The purpose of this study was to assess the efficacy and practicality of precision reading, a constructive reading intervention, with students with cognitive impairments, extreme academic deficits in reading, and severe social, emotional, and psychiatric problems. As precision reading had shown promise with students with low achievement, learning…

Long-Term Enrichment Enhances the Cognitive Behavior of the Aging Neurogranin Null Mice without Affecting Their Hippocampal LTP

ERIC Educational Resources Information Center

Huang, Freesia L.; Huang, Kuo-Ping; Boucheron, Catherine

2007-01-01

Neurogranin (Ng), a PKC substrate, is abundantly expressed in brain regions important for cognitive functions. Deletion of Ng caused severe deficits in spatial learning and LTP in the hippocampal CA1 region of mice. These Ng-/- mice also exhibit deficits in the amplification of their hippocampal signaling pathways critical for learning and memory.…

Social Cognitive Training in Adolescents with Chromosome 22q11.2 Deletion Syndrome: Feasibility and Preliminary Effects of the Intervention

ERIC Educational Resources Information Center

Shashi, V.; Harrell, W.; Eack, S.; Sanders, C.; McConkie-Rosell, A.; Keshavan, M. S.; Bonner, M. J.; Schoch, K.; Hooper, S. R.

2015-01-01

Background: Children with chromosome 22q11.2 deletion syndrome (22q11DS) often have deficits in social cognition and social skills that contribute to poor adaptive functioning. These deficits may be of relevance to the later occurrence of serious psychiatric illnesses such as schizophrenia. Yet, there are no evidence-based interventions to improve…

Juvenile treatment with a novel mGluR2 agonist/mGluR3 antagonist compound, LY395756, reverses learning deficits and cognitive flexibility impairments in adults in a neurodevelopmental model of schizophrenia.

PubMed

Li, Meng-Lin; Gulchina, Yelena; Monaco, Sarah A; Xing, Bo; Ferguson, Brielle R; Li, Yan-Chun; Li, Feng; Hu, Xi-Quan; Gao, Wen-Jun

2017-04-01

Schizophrenia (SCZ) is a neurodevelopmental psychiatric disorder, in which cognitive function becomes disrupted at early stages of the disease. Although the mechanisms underlying cognitive impairments remain unclear, N-methyl-D-aspartate receptors (NMDAR) hypofunctioning in the prefrontal cortex (PFC) has been implicated. Moreover, cognitive symptoms in SCZ are usually unresponsive to treatment with current antipsychotics and by onset, disruption of the dopamine system, not NMDAR hypofunctioning, dominates the symptoms. Therefore, treating cognitive deficits at an early stage is a realistic approach. In this study, we tested whether an early treatment targeting mGluR2 would be effective in ameliorating cognitive impairments in the methylazoxymethanol acetate (MAM) model of SCZ. We investigated the effects of an mGluR2 agonist/mGluR3 antagonist, LY395756 (LY39), on the NMDAR expression and function in juveniles, as well as cognitive deficits in adult rats after juvenile treatment. We found that gestational MAM exposure induced a significant decrease in total protein levels of the NMDAR subunit, NR2B, and a significant increase of pNR2BTyr1472 in the juvenile rat PFC. Treatment with LY39 in juvenile MAM-exposed rats effectively recovered the disrupted NMDAR expression. Furthermore, a subchronic LY39 treatment in juvenile MAM-exposed rats also alleviated the learning deficits and cognitive flexibility impairments when tested with a cross-maze based set-shifting task in adults. Therefore, our study demonstrates that targeting dysfunctional NMDARs with an mGluR2 agonist during the early stage of SCZ could be an effective strategy in preventing the development and progression in addition to ameliorating cognitive impairments of SCZ. Copyright © 2017 Elsevier Inc. All rights reserved.

Targeting the neurophysiology of cognitive systems with transcranial alternating current stimulation (tACS)

PubMed Central

Fröhlich, Flavio; Sellers, Kristin K.; Cordle, Asa L.

2015-01-01

Cognitive impairment represents one of the most debilitating and most difficult symptom to treat of many psychiatric illnesses. Human neurophysiology studies have suggested specific pathologies of cortical network activity correlate with cognitive impairment. However, we lack (1) demonstration of causal relationships between specific network activity patterns and cognitive capabilities and (2) treatment modalities that directly target impaired network dynamics of cognition. Transcranial alternating current stimulation (tACS), a novel non-invasive brain stimulation approach, may provide a crucial tool to tackle these challenges. We here propose that tACS can be used to elucidate the causal role of cortical synchronization in cognition and, eventually, to enhance pathologically weakened synchrony that may underlie cognitive deficits. To accelerate such development of tACS as a treatment for cognitive deficits, we discuss studies on tACS and cognition (all performed in healthy participants) according to the Research Domain Criteria (RDoC) of the National Institute of Mental Health. PMID:25547149

Trajectories of cognitive development during adolescence among youth at-risk for schizophrenia.

PubMed

Dickson, Hannah; Cullen, Alexis E; Jones, Rebecca; Reichenberg, Abraham; Roberts, Ruth E; Hodgins, Sheilagh; Morris, Robin G; Laurens, Kristin R

2018-04-23

Among adults with schizophrenia, evidence suggests that premorbid deficits in different cognitive domains follow distinct developmental courses during childhood and adolescence. The aim of this study was to delineate trajectories of adolescent cognitive functions prospectively among different groups of youth at-risk for schizophrenia, relative to their typically developing (TD) peers. Using linear mixed models adjusted for sex, ethnicity, parental occupation and practice effects, cognitive development between ages 9 and 16 years was compared for youth characterised by a triad of well-replicated developmental antecedents of schizophrenia (ASz; N = 32) and youth with a least one affected relative with schizophrenia or schizoaffective disorder (FHx; N = 29), relative to TD youth (N = 45). Participants completed measures of IQ, scholastic achievement, memory and executive function at three time-points, separated by approximately 24-month intervals. Compared to TD youth, both ASz and FHx youth displayed stable developmental deficits in verbal working memory and inhibition/switching executive functions. ASz youth additionally presented with stable deficits in measures of vocabulary (IQ), word reading, numerical operations, and category fluency executive function, and a slower rate of growth (developmental lag) on spelling from 9 to 16 years than TD peers. Conversely, faster rates of growth relative to TD peers (developmental delay) were observed on visual and verbal memory, and on category fluency executive function (ASz youth only) and on matrix reasoning (IQ) and word reading (FHx youth only). These differential patterns of deviation from normative adolescent cognitive development among at-risk youth imply potential for cognitive rehabilitation targeting of specific cognitive deficits at different developmental phases. © 2018 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.

The effect of positive symptoms on social cognition in first-episode schizophrenia is modified by the presence of negative symptoms.

PubMed

Bliksted, Vibeke; Videbech, Poul; Fagerlund, Birgitte; Frith, Chris

2017-02-01

There is considerable evidence that patients with schizophrenia have neurocognitive and social-cognitive deficits. It is unclear how such deficits in first-episode schizophrenia relate to current clinical symptoms. Fifty-nine patients with first-episode schizophrenia (FES) were tested using the Danish version of NART (premorbid IQ), subtests from WAIS-III (current IQ), and global cognition using Brief Assessment of Cognition in Schizophrena (BACS), a neurocognitive test battery. Social perception was tested using film clips of everyday interactions (TASIT). Theory of mind (ToM) was tested using silent animations (Animated Triangles Task). The FES subjects had been experiencing psychotic symptoms for several years (mean duration 9.5 years 95% confidence interval (CI [7.6;11.3]). The FES patients were divided into clinical subgroups based on their level of positive and negative symptoms (using SANS and SAPS). Healthy controls were matched to the patients. High levels of negative symptoms were associated with low estimated functional IQ and poor neurocognition and social cognition. All SANS subscales, but Avolition-Apathy, had significant negative impact on social cognition. The effects of positive symptoms were complex. High levels of delusions were associated with higher premorbid IQ. In the presence of high levels of negative symptoms, high levels of positive symptoms were associated with the most comprehensive deficits in social perception, while, in the absence of negative symptoms, high levels of positive symptoms were not associated with such deficits. The results suggest that social-cognitive training will need to take account of the above mentioned effects of symptoms. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

Adolescent social defeat decreases spatial working memory performance in adulthood

PubMed Central

2013-01-01

Background Adolescent social stress is associated with increased incidence of mental illnesses in adulthood that are characterized by deficits in cognitive focus and flexibility. Such enhanced vulnerability may be due to psychosocial stress-induced disruption of the developing mesocortical dopamine system, which plays a fundamental role in facilitating complex cognitive processes such as spatial working memory. Adolescent rats exposed to repeated social defeat as a model of social stress develop dopaminergic hypofunction in the medial prefrontal cortex as adults. To evaluate a direct link between adolescent social stress and later deficits in cognitive function, the present study tested the effects of adolescent social defeat on two separate tests of spatial working memory performance. Methods Adult rats exposed to adolescent social defeat and their controls were trained on either the delayed win-shift task or the delayed alternating T-Maze task and then challenged with various delay periods. To evaluate potential differences in motivation for the food reward used in memory tasks, consumption and conditioned place preference for sweetened condensed milk were tested in a separate cohort of previously defeated rats and controls. Results Compared to controls, adult rats defeated in adolescence showed a delay-dependent deficit in spatial working memory performance, committing more errors at a 90 s and 5 min delay period on the T-maze and win-shift tasks, respectively. Observed memory deficits were likely independent of differences in reward motivation, as conditioned place preference for the palatable food used on both tasks was similar between the adolescent social defeat group and control. Conclusions The results demonstrate that severe social stressors during adolescence can produce long term deficits in aspects of cognitive function. Given the dependence of spatial working memory on prefrontal dopamine, pharmacologically reversing dopaminergic deficiencies caused by adolescent social stress has the potential to treat such cognitive deficits. PMID:24134918

Neurocognitive profile in psychotic versus nonpsychotic individuals with 22q11.2 deletion syndrome.

PubMed

Weinberger, Ronnie; Yi, James; Calkins, Monica; Guri, Yael; McDonald-McGinn, Donna M; Emanuel, Beverly S; Zackai, Elaine H; Ruparel, Kosha; Carmel, Miri; Michaelovsky, Elena; Weizman, Abraham; Gur, Ruben C; Gur, Raquel E; Gothelf, Doron

2016-10-01

The 22q11.2 deletion syndrome (22q11DS) is associated with increased rates of psychotic disorders and cognitive deficits, but large scale studies are needed to elucidate their interaction. The objective of this two-center study was to identify the neurocognitive phenotype of individuals with 22q11DS and psychotic disorders. We hypothesized that psychotic 22q11DS individuals compared to nonpsychotic deleted individuals would have more severe neurocognitive deficits, especially in executive function and social cognition. These deficits would be present when compared to IQ- matched individuals with Williams Syndrome (WS). Three groups were ascertained from the Tel Aviv and Philadelphia centers: 22q11DS individuals with a psychotic disorder (n=31), nonpsychotic 22q11DS (n=86) and typically-developing controls (TD, n=828). In Tel Aviv a group of individuals with WS (n=18) matched in IQ to the 22q11DS psychotic group was also included. The Penn Computerized Neurocognitive Battery (CNB) was used to assess a wide-range of cognitive functions and all patients underwent structured psychiatric evaluations. 22q11DS individuals performed poorly on all CNB domains compared to TD. Participants with 22q11DS and psychosis, compared to nonpsychotic 22q11DS, had more severe deficits in global neurocognitive performance (GNP), executive function, social cognition and episodic memory domains. The primary deficits were also significant when comparing the Tel Aviv 22q11DS psychotic group to IQ-matched individuals with WS. In conclusion, 22q11DS individuals with a psychotic disorder have specific neurocognitive deficits that are reliably identified cross nationality using the CNB. These cognitive dysfunctions should be further studied as potential endophenotypes of psychosis in 22q11DS and as targets for intervention. Copyright © 2016 Elsevier B.V. and ECNP. All rights reserved.

The α2C-adrenoceptor antagonist, ORM-10921, has antipsychotic-like effects in social isolation reared rats and bolsters the response to haloperidol.

PubMed

Uys, Madeleine; Shahid, Mohammed; Sallinen, Jukka; Dreyer, Walter; Cockeran, Marike; Harvey, Brian H

2016-11-03

Early studies suggest that selective α2C-adrenoceptor (AR)-antagonism has anti-psychotic-like and pro-cognitive properties. However, this has not been demonstrated in an animal model of schizophrenia with a neurodevelopmental construct. The beneficial effects of clozapine in refractory schizophrenia and associated cognitive deficits have, among others, been associated with its α2C-AR modulating activity. Altered brain-derived neurotrophic factor (BDNF) has been linked to schizophrenia and cognitive deficits. We investigated whether the α2C-AR antagonist, ORM-10921, could modulate sensorimotor gating and cognitive deficits, as well as alter striatal BDNF levels in the social isolation reared (SIR) model of schizophrenia, comparing its effects to clozapine and the typical antipsychotic, haloperidol, the latter being devoid of α2C-AR-activity. Moreover, the ability of ORM-10921 to augment the effects of haloperidol on the above parameters was also investigated. Animals received subcutaneous injection of either ORM-10921 (0.01mg/kg), clozapine (5mg/kg), haloperidol (0.2mg/kg), haloperidol (0.2mg/kg)+ORM-10921 (0.01mg/kg) or vehicle once daily for 14days, followed by assessment of novel object recognition (NOR), prepulse inhibition (PPI) of startle response and striatal BDNF levels. SIR significantly attenuated NOR memory as well as PPI, and reduced striatal BDNF levels vs. social controls. Clozapine, ORM-10921 and haloperidol+ORM-10921, but not haloperidol alone, significantly improved SIR-associated deficits in PPI and NOR, with ORM-10921 also significantly improving PPI deficits vs. haloperidol-treated SIR animals. Haloperidol+ORM-10921 significantly reversed reduced striatal BDNF levels in SIR rats. α2C-AR-antagonism improves deficits in cognition and sensorimotor gating in a neurodevelopmental animal model of schizophrenia and bolsters the effects of a typical antipsychotic, supporting a therapeutic role for α2C-AR-antagonism in schizophrenia. Copyright © 2016 Elsevier Inc. All rights reserved.

Memory deficits in amyotrophic lateral sclerosis are not exclusively caused by executive dysfunction: a comparative neuropsychological study of amnestic mild cognitive impairment.

PubMed

Machts, Judith; Bittner, Verena; Kasper, Elisabeth; Schuster, Christina; Prudlo, Johannes; Abdulla, Susanne; Kollewe, Katja; Petri, Susanne; Dengler, Reinhard; Heinze, Hans-Jochen; Vielhaber, Stefan; Schoenfeld, Mircea A; Bittner, Daniel M

2014-06-30

Recent work suggests that ALS and frontotemporal dementia can occur together and share at least in part the same underlying pathophysiology. However, it is unclear at present whether memory deficits in ALS stem from a temporal lobe dysfunction, or are rather driven by frontal executive dysfunction. In this study we sought to investigate the nature of memory deficits by analyzing the neuropsychological performance of 40 ALS patients in comparison to 39 amnestic mild cognitive impairment (aMCI) patients and 40 healthy controls (HC). The neuropsychological battery tested for impairment in executive functions, as well as memory and visuo-spatial skills, the results of which were compared across study groups. In addition, we calculated composite scores for memory (learning, recall, recognition) and executive functions (verbal fluency, cognitive flexibility, working memory). We hypothesized that the nature of memory impairment in ALS will be different from those exhibited by aMCI patients. Patient groups exhibited significant differences in their type of memory deficit, with the ALS group showing impairment only in recognition, whereas aMCI patients showed short and delayed recall performance deficits as well as reduced short-term capacity. Regression analysis revealed a significant impact of executive function on memory performance exclusively for the ALS group, accounting for one fifth of their memory performance. Interestingly, merging all sub scores into a single memory and an executive function score obscured these differences. The presented results indicate that the interpretation of neuropsychological scores needs to take the distinct cognitive profiles in ALS and aMCI into consideration. Importantly, the observed memory deficits in ALS were distinctly different from those observed in aMCI and can be explained only to some extent in the context of comorbid (coexisting) executive dysfunction. These findings highlight the qualitative differences in temporal lobe dysfunction between ALS and aMCI patients, and support temporal lobe dysfunction as a mechanism underlying the distinct cognitive impairments observed in ALS.

University Students With Poor Reading Comprehension: The Hidden Cognitive Processing Deficit.

PubMed

Georgiou, George K; Das, J P

2015-01-01

The present study aimed to examine the nature of the working memory and general cognitive ability deficits experienced by university students with a specific reading comprehension deficit. A total of 32 university students with poor reading comprehension but average word-reading skills and 60 age-matched controls with no comprehension difficulties participated in the study. The participants were assessed on three verbal working memory tasks that varied in terms of their processing demands and on the Das-Naglieri Cognitive Assessment System, which was used to operationalize intelligence. The results indicated first that the differences between poor and skilled comprehenders on working memory were amplified as the processing demands of the tasks increased. In addition, although poor comprehenders as a group had average intelligence, they experienced significant difficulties in simultaneous and successive processing. Considering that working memory and general cognitive ability are highly correlated processes, these findings suggest that the observed differences between poor and skilled comprehenders are likely a result of a deficient information processing system. © Hammill Institute on Disabilities 2013.

Effects of long-term administration of a cocoa polyphenolic extract (Acticoa powder) on cognitive performances in aged rats.

PubMed

Bisson, Jean-François; Nejdi, Amine; Rozan, Pascale; Hidalgo, Sophie; Lalonde, Robert; Messaoudi, Michaël

2008-07-01

Numerous studies have indicated that increased vulnerability to oxidative stress may be the main factor involved in functional declines during normal and pathological ageing, and that antioxidant agents, such as polyphenols, may improve or prevent these deficits. We examined whether 1-year administration of a cocoa polyphenolic extract (Acticoa powder), orally delivered at the dose of 24 mg/kg per d between 15 and 27 months of age, affects the onset of age-related cognitive deficits, urinary free dopamine levels and lifespan in old Wistar-Unilever rats. Acticoa powder improved cognitive performances in light extinction and water maze paradigms, increased lifespan and preserved high urinary free dopamine levels. These results suggest that Acticoa powder may be beneficial in retarding age-related brain impairments, including cognitive deficits in normal ageing and perhaps neurodegenerative diseases. Further studies are required to elucidate the mechanisms of cocoa polyphenols in neuroprotection and to explore their effects in man.

Differential profiles in auditory social cognition deficits between adults with autism and schizophrenia spectrum disorders: A preliminary analysis.

PubMed

Tobe, Russell H; Corcoran, Cheryl M; Breland, Melissa; MacKay-Brandt, Anna; Klim, Casimir; Colcombe, Stanley J; Leventhal, Bennett L; Javitt, Daniel C

2016-08-01

Impairment in social cognition, including emotion recognition, has been extensively studied in both Autism Spectrum Disorders (ASD) and Schizophrenia (SZ). However, the relative patterns of deficit between disorders have been studied to a lesser degree. Here, we applied a social cognition battery incorporating both auditory (AER) and visual (VER) emotion recognition measures to a group of 19 high-functioning individuals with ASD relative to 92 individuals with SZ, and 73 healthy control adult participants. We examined group differences and correlates of basic auditory processing and processing speed. Individuals with SZ were impaired in both AER and VER while ASD individuals were impaired in VER only. In contrast to SZ participants, those with ASD showed intact basic auditory function. Our finding of a dissociation between AER and VER deficits in ASD relative to Sz support modality-specific theories of emotion recognition dysfunction. Future studies should focus on visual system-specific contributions to social cognitive impairment in ASD. Copyright © 2016 Elsevier Ltd. All rights reserved.

Nondeclarative learning in children with specific language impairment: predicting regularities in the visuomotor, phonological, and cognitive domains.

PubMed

Mayor-Dubois, C; Zesiger, P; Van der Linden, M; Roulet-Perez, E

2014-01-01

Ullman (2004) suggested that Specific Language Impairment (SLI) results from a general procedural learning deficit. In order to test this hypothesis, we investigated children with SLI via procedural learning tasks exploring the verbal, motor, and cognitive domains. Results showed that compared with a Control Group, the children with SLI (a) were unable to learn a phonotactic learning task, (b) were able but less efficiently to learn a motor learning task and (c) succeeded in a cognitive learning task. Regarding the motor learning task (Serial Reaction Time Task), reaction times were longer and learning slower than in controls. The learning effect was not significant in children with an associated Developmental Coordination Disorder (DCD), and future studies should consider comorbid motor impairment in order to clarify whether impairments are related to the motor rather than the language disorder. Our results indicate that a phonotactic learning but not a cognitive procedural deficit underlies SLI, thus challenging Ullmans' general procedural deficit hypothesis, like a few other recent studies.

[Lack of insight in schizophrenia: a review].

PubMed

Raffard, S; Bayard, S; Capdevielle, D; Garcia, F; Boulenger, J-P; Gely-Nargeot, M-C

2008-10-01

Relative to other psychiatric disorders, patients with schizophrenia are often unaware of the consequences of their disease and their need for treatment. These deficits in awareness referred in general in the English literature as "poor insight", have been the focus of many clinical studies over recent years. This phenomenon, which is considered as fundamental in clinical evaluations of schizophrenia, should be understood as a multidimensional process rather than a dichotomic phenomenon, as is presently the case. The links between insight deficits and responses to vocational rehabilitation efforts represent a major interest in research, including those related to medication compliance and clinical outcome. To conduct such studies, various evaluation tools have been developed, enabling the assessment of insight, of its time-course and of its components in psychosis and schizophrenia spectrum disorders. The Scale to Assess Unawareness of illness in Mental Disorders (SUMD) developed by Amador and Strauss appears to be the most frequently used scale for the evaluation of awareness of the disorder in schizophrenia. Although the model proposed by Amador and Strauss is considered as the privileged model in the multidimensional approach of insight, it corresponds only to a phenomenological analysis of this concept. In the second part of this article, we thus review the current models attempting to explain the lack of insight in schizophrenia. Four current explanatory models of lack of insight will be described as follows: resulting either from adaptation or defence mechanisms to environmental stressors, resulting from cognitive bias of data processing, resulting from neuropsychological functional deficits and resulting from metacognitive deficits. Several hypotheses concerning these deficits arise from clinical studies. Although coping, and defence mechanisms to the consequences and stigmatization of the disease were hardly studied, the fact that poor insight does not appear related to the severity of symptomatology or to the emotional state of the patients argue against this hypothesis. Conversely, a considerable body of literature emphasized how unawareness may result from cognitive deficits. Research in neuropsychology and cognitive psychology has provided consistent results concerning the link between deficit in executive functions, frontal lobe dysfunction and poor insight. Recent studies on bias in cognitive information treatment and social cognition theories currently open new prospects.

[Theory of mind in schizophrenia spectrum disorders].

PubMed

Bora, Emre

2009-01-01

To review studies that investigated theory of mind (ToM) deficits in schizophrenia spectrum disorders. After a thorough literature search, 71 studies were included in this review. Data regarding the relationship between ToM, and other cognitive skills, symptoms, and the impact of the state of illness were reviewed. ToM instruments used in schizophrenia spectrum disorders have some major psychometric limitations; however, previous research was still able to provide some important findings regarding mentalizing impairments in schizophrenia. While ToM deficits are more pronounced in the acute phase of illness, it seems to persist during periods of remission. There is also evidence of ToM deficits in the healthy relatives of schizophrenics, patients with delusional disorder and bipolar disorder (BD), and individuals with high schizotypy scores. ToM dysfunction might be secondary to other cognitive deficits in patients with schizophrenia that have a good prognosis, asymptomatic schizophrenia, delusional disorder, and BD. Other cognitive deficits do not seem to explain ToM dysfunction in patients with psychosis and severe negative symptoms. These findings support the contribution of impairment in both domain-general and domain-specific mechanisms to ToM deficits in schizophrenia spectrum disorders. ToM deficits may be important for understanding poor social functioning and poor insight in psychotic disorders. While ToM is influenced by state variables, it might be an endophenotype of schizophrenia; however, ToM is likely to be an indicator of other frontal lobe-related endophenotypes. Longitudinal studies conducted with high-risk individuals are particularly important.

Cognitive skill learning and schizophrenia: implications for cognitive remediation.

PubMed

Michel, L; Danion, J M; Grangé, D; Sandner, G

1998-10-01

The ability to acquire a motor and cognitive skill was investigated in 26 patients with schizophrenia and 26 normal participants using repeated testing on the Tower of Toronto puzzle. Seven patients with defective performance were retested using additional trials and immediate feedback designed to facilitate problem solving. A component analysis of performance was used based on J. R. Anderson's (1987) model of cognitive skill learning. Patients exhibited a performance deficit on both motor and cognitive skills. However, their acquisition rate was similar to that of normal participants on most parameters, indicating that skill learning suffered little or no impairment. Performance deficit was accounted for by poor problem-solving ability, explicit memory, and general intellectual capacities. It was remediable in some, but not all, patients. Remediation failure was also related to severe defects of cognitive functions.

Multifamily group psychoeducation and cognitive remediation for first-episode psychosis: a randomized controlled trial.

PubMed

Breitborde, Nicholas Jk; Moreno, Francisco A; Mai-Dixon, Natalie; Peterson, Rachele; Durst, Linda; Bernstein, Beth; Byreddy, Seenaiah; McFarlane, William R

2011-01-12

Multifamily group psychoeducation (MFG) has been shown to reduce relapse rates among individuals with first-episode psychosis. However, given the cognitive demands associated with participating in this intervention (e.g., learning and applying a structured problem-solving activity), the cognitive deficits that accompany psychotic disorders may limit the ability of certain individuals to benefit from this intervention. Thus, the goal of this study is to examine whether individuals with first-episode psychosis who participate simultaneously in MFG and cognitive remediation--an intervention shown to improve cognitive functioning among individuals with psychotic disorders--will be less likely to experience a relapse than individuals who participate in MFG alone. Forty individuals with first-episode psychosis and their caregiving relative will be recruited to participate in this study. Individuals with first-episode psychosis will be randomized to one of two conditions: (i) MFG with concurrent participation in cognitive remediation or (ii) MFG alone. The primary outcome for this study is relapse of psychotic symptoms. We will also examine secondary outcomes among both individuals with first-episode psychosis (i.e., social and vocational functioning, health-related quality of life, service utilization, independent living status, and cognitive functioning) and their caregiving relatives (i.e., caregiver burden, anxiety, and depression) Cognitive remediation offers the possibility of ameliorating a specific deficit (i.e., deficits in cognitive functioning) that often accompanies psychotic symptoms and may restrict the magnitude of the clinical benefits derived from MFG. ClinicalTrials (NCT): NCT01196286.

Integrating intention and context: assessing social cognition in adults with Asperger syndrome

PubMed Central

Baez, Sandra; Rattazzi, Alexia; Gonzalez-Gadea, María L.; Torralva, Teresa; Vigliecca, Nora Silvana; Decety, Jean; Manes, Facundo; Ibanez, Agustin

2012-01-01

Deficits in social cognition are an evident clinical feature of the Asperger syndrome (AS). Although many daily life problems of adults with AS are related to social cognition impairments, few studies have conducted comprehensive research in this area. The current study examined multiple domains of social cognition in adults with AS assessing the executive functions (EF) and exploring the intra and inter-individual variability. Fifteen adult's diagnosed with AS and 15 matched healthy controls completed a battery of social cognition tasks. This battery included measures of emotion recognition, theory of mind (ToM), empathy, moral judgment, social norms knowledge, and self-monitoring behavior in social settings. We controlled for the effect of EF and explored the individual variability. The results indicated that adults with AS had a fundamental deficit in several domains of social cognition. We also found high variability in the social cognition tasks. In these tasks, AS participants obtained mostly subnormal performance. EF did not seem to play a major role in the social cognition impairments. Our results suggest that adults with AS present a pattern of social cognition deficits characterized by the decreased ability to implicitly encode and integrate contextual information in order to access to the social meaning. Nevertheless, when social information is explicitly presented or the situation can be navigated with abstract rules, performance is improved. Our findings have implications for the diagnosis and treatment of individuals with AS as well as for the neurocognitive models of this syndrome. PMID:23162450

The relationship between specific cognitive impairment and behaviour in Prader-Willi syndrome.

PubMed

Woodcock, K A; Oliver, C; Humphreys, G W

2011-02-01

Individuals with Prader-Willi syndrome (PWS) have been shown to demonstrate a particular cognitive deficit in attention switching and high levels of preference for routine and temper outbursts. This study assesses whether a specific pathway between a cognitive deficit and behaviour via environmental interaction can exist in individuals with PWS. Four individuals with PWS participated in a series of three single-case experiments including laboratory-based and natural environment designs. Cognitive (computer-based) challenges placed varying demands on attention switching or controlled for the cognitive demands of the tasks while placing no demands on switching. Unexpected changes to routines or expectations were presented in controlled games, or imposed on participants' natural environments and compared with control conditions during which no unexpected changes occurred. Behaviour was observed and heart rate was measured. Participants showed significantly increased temper outburst related behaviours during cognitive challenges that placed demands on attention switching, relative to the control cognitive challenges. Participants showed significantly increased temper outburst related behaviours when unexpected changes occurred in an experimental or the natural environment compared with when no changes occurred. Difficult behaviours that could be triggered reliably in an individual by a specific cognitive demand could also be triggered via manipulation of the environment. Results suggest that a directional relationship between a specific cognitive deficit and behaviour, via environmental interaction, can exist in individuals with PWS. © 2011 The Authors. Journal of Intellectual Disability Research © 2011 Blackwell Publishing Ltd.

Synaptic correlates of increased cognitive vulnerability with aging: peripheral immune challenge and aging interact to disrupt theta-burst late-phase long-term potentiation in hippocampal area CA1.

PubMed

Chapman, Timothy R; Barrientos, Ruth M; Ahrendsen, Jared T; Maier, Steven F; Patterson, Susan L

2010-06-02

Variability in cognitive functioning increases markedly with age, as does cognitive vulnerability to physiological and psychological challenges. Exploring the basis of this vulnerability may provide important insights into the mechanisms underlying aging-associated cognitive decline. As we have previously reported, the cognitive abilities of aging (24-month-old) F344 x BN rats are generally good, but are more vulnerable to the consequences of a peripheral immune challenge (an intraperitoneal injection of live Escherichia coli) than those of their younger (3-month-old) counterparts. Four days after the injection, the aging, but not the young rats show profound memory deficits, specific to the consolidation of hippocampus-dependent memory processes. Here, we have extended these observations, using hippocampal slices to examine for the first time the combined effects of aging and a recent infection on several forms of synaptic plasticity. We have found that the specific deficit in long-lasting memory observed in the aged animals after infection is mirrored by a specific deficit in a form of long-lasting synaptic plasticity. The late-phase long-term potentiation induced in area CA1 using theta-burst stimulation is particularly compromised by the combined effects of aging and infection-a deficit that can be ameliorated by intra-cisterna magna administration of the naturally occurring antiinflammatory cytokine IL-1Ra (interleukin-1 receptor antagonist). These data support the idea that the combination of aging and a negative life event such as an infection might produce selective, early-stage failures of synaptic plasticity in the hippocampus, with corresponding selective deficits in memory.

Citalopram Ameliorates Synaptic Plasticity Deficits in Different Cognition-Associated Brain Regions Induced by Social Isolation in Middle-Aged Rats.

PubMed

Gong, Wei-Gang; Wang, Yan-Juan; Zhou, Hong; Li, Xiao-Li; Bai, Feng; Ren, Qing-Guo; Zhang, Zhi-Jun

2017-04-01

Our previous experiments demonstrated that social isolation (SI) caused AD-like tau hyperphosphorylation and spatial memory deficits in middle-aged rats. However, the underlying mechanisms of SI-induced spatial memory deficits remain elusive. Middle-aged rats (10 months) were group or isolation reared for 8 weeks. Following the initial 4-week period of rearing, citalopram (10 mg/kg i.p.) was administered for 28 days. Then, pathophysiological changes were assessed by performing behavioral, biochemical, and pathological analyses. We found that SI could cause cognitive dysfunction and decrease synaptic protein (synaptophysin or PSD93) expression in different brain regions associated with cognition, such as the prefrontal cortex, dorsal hippocampus, ventral hippocampus, amygdala, and caudal putamen, but not in the entorhinal cortex or posterior cingulate. Citalopram could significantly improve learning and memory and partially restore synaptophysin or PSD93 expression in the prefrontal cortex, hippocampus, and amygdala in SI rats. Moreover, SI decreased the number of dendritic spines in the prefrontal cortex, dorsal hippocampus, and ventral hippocampus, which could be reversed by citalopram. Furthermore, SI reduced the levels of BDNF, serine-473-phosphorylated Akt (active form), and serine-9-phosphorylated GSK-3β (inactive form) with no significant changes in the levels of total GSK-3β and Akt in the dorsal hippocampus, but not in the posterior cingulate. Our results suggest that decreased synaptic plasticity in cognition-associated regions might contribute to SI-induced cognitive deficits, and citalopram could ameliorate these deficits by promoting synaptic plasticity mainly in the prefrontal cortex, dorsal hippocampus, and ventral hippocampus. The BDNF/Akt/GSK-3β pathway plays an important role in regulating synaptic plasticity in SI rats.

Neurally dissociable cognitive components of reading deficits in subacute stroke.

PubMed

Boukrina, Olga; Barrett, A M; Alexander, Edward J; Yao, Bing; Graves, William W

2015-01-01

According to cognitive models of reading, words are processed by interacting orthographic (spelling), phonological (sound), and semantic (meaning) information. Despite extensive study of the neural basis of reading in healthy participants, little group data exist on patients with reading deficits from focal brain damage pointing to critical neural systems for reading. Here, we report on one such study. We have performed neuropsychological testing and magnetic resonance imaging on 11 patients with left-hemisphere stroke (<=5 weeks post-stroke). Patients completed tasks assessing cognitive components of reading such as semantics (matching picture or word choices to a target based on meaning), phonology (matching word choices to a target based on rhyming), and orthography (a two-alternative forced choice of the most plausible non-word). They also read aloud pseudowords and words with high or low levels of usage frequency, imageability, and spelling-sound consistency. As predicted by the cognitive model, when averaged across patients, the influence of semantics was most salient for low-frequency, low-consistency words, when phonological decoding is especially difficult. Qualitative subtraction analyses revealed lesion sites specific to phonological processing. These areas were consistent with those shown previously to activate for phonology in healthy participants, including supramarginal, posterior superior temporal, middle temporal, inferior frontal gyri, and underlying white matter. Notable divergence between this analysis and previous functional imaging is the association of lesions in the mid-fusiform gyrus and anterior temporal lobe with phonological reading deficits. This study represents progress toward identifying brain lesion-deficit relationships in the cognitive components of reading. Such correspondences are expected to help not only better understand the neural mechanisms of reading, but may also help tailor reading therapy to individual neurocognitive deficit profiles.

Meta-analyses of cognitive and motor function in youth aged 16 years and younger who subsequently develop schizophrenia.

PubMed

Dickson, H; Laurens, K R; Cullen, A E; Hodgins, S

2012-04-01

Previous reviews have reported cognitive and motor deficits in childhood and adolescence among individuals who later develop schizophrenia. However, these reviews focused exclusively on studies of individuals with affected relatives or on population/birth cohorts, incorporated studies with estimated measures of pre-morbid intelligence, or included investigations that examined symptomatic at-risk participants or participants 18 years or older. Thus, it remains unclear whether cognitive and motor deficits constitute robust antecedents of schizophrenia. Meta-analyses were conducted on published studies that examined cognitive or motor function in youth aged 16 years or younger who later developed schizophrenia or a schizophrenia spectrum disorder (SSD) and those who did not. Twenty-three studies fulfilled the following inclusion criteria: (1) written in English; (2) prospective investigations of birth or genetic high-risk cohorts, or follow-back investigations of population samples; (3) objective measures of cognitive or motor performance at age 16 or younger; (4) results provided for individuals who did and who did not develop schizophrenia/SSD later in life; and (5) sufficient data to calculate effect sizes. Four domains of function were examined: IQ; Motor Function; General Academic Achievement; and Mathematics Achievement. Meta-analyses showed that, by age 16, individuals who subsequently developed schizophrenia/SSD displayed significant deficits in IQ (d=0.51) and motor function (d=0.56), but not in general academic achievement (d=0.25) or mathematics achievement (d=0.21). Subsidiary analysis indicated that the IQ deficit was present by age 13. These results demonstrate that deficits in IQ and motor performance precede the prodrome and the onset of illness.

Auditory emotion recognition impairments in Schizophrenia: Relationship to acoustic features and cognition

PubMed Central

Gold, Rinat; Butler, Pamela; Revheim, Nadine; Leitman, David; Hansen, John A.; Gur, Ruben; Kantrowitz, Joshua T.; Laukka, Petri; Juslin, Patrik N.; Silipo, Gail S.; Javitt, Daniel C.

2013-01-01

Objective Schizophrenia is associated with deficits in ability to perceive emotion based upon tone of voice. The basis for this deficit, however, remains unclear and assessment batteries remain limited. We evaluated performance in schizophrenia on a novel voice emotion recognition battery with well characterized physical features, relative to impairments in more general emotional and cognitive function. Methods We studied in a primary sample of 92 patients relative to 73 controls. Stimuli were characterized according to both intended emotion and physical features (e.g., pitch, intensity) that contributed to the emotional percept. Parallel measures of visual emotion recognition, pitch perception, general cognition, and overall outcome were obtained. More limited measures were obtained in an independent replication sample of 36 patients, 31 age-matched controls, and 188 general comparison subjects. Results Patients showed significant, large effect size deficits in voice emotion recognition (F=25.4, p<.00001, d=1.1), and were preferentially impaired in recognition of emotion based upon pitch-, but not intensity-features (group X feature interaction: F=7.79, p=.006). Emotion recognition deficits were significantly correlated with pitch perception impairments both across (r=56, p<.0001) and within (r=.47, p<.0001) group. Path analysis showed both sensory-specific and general cognitive contributions to auditory emotion recognition deficits in schizophrenia. Similar patterns of results were observed in the replication sample. Conclusions The present study demonstrates impairments in auditory emotion recognition in schizophrenia relative to acoustic features of underlying stimuli. Furthermore, it provides tools and highlights the need for greater attention to physical features of stimuli used for study of social cognition in neuropsychiatric disorders. PMID:22362394

Deficient attention is hard to find: applying the perceptual load model of selective attention to attention deficit hyperactivity disorder subtypes.

PubMed

Huang-Pollock, Cynthia L; Nigg, Joel T; Carr, Thomas H

2005-11-01

Whether selective attention is a primary deficit in childhood Attention Deficit Hyperactivity Disorder (ADHD) remains in active debate. We used the perceptual load paradigm to examine both early and late selective attention in children with the Primarily Inattentive (ADHD-I) and Combined subtypes (ADHD-C) of ADHD. No evidence emerged for selective attention deficits in either of the subtypes, but sluggish cognitive tempo was associated with abnormal early selection. At least some, and possibly most, children with DSM-IV ADHD have normal selective attention. Results support the move away from theories of attention dysfunction as primary in ADHD-C. In ADHD-I, this was one of the first formal tests of posterior attention network dysfunction, and results did not support that theory. However, ADHD children with sluggish cognitive tempo (SCT) warrant more study for possible early selective attention deficits.

Psychopathy: cognitive and neural dysfunction.

PubMed

R Blair, R James

2013-06-01

Psychopathy is a developmental disorder marked by emotional deficits and an increased risk for antisocial behavior. It is not equivalent to the diagnosis Antisocial Personality Disorder, which concentrates only on the increased risk for antisocial behavior and not a specific cause-ie, the reduced empathy and guilt that constitutes the emotional deficit. The current review considers data from adults with psychopathy with respect to the main cognitive accounts of the disorder that stress either a primary attention deficit or a primary emotion deficit. In addition, the current review considers data regarding the neurobiology of this disorder. Dysfunction within the amygdala's role in reinforcement learning and the role of ventromedial frontal cortex in the representation of reinforcement value is stressed. Data is also presented indicating potential difficulties within parts of temporal and posterior cingulate cortex. Suggestions are made with respect to why these deficits lead to the development of the disorder.

Psychopathy: cognitive and neural dysfunction

PubMed Central

R. Blair, R. James

2013-01-01

Psychopathy is a developmental disorder marked by emotional deficits and an increased risk for antisocial behavior. It is not equivalent to the diagnosis Antisocial Personality Disorder, which concentrates only on the increased risk for antisocial behavior and not a specific cause—ie, the reduced empathy and guilt that constitutes the emotional deficit. The current review considers data from adults with psychopathy with respect to the main cognitive accounts of the disorder that stress either a primary attention deficit or a primary emotion deficit. In addition, the current review considers data regarding the neurobiology of this disorder. Dysfunction within the amygdala's role in reinforcement learning and the role of ventromedial frontal cortex in the representation of reinforcement value is stressed. Data is also presented indicating potential difficulties within parts of temporal and posterior cingulate cortex. Suggestions are made with respect to why these deficits lead to the development of the disorder. PMID:24174892

Cognitive Effects of ThinkRx Cognitive Rehabilitation Training for Eleven Soldiers with Brain Injury: A Retrospective Chart Review

PubMed Central

Ledbetter, Christina; Moore, Amy Lawson; Mitchell, Tanya

2017-01-01

Cognitive rehabilitation training is a promising technique for remediating the cognitive deficits associated with brain injury. Extant research is dominated by computer-based interventions with varied results. Results from clinician-delivered cognitive rehabilitation are notably lacking in the literature. The current study examined the cognitive outcomes following ThinkRx, a clinician-delivered cognitive rehabilitation training program for soldiers recovering from traumatic brain injury and acquired brain injury. In a retrospective chart review, we examined cognitive outcomes of 11 cases who had completed an average of 80 h of ThinkRx cognitive rehabilitation training delivered by clinicians and supplemented with digital training exercises. Outcome measures included scores from six cognitive skill batteries on the Woodcock Johnson – III Tests of Cognitive Abilities. Participants achieved gains in all cognitive skills tested and achieved statistically significant changes in long-term memory, processing speed, auditory processing, and fluid reasoning with very large effect sizes. Clinically significant changes in multiple cognitive skills were also noted across cases. Results of the study suggest that ThinkRx clinician-delivered cognitive training supplemented with digital exercises may be a viable method for targeting the cognitive deficits associated with brain injury. PMID:28588534

Cognitive deficits and educational loss in children with schistosome infection—A systematic review and meta-analysis

PubMed Central

Bustinduy, Amaya L.; Nkwata, Allan K.; Martinez, Leonardo; Pabalan, Noel; Boivin, Michael J.; King, Charles H.

2018-01-01

Background By means of meta-analysis of information from all relevant epidemiologic studies, we examined the hypothesis that Schistosoma infection in school-aged children (SAC) is associated with educational loss and cognitive deficits. Methodology/Principal findings This review was prospectively registered in the PROSPERO database (CRD42016040052). Medline, Biosis, and Web of Science were searched for studies published before August 2016 that evaluated associations between Schistosoma infection and cognitive or educational outcomes. Cognitive function was defined in four domains—learning, memory, reaction time, and innate intelligence. Educational outcome measures were defined as attendance and scholastic achievement. Risk of bias (ROB) was evaluated using the Newcastle-Ottawa quality assessment scale. Standardized mean differences (SMD) and 95% confidence intervals (CI) were calculated to compare cognitive and educational measures for Schistosoma infected /not dewormed vs. uninfected/dewormed children. Sensitivity analyses by study design, ROB, and sequential exclusion of individual studies were implemented. Thirty studies from 14 countries, including 38,992 SAC between 5–19 years old, were identified. Compared to uninfected children and children dewormed with praziquantel, the presence of Schistosoma infection and/or non-dewormed status was associated with deficits in school attendance (SMD = -0.36, 95%CI: -0.60, -0.12), scholastic achievement (SMD = -0.58, 95%CI: -0.96, -0.20), learning (SMD = -0.39, 95%CI: -0.70, -0.09) and memory (SMD = -0.28, 95%CI: -0.52, -0.04) tests. By contrast, Schistosoma-infected/non-dewormed and uninfected/dewormed children were similar with respect to performance in tests of reaction time (SMD = -0.06, 95%CI: -0.42, 0.30) and intelligence (SMD = -0.25, 95%CI: -0.57, 0.06). Schistosoma infection-associated deficits in educational measures were robust among observational studies, but not among interventional studies. The significance of infection-associated deficits in scholastic achievement was sensitive to ROB. Schistosoma infection-related deficits in learning and memory tests were invariant by ROB and study design. Conclusion/Significance Schistosoma infection/non-treatment was significantly associated with educational, learning, and memory deficits in SAC. Early treatment of children in Schistosoma-endemic regions could potentially mitigate these deficits. Trial registration ClinicalTrials.gov CRD42016040052 PMID:29329293

Neuropsychological and social cognitive function in young people at genetic risk of bipolar disorder.

PubMed

McCormack, C; Green, M J; Rowland, J E; Roberts, G; Frankland, A; Hadzi-Pavlovic, D; Joslyn, C; Lau, P; Wright, A; Levy, F; Lenroot, R K; Mitchell, P B

2016-03-01

Impairments in key neuropsychological domains (e.g. working memory, attention) and social cognitive deficits have been implicated as intermediate (endo) phenotypes for bipolar disorder (BD), and should therefore be evident in unaffected relatives. Neurocognitive and social cognitive ability was examined in 99 young people (age range 16-30 years) with a biological parent or sibling diagnosed with the disorder [thus deemed to be at risk (AR) of developing BD], compared with 78 healthy control (HC) subjects, and 52 people with a confirmed diagnosis of BD. Only verbal intelligence and affective response inhibition were significantly impaired in AR relative to HC participants; the BD participants showed significant deficits in attention tasks compared with HCs. Neither AR nor BD patients showed impairments in general intellectual ability, working memory, visuospatial or language ability, relative to HC participants. Analysis of BD-I and BD-II cases separately revealed deficits in attention and immediate memory in BD-I patients (only), relative to HCs. Only the BD (but not AR) participants showed impaired emotion recognition, relative to HCs. Selective cognitive deficits in the capacity to inhibit negative affective information, and general verbal ability may be intermediate markers of risk for BD; however, the extent and severity of impairment in this sample was less pronounced than has been reported in previous studies of older family members and BD cases. These findings highlight distinctions in the cognitive profiles of AR and BD participants, and provide limited support for progressive cognitive decline in association with illness development in BD.

Cognitive deficits of executive functions and decision-making in obsessive-compulsive disorder.

PubMed

Dittrich, Winand H; Johansen, Thomas

2013-10-01

The nature of cognitive deficits in obsessive-compulsive disorder (OCD) is characterized by contradictory findings in terms of specific neuropsychological deficits. Selective impairments have been suggested to involve visuospatial memory, set shifting, decision-making and response inhibition. The aim of this study was to investigate cognitive deficits in decision-making and executive functioning in OCD. It was hypothesized that the OCD patients would be less accurate in their responses compared to the healthy controls in rational decision-making on a version of the Cambridge gambling task (CGT) and on the color-word interference test and on a version of the Tower of Hanoi test (tower test) of executive functioning. Thirteen participants with OCD were compared to a group of healthy controls (n = 13) matched for age, gender, education and verbal IQ. Results revealed significant differences between the OCD group and the healthy control group on quality of decision-making on the CGT and for achievement score on the tower test. On these two tasks the OCD group performed worse than the healthy control group. The symptom-dimension analysis revealed performance differences where safety checking patients were impaired on the tower test compared to contamination patients. Results are discussed in the framework of cognition and emotion processing and findings implicate that OCD models should address, specifically, the interaction between cognition and emotion. Here the emotional disruption hypothesis is forwarded to account for the dysfunctional behaviors in OCD. Further implications regarding methodological and inhibitory factors affecting cognitive information processing are highlighted. © 2013 The Scandinavian Psychological Associations.

Cognitive deficits in obese persons with and without binge eating disorder. Investigation using a mental flexibility task.

PubMed

Mobbs, Olivia; Iglesias, Katia; Golay, Alain; Van der Linden, Martial

2011-08-01

Studies suggest that cognitive deficits and attentional biases play a role in the development and maintenance of obesity and eating disorders. In this study, we simultaneously examine attentional biases, as well as inhibitory control and mental flexibility, which are keys to controlling unwanted behaviors and thoughts in obese patients with and without binge eating disorder. 16 obese patients with binge eating disorder and 16 patients without binge eating disorder were compared with 16 normal-weight controls on a "food/body-mental flexibility task", which allows the investigation of inhibitory control, mental flexibility and attention for stimuli related to the body and food. All obese patients made significantly more errors (i.e., pressing a key when a distracter displayed) and more omissions (i.e., not pressing a key when a target displayed) than controls in both food and body sections of the task. Obese participants with binge eating disorder made significantly more errors and omissions than those without binge eating disorder. No difference between groups was found concerning mental flexibility and cognitive biases for food- and body-related targets. These results suggest that obese patients have a general inhibition problem and difficulty focusing attention, which do not depend on the types of stimuli processed. The results also suggest that these cognitive deficits are more severe in obese patients with binge eating disorder, which indicates that there is a continuum of increasing inhibition and cognitive problems with increasingly disordered eating. These cognitive deficits may contribute to problematic eating behaviors. Copyright © 2011 Elsevier Ltd. All rights reserved.

Effects of β-hydroxy-β-methyl butyrate on working memory and cognitive flexibility in an animal model of aging.

PubMed

Hankosky, Emily R; Sherrill, Luke K; Ruvola, Lauren A; Haake, Rachel M; Kim, Taehyeon; Hammerslag, Lindsey R; Kougias, Daniel G; Juraska, Janice M; Gulley, Joshua M

2017-09-01

Normal aging results in cognitive decline and nutritional interventions have been suggested as potential approaches for mitigating these deficits. Here, we used rats to investigate the effects of short- and long-term dietary supplementation with the leucine metabolite β-hydroxy-β-methyl butyrate (HMB) on working memory and cognitive flexibility. Beginning ∼12 months of age, male and female Long-Evans rats were given twice daily access to sipper tubes containing calcium HMB (450 mg/kg) or vehicle (285 mg/kg calcium lactate) in a sucrose solution (20% w/v). Supplementation continued for 1 or 7 months (middle- and old-age (OA) groups, respectively) before testing began. Working memory was assessed by requiring rats to respond on a previously sampled lever following various delays. Cognitive flexibility was assessed by training rats to earn food according to a visual strategy and then, once acquired, shifting to an egocentric response strategy. Treatment with HMB improved working memory performance in middle-age (MA) males and OA rats of both sexes. In the cognitive flexibility task, there was a significant age-dependent deficit in acquisition of the visual strategy that was not apparent in OA males treated with HMB. Furthermore, HMB ameliorated an apparent deficit in visual strategy acquisition in MA females. Together, these findings suggest that daily nutritional supplementation with HMB facilitates learning and improves working memory performance. As such, HMB supplementation may mitigate age-related cognitive deficits and may therefore be an effective tool to combat this undesirable feature of the aging process.

Cognitive-behavioral screening in elderly patients with new-onset epilepsy before treatment.

PubMed

Witt, J-A; Werhahn, K J; Krämer, G; Ruckes, C; Trinka, E; Helmstaedter, C

2014-09-01

Cognitive comorbidity at epilepsy onset reflects disease severity and provides a baseline estimate of reserve capacities with regard to the effects of epilepsy and its treatment. Given the high incidence of epilepsy at an older age, this study analyzed objective and subjective cognition as well as quality of life in elderly patients with new-onset focal epilepsy before initiation of anti-epileptic treatment. A total of 257 untreated patients (60-95 years of age) with new-onset epilepsy underwent objective assessment of executive function (EpiTrack) and performed subjective ratings of cognition (Portland Neurotoxicity Scale) and quality of life (QoL; QOLIE-31). According to age-corrected norms, 58% of patients (N=257) demonstrated deficits in executive function; major determinants were cerebrovascular etiology, neurological comorbidity, and higher body mass index. Subjective ratings indicated deficits in up to 27% of patients. Self-perceived deficits were associated with neurological, cardiovascular, and/or psychiatric comorbidity, whereas poorer QoL was related to neurological comorbidity and female gender. Objectively assessed executive functions correlated with subjective social functioning, energy, motor function, and vigilance. We found a relatively high QoL, a low rate of subjective impairment, but a high incidence of objective executive deficits in untreated elderly patients with new-onset epilepsy. Neurological status and body mass index, rather than seizure frequency or severity, were risk factors for cognitive impairment. Given the relevance of cognition in the course of epilepsy and its treatment, routine screening before treatment initiation is highly recommended. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Chotosan, a kampo formula, ameliorates chronic cerebral hypoperfusion-induced deficits in object recognition behaviors and central cholinergic systems in mice.

PubMed

Zhao, Qi; Murakami, Yukihisa; Tohda, Michihisa; Obi, Ryosuke; Shimada, Yutaka; Matsumoto, Kinzo

2007-04-01

We previously demonstrated that the Kampo formula chotosan (CTS) ameliorated spatial cognitive impairment via central cholinergic systems in a chronic cerebral hypoperfusion (P2VO) mouse model. In this study, the object discrimination tasks were used to determine if the ameliorative effects of CTS on P2VO-induced cognitive deficits are a characteristic pharmacological profile of this formula, with the aim of clarifying the mechanisms by which CTS enhances central cholinergic function in P2VO mice. The cholinesterase inhibitor tacrine (THA) and Kampo formula saikokeishito (SKT) were used as controls. P2VO impaired object discrimination performance in the object recognition, location, and context tests. Daily administration of CTS (750 mg/kg, p.o.) and THA (2.5 mg/kg, i.p.) improved the object discrimination deficits, whereas SKT (750 mg/kg, p.o.) did not. In ex vivo assays, tacrine but not CTS or SKT inhibited cortical cholinesterase activity. P2VO reduced the mRNA expression of m(3) and m(5) muscarinic receptors and choline acetyltransferase but not that of other muscarinic receptor subtypes in the cerebral cortex. Daily administration of CTS and THA but not SKT reversed these expression changes. These results suggest that CTS and THA improve P2VO-induced cognitive impairment by normalizing the deficit of central cholinergic systems and that the beneficial effect on P2VO-induced cognitive deficits is a distinctive pharmacological characteristic of CTS.

Indoleamine 2,3-dioxygenase-dependent neurotoxic kynurenine metabolism mediates inflammation-induced deficit in recognition memory

PubMed Central

Heisler, Jillian M.; O’Connor, Jason C.

2015-01-01

Cognitive dysfunction in depression is a prevalent and debilitating symptom that is poorly treated by the currently available pharmacotherapies. Research over the past decade has provided evidence for proinflammatory involvement in the neurobiology of depressive disorders and symptoms associated with these disorders, including aspects of memory dysfunction. Recent clinical studies implicate inflammation-related changes in kynurenine metabolism as a potential pathogenic factor in the development of a range of depressive symptoms, including deficits in cognition and memory. Additionally, preclinical work has demonstrated a number of mood-related depressive-like behaviors to be dependent on indoleamine 2,3-dioxygenase-1 (IDO1), the inflammation-induced rate-limiting enzyme of the kynurenine pathway. Here, we demonstrate in a mouse model, that peripheral administration of endotoxin induced a deficit in recognition memory. Mice deficient in IDO were protected from cognitive impairment. Furthermore, endotoxin-induced inflammation increased kynurenine metabolism within the perirhinal/entorhinal cortices, brain regions which have been implicated in recognition memory. A single peripheral injection of kynurenine, the metabolic product of IDO1, was sufficient to induce a deficit in recognition memory in both control and IDO null mice. Finally, kynurenine monooxygenase (KMO) deficient mice were also protected from inflammation-induced deficits on novel object recognition. These data implicate IDO-dependent neurotoxic kynurenine metabolism as a pathogenic factor for cognitive dysfunction in inflammation-induced depressive disorders and a potential novel target for the treatment of these disorders. PMID:26130057

Neuropsychological deficits in temporal lobe epilepsy: A comprehensive review

PubMed Central

Zhao, Fengqing; Kang, Hai; You, LIbo; Rastogi, Priyanka; Venkatesh, D.; Chandra, Mina

2014-01-01

Temporal lobe epilepsy (TLE) is the most prevalent form of complex partial seizures with temporal lobe origin of electrical abnormality. Studies have shown that recurrent seizures affect all aspects of cognitive functioning, including memory, language, praxis, executive functions, and social judgment, among several others. In this article, we will review these cognitive impairments along with their neuropathological correlates in a comprehensive manner. We will see that neuropsychological deficits are prevalent in TLE. Much of the effort has been laid on memory due to the notion that temporal lobe brain structures involved in TLE play a central role in consolidating information into memory. It seems that damage to the mesial structure of the temporal lobe, particularly the amygdale and hippocampus, has the main role in these memory difficulties and the neurobiological plausibility of the role of the temporal lobe in different aspects of memory. Here, we will cover the sub-domains of working memory and episodic memory deficits. This is we will further proceed to evaluate the evidences of executive function deficits in TLE and will see that set-shifting among other EFs is specifically affected in TLE as is social cognition. Finally, critical components of language related deficits are also found in the form of word-finding difficulties. To conclude, TLE affects several of cognitive function domains, but the etiopathogenesis of all these dysfunctions remain elusive. Further well-designed studies are needed for a better understanding of these disorders. PMID:25506156

Profile of cognitive impairment and underlying pathology in multiple system atrophy.

PubMed

Koga, Shunsuke; Parks, Adam; Uitti, Ryan J; van Gerpen, Jay A; Cheshire, William P; Wszolek, Zbigniew K; Dickson, Dennis W

2017-03-01

The objectives of this study were to elucidate any potential association between α-synuclein pathology and cognitive impairment and to determine the profile of cognitive impairment in multiple system atrophy (MSA) patients. To do this, we analyzed the clinical and pathologic features in autopsy-confirmed MSA patients. We retrospectively reviewed medical records, including neuropsychological test data, in 102 patients with autopsy-confirmed MSA in the Mayo Clinic brain bank. The burden of glial cytoplasmic inclusions and neuronal cytoplasmic inclusions were semiquantitatively scored in the limbic regions and middle frontal gyrus. We also assessed concurrent pathologies potentially causing dementia including Alzheimer's disease, hippocampal sclerosis, and cerebrovascular pathology. Of 102 patients, 33 (32%) were documented to have cognitive impairment. Those that received objective testing, deficits primarily in processing speed and attention/executive functions were identified, which suggests a frontal-subcortical pattern of dysfunction. Of these 33 patients with cognitive impairment, 8 patients had concurrent pathologies of dementia. MSA patients with cognitive impairment had a greater burden of neuronal cytoplasmic inclusions in the dentate gyrus than patients without cognitive impairment, both including and excluding patients with concurrent pathologies of dementia. The cognitive deficits observed in this study were more evident on neuropsychological assessment than with cognitive screens. Based on these findings, we recommend that clinicians consider more in-depth neuropsychological assessments if patients with MSA present with cognitive complaints. Although we did not identify the correlation between cognitive deficits and responsible neuroanatomical regions, a greater burden of neuronal cytoplasmic inclusions in the limbic regions was associated with cognitive impairment in MSA. © 2016 International Parkinson and Movement Disorder Society. © 2016 International Parkinson and Movement Disorder Society.

Independent contribution of temporal beta-amyloid deposition to memory decline in the pre-dementia phase of Alzheimer's disease.

PubMed

Chételat, Gaël; Villemagne, Victor L; Pike, Kerryn E; Ellis, Kathryn A; Bourgeat, Pierrick; Jones, Gareth; O'Keefe, Graeme J; Salvado, Olivier; Szoeke, Cassandra; Martins, Ralph N; Ames, David; Masters, Colin L; Rowe, Christopher C

2011-03-01

The relationship between β-amyloid deposition and memory deficits in early Alzheimer's disease is unresolved, as past studies show conflicting findings. The present study aims to determine the relative contribution of regional β-amyloid deposition, hippocampal atrophy and white matter integrity to episodic memory deficits in non-demented older individuals harbouring one of the characteristic hallmarks of Alzheimer's disease, i.e. with β-amyloid pathology. Understanding these relationships is critical for effective therapeutic development. Brain magnetic resonance imaging and [(11)C]Pittsburgh Compound B-positron emission tomography scans were obtained in 136 non-demented individuals aged over 60 years, including 93 healthy elderly and 43 patients with mild cognitive impairment. Voxel-based correlations were computed between a memory composite score and grey matter volume, white matter volume and β-amyloid deposition imaging datasets. Hierarchical linear regression analyses were then performed using values extracted in regions of most significant correlations to determine the relative contribution of each modality to memory deficits. All analyses were conducted pooling all groups together as well as within separate subgroups of cognitively normal elderly, patients with mild cognitive impairment and individuals with high versus low neocortical β-amyloid. Brain areas of highest correlation with episodic memory deficits were the hippocampi for grey matter volume, the perforant path for white matter volume and the temporal neocortex for β-amyloid deposition. When considering these three variables together, only hippocampal volume and temporal β-amyloid deposition provided independent contributions to memory deficits. In contrast to global β-amyloid deposition, temporal β-amyloid deposition was still related to memory independently from hippocampal atrophy within subgroups of cognitively normal elderly, patients with mild cognitive impairment or cases with high neocortical β-amyloid. In the pre-dementia stage of Alzheimer's disease, subtle episodic memory impairment is related to β-amyloid deposition, especially in the temporal neocortex, and independently from hippocampal atrophy, suggesting that both factors should be independently targeted in therapeutic trials aimed at reducing cognitive decline.

Modelling the cognitive and neuropathological features of schizophrenia with phencyclidine.

PubMed

Reynolds, Gavin P; Neill, Joanna C

2016-11-01

Here, Reynolds and Neill describe the studies that preceded and followed publication of this paper, which reported a deficit in parvalbumin (PV), a calcium-binding protein found in GABA interneurons known to be reduced in schizophrenia patients, in conjunction with a deficit in reversal learning in an animal model for schizophrenia. This publication resulted from common research interests: Reynolds in the neurotransmitter pathology of schizophrenia, and Neill in developing animal models for schizophrenia symptomatology. The animal model, using a sub-chronic dosing regimen (sc) with the non-competitive NMDA receptor antagonist PCP (phencyclidine), evolved from previous work in rats (for PCP) and primates (for cognition). The hypothesis of a PV deficit came from emerging evidence for a GABAergic dysfunction in schizophrenia, in particular a deficit in PV-containing GABA interneurons. Since this original publication, a PV deficit has been identified in other animal models for schizophrenia, and the PV field has expanded considerably. This includes mechanistic work attempting to identify the link between oxidative stress and GABAergic dysfunction using this scPCP model, and assessment of the potential of the PV neuron as a target for new antipsychotic drugs. The latter has included development of a molecule targeting KV3.1 channels located on PV-containing GABA interneurons which can restore both PV expression and cognitive deficits in the scPCP model. © The Author(s) 2016.

Prescription Stimulants and the Development of Post-Traumatic Stress Disorder among U.S. Service Members

DTIC Science & Technology

2013-08-13

attention deficit disorder (ADD)/ attention deficit hyperactivity disorder ( ADHD ) or to enhance performance, and such use has...individuals with and without attention deficit hyperactivity disorder : misuse, cognitive impact, and adverse effects. Brain Behav 2012, 2(5), 661-77. 11...36. Antshel KM, Kaul P, Biederman J, et al., Posttraumatic stress disorder in adult attention - deficit / hyperactivity

Concussive Brain Trauma in the Mouse Results in Acute Cognitive Deficits and Sustained Impairment of Axonal Function

PubMed Central

Creed, Jennifer A.; DiLeonardi, Ann Mae; Fox, Douglas P.; Tessler, Alan R.

2011-01-01

Abstract Concussive brain injury (CBI) accounts for approximately 75% of all brain-injured people in the United States each year and is particularly prevalent in contact sports. Concussion is the mildest form of diffuse traumatic brain injury (TBI) and results in transient cognitive dysfunction, the neuropathologic basis for which is traumatic axonal injury (TAI). To evaluate the structural and functional changes associated with concussion-induced cognitive deficits, adult mice were subjected to an impact on the intact skull over the midline suture that resulted in a brief apneic period and loss of the righting reflex. Closed head injury also resulted in an increase in the wet weight:dry weight ratio in the cortex suggestive of edema in the first 24 h, and the appearance of Fluoro-Jade-B-labeled degenerating neurons in the cortex and dentate gyrus of the hippocampus within the first 3 days post-injury. Compared to sham-injured mice, brain-injured mice exhibited significant deficits in spatial acquisition and working memory as measured using the Morris water maze over the first 3 days (p<0.001), but not after the fourth day post-injury. At 1 and 3 days post-injury, intra-axonal accumulation of amyloid precursor protein in the corpus callosum and cingulum was accompanied by neurofilament dephosphorylation, impaired transport of Fluoro-Gold and synaptophysin, and deficits in axonal conductance. Importantly, deficits in retrograde transport and in action potential of myelinated axons continued to be observed until 14 days post-injury, at which time axonal degeneration was apparent. These data suggest that despite recovery from acute cognitive deficits, concussive brain trauma leads to axonal degeneration and a sustained perturbation of axonal function. PMID:21299360

Visual orienting and attention deficits in 5- and 10-month-old preterm infants.

PubMed

Ross-Sheehy, Shannon; Perone, Sammy; Macek, Kelsi L; Eschman, Bret

2017-02-01

Cognitive outcomes for children born prematurely are well characterized, including increased risk for deficits in memory, attention, processing speed, and executive function. However, little is known about deficits that appear within the first 12 months, and how these early deficits contribute to later outcomes. To probe for functional deficits in visual attention, preterm and full-term infants were tested at 5 and 10 months with the Infant Orienting With Attention task (IOWA; Ross-Sheehy, Schneegans and Spencer, 2015). 5-month-old preterm infants showed significant deficits in orienting speed and task related error. However, 10-month-old preterm infants showed only selective deficits in spatial attention, particularly reflexive orienting responses, and responses that required some inhibition. These emergent deficits in spatial attention suggest preterm differences may be related to altered postnatal developmental trajectories. Moreover, we found no evidence of a dose-response relation between increased gestational risk and spatial attention. These results highlight the critical role of postnatal visual experience, and suggest that visual orienting may be a sensitive measure of attentional delay. Results reported here both inform current theoretical models of early perceptual/cognitive development, and future intervention efforts. Copyright © 2016 Elsevier Inc. All rights reserved.

Dyslexia in Regular Orthographies: Manifestation and Causation

ERIC Educational Resources Information Center

Wimmer, Heinz; Schurz, Matthias

2010-01-01

This article summarizes our research on the manifestation of dyslexia in German and on cognitive deficits, which may account for the severe reading speed deficit and the poor orthographic spelling performance that characterize dyslexia in regular orthographies. An only limited causal role of phonological deficits (phonological awareness,…

Cognitive Resilience and Psychological Responses across a Collegiate Rowing Season.

PubMed

Shields, Morgan R; Brooks, M Alison; Koltyn, Kelli F; Kim, Jee-Seon; Cook, Dane B

2017-11-01

Student-athletes face numerous challenges across their competitive season. Although mood states have been previously studied, little is known about adaptations in other psychological responses, specifically cognition. The purpose of this study was to characterize cognitive function, mood, sleep, and stress responses at select time points of a season in collegiate rowers. It was hypothesized that during baseline, typical training, and recovery, athletes would show positive mental health profiles, in contrast to decreases in cognition with increases in negative mood and measurements of stress during peak training. Male and female Division I rowers (N = 43) and healthy controls (N = 23) were enrolled and assessed at baseline, typical training, peak training, and recovery. At each time point, measures of cognitive performance (Stroop color-naming task), academic and exercise load, perceived cognitive deficits, mood states, sleep, and stress (via self-report and salivary cortisol) were recorded. Repeated-measures ANOVA revealed significant group-time interactions for perceived exercise load, cognitive deficits, mood states, and perceived stress (P < 0.05). For athletes during peak training, the perception of cognitive deficits was positively correlated with mood disturbance (r = 0.54, P < 0.05) and perceived stress (r = 0.55, P < 0.05) and negatively correlated with response accuracy during incongruent Stroop trials (r = -0.38, P < 0.05). Cognitive performance did not change over the course of the season for either group. Cortisol and sleepiness changed over the course of the season but no significant interactions were observed. These results demonstrate that various psychological responses change over the course of a season, but they also highlight adaptation indicative of cognitive resilience among student-athletes.

How culture shapes social cognition deficits in mental disorders: A review.

PubMed

Koelkebeck, Katja; Uwatoko, Teruhisa; Tanaka, Jiro; Kret, Mariska Esther

2017-04-01

Social cognitive skills are indispensable for successful communication with others. Substantial research has determined deficits in these abilities in patients with mental disorders. In neurobiological development and continuing into adulthood, cross-cultural differences in social cognition have been demonstrated. Moreover, symptomatic patterns in mental disorders may vary according to the cultural background of an individual. Cross-cultural studies can thus help in understanding underlying (biological) mechanisms and factors that influence behavior in health and disease. In addition, studies that apply novel paradigms assessing the impact of culture on cognition may benefit and advance neuroscience research. In this review, the authors give an overview of cross-cultural research in the field of social cognition in health and in mental disorders and provide an outlook on future research directions, taking a neuroscience perspective.

Social outcome related to cognitive performance and computed tomographic findings after surgery for a ruptured intracranial aneurysm.

PubMed

Vilkki, J; Holst, P; Ohman, J; Servo, A; Heiskanen, O

1990-04-01

A series of 83 patients was examined with a battery of cognitive tests, a clinical interview, and computed tomography 1 year after surgery for a ruptured intracranial aneurysm. Disability on the Glasgow Outcome Scale (33%), failure to return to work (25%), impaired social relations (25%), and subjective or clinical mental impairment (56%) were found to be related to each other and to poor performance on cognitive tests, especially to verbal impairments in patients with left lateral infarctions and to memory deficits and cognitive inflexibility in patients with frontal medial infarctions. Furthermore, cognitive deficits and poor outcome were associated with diffuse brain damage. Depression and anxiety were unrelated to test performances, but were frequently reported by patients with right lateral infarctions.

Cognitive Performance Is Highly Sensitive to Prior Experience in Mice with a Learning and Memory Deficit: Failure Leads to More Failure

ERIC Educational Resources Information Center

Hebda-Bauer, Elaine K.; Watson, Stanley J.; Akil, Huda

2005-01-01

The impact of a previously successful or unsuccessful experience on the subsequent acquisition of a related task is not well understood. The nature of past experience may have even greater impact in individuals with learning deficits, as their cognitive processes can be easily disrupted. Mice with a targeted disruption of the [alpha] and [delta]…

Cognitive influences on self-care decision making in persons with heart failure.

PubMed

Dickson, Victoria V; Tkacs, Nancy; Riegel, Barbara

2007-09-01

Despite advances in management, heart failure is associated with high rates of hospitalization, poor quality of life, and early death. Education intended to improve patients' abilities to care for themselves is an integral component of disease management programs. True self-care requires that patients make decisions about symptoms, but the cognitive deficits documented in 30% to 50% of the heart failure population may make daily decision making challenging. After describing heart failure self-care as a naturalistic decision making process, we explore cognitive deficits known to exist in persons with heart failure. Problems in heart failure self-care are analyzed in relation to neural alterations associated with heart failure. As a neural process, decision making has been traced to regions of the prefrontal cortex, the same areas that are affected by ischemia, infarction, and hypoxemia in heart failure. Resulting deficits in memory, attention, and executive function may impair the perception and interpretation of early symptoms and reasoning and, thereby, delay early treatment implementation. There is compelling evidence that the neural processes critical to decision making are located in the same structures that are affected by heart failure. Because self-care requires the cognitive ability to learn, perceive, interpret, and respond, research is needed to discern how neural deficits affects these abilities, decision-making, and self-care behaviors.

Modeling cognitive deficits following neurodegenerative diseases and traumatic brain injuries with deep convolutional neural networks.

PubMed

Lusch, Bethany; Weholt, Jake; Maia, Pedro D; Kutz, J Nathan

2018-06-01

The accurate diagnosis and assessment of neurodegenerative disease and traumatic brain injuries (TBI) remain open challenges. Both cause cognitive and functional deficits due to focal axonal swellings (FAS), but it is difficult to deliver a prognosis due to our limited ability to assess damaged neurons at a cellular level in vivo. We simulate the effects of neurodegenerative disease and TBI using convolutional neural networks (CNNs) as our model of cognition. We utilize biophysically relevant statistical data on FAS to damage the connections in CNNs in a functionally relevant way. We incorporate energy constraints on the brain by pruning the CNNs to be less over-engineered. Qualitatively, we demonstrate that damage leads to human-like mistakes. Our experiments also provide quantitative assessments of how accuracy is affected by various types and levels of damage. The deficit resulting from a fixed amount of damage greatly depends on which connections are randomly injured, providing intuition for why it is difficult to predict impairments. There is a large degree of subjectivity when it comes to interpreting cognitive deficits from complex systems such as the human brain. However, we provide important insight and a quantitative framework for disorders in which FAS are implicated. Copyright © 2018 Elsevier Inc. All rights reserved.

Gestational methylazoxymethanol exposure leads to NMDAR dysfunction in hippocampus during early development and lasting deficits in learning.

PubMed

Snyder, Melissa A; Adelman, Alicia E; Gao, Wen-Jun

2013-01-01

The N-methyl-D-aspartate (NMDA) receptor has long been associated with learning and memory processes as well as diseased states, particularly in schizophrenia (SZ). Additionally, SZ is increasingly recognized as a neurodevelopmental disorder with cognitive impairments often preceding the onset of psychosis. However, the cause of these cognitive deficits and what initiates the pathological process is unknown. Growing evidence has implicated the glutamate system and, in particular, N-methyl-D-aspartate receptor (NMDAR) dysfunction in the pathophysiology of SZ. Yet, the vast majority of SZ-related research has focused on NMDAR function in adults leaving the role of NMDARs during development uncharacterized. We used the prenatal methylazoxymethanol acetate (MAM, E17) exposure model to determine the alterations of NMDAR protein levels and function, as well as associated cognitive deficits during development. We found that MAM-exposed animals have significantly altered NMDAR protein levels and function in the juvenile and adolescent hippocampus. Furthermore, these changes are associated with learning and memory deficits in the Morris Water Maze. Thus, in the prenatal MAM-exposure SZ model, NMDAR expression and function is altered during the critical period of hippocampal development. These changes may be involved in disease initiation and cognitive impairment in the early stage of SZ.

Musical deficits and cortical thickness in people with schizophrenia.

PubMed

Fujito, Ryosuke; Minese, Masayoshi; Hatada, Sanae; Kamimura, Naoto; Morinobu, Shigeru; Lang, Donna J; Honer, William G; Sawada, Ken

2018-02-14

Investigation of acquired amusia caused by brain damage suggested that cortical lesions of the right hemisphere contributed to musical deficits. We previously reported reduced musical ability in schizophrenia; these deficits were correlated with clinical manifestations such as cognitive dysfunction and negative symptoms. However, the neural substrate underlying the musical disability in schizophrenia remains unclear. We investigated the relationship between musical deficits and cortical thickness in patients with schizophrenia using structural MRI. We recruited 24 patients (13 males; age mean=45.9years old), and 22 controls (14 males, age mean=43.5years old). Musical ability was assessed with the Montreal Battery for Evaluation of Amusia (MBEA), cognitive function with the Brief Assessment of Cognition in Schizophrenia (BACS) and clinical features of illness with the Positive and Negative Syndrome Scale (PANSS). MRI Images were acquired and processed using FreeSurfer. Surface-based analysis showed that thinner cortex in left temporal and inferior frontal region was associated with lower musical ability in schizophrenia. In contrast, in controls thicker cortex in the left supramarginal region was correlated with lower musical ability. These results shed light on the clinical pathology underlying the associations of musical ability, cognitive dysfunction and negative symptoms in patients with schizophrenia. Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.

Opposing effects of AMPA and 5-HT1A receptor blockade on passive avoidance and object recognition performance: correlation with AMPA receptor subunit expression in rat hippocampus.

PubMed

Schiapparelli, L; Simón, A M; Del Río, J; Frechilla, D

2006-06-01

It has been suggested that antagonists at serotonin 5-HT1A receptors may exert a procognitive effect by facilitating glutamatergic neurotransmission. Here we further explored this issue by looking for the ability of a 5-HT1A antagonist to prevent the learning deficit induced by AMPA receptor blockade in two behavioural procedures in rats, and for concomitant molecular changes presumably involved in memory formation in the hippocampus. Pretraining administration of the competitive AMPA receptor antagonist, NBQX, produced a dose-related retention impairment in a passive avoidance task 24h later, and also impaired retention in a novel object recognition test when an intertrial interval of 3h was selected. Pretreatment with the selective 5-HT1A receptor antagonist, WAY-100635, prevented the learning deficit induced by NBQX in the two behavioural procedures. In biochemical studies performed on rat hippocampus after the retention tests, we found that learning increased the membrane levels of AMPA receptor GluR1 and GluR2/3 subunits, as well as the phosphorylated forms of GluR1, effects that were abolished by NBQX administration before the training session. Pretreatment with WAY-100635 counteracted the NBQX effects and restored the initial learning-specific increase in Ca2+/calmodulin-dependent protein kinase II (CaMKII) function and the later increase in GluR2/3 and phosphorylated GluR1 surface expression. Moreover, administration of WAY-100635 before object recognition training improved recognition memory 24h later and potentiated the learning-associated increase in AMPA receptor subunits. The results support the proposed utility of 5-HT1A antagonists in the treatment of cognitive disorders.

Cognitive remediation of attention deficits following acquired brain injury: A systematic review and meta-analysis.

PubMed

Virk, Sohaib; Williams, Tracey; Brunsdon, Ruth; Suh, Flora; Morrow, Angie

2015-01-01

Attention deficits are common after acquired brain injury (ABI) and adversely impact academic, vocational and social outcomes. The role of cognitive interventions in post-ABI attention rehabilitation remains unclear. To evaluate effectiveness of cognitive interventions in treating attention deficits following ABI and to explore differences in treatment effect between ABI etiologies. MEDLINE, EMBASE, PsycINFO and CENTRAL databases were searched for randomized controlled trials (RCTs). Studies were selected by three reviewers. Study quality was assessed using Cochrane Collaboration tool for RCTs. Effect sizes (Hedge's g) for each attentional domain were meta-analyzed with subgroup analysis by ABI etiology. Twelve RCTs with 584 participants were included, representing individuals with stroke, traumatic brain injury (TBI) and CNS-impacting malignancy. Cognitive rehabilitation improved divided attention in stroke survivors (g 0.67; 95% confidence interval, 0.35-0.98; p <  0.0001) but not other ABI populations. Sustained, selective and alternating attention, and inhibition were not significantly improved in any ABI population. Follow-up data showed no evidence of long-term benefit. Cognitive rehabilitation resulted in short-term improvements in divided attention following stroke, but not after TBI or CNS-impacting malignancy. Cognitive interventions did not significantly improve other attentional domains in participants with stroke, TBI or CNS-impacting malignancy.

The narcoleptic cognitive pupillary response.

PubMed

O'Neill, W D; Trick, K P

2001-09-01

It has been reported that narcoleptics exhibit deficits in short-term memory, list recall, and stimulus frequency estimation compared with control subjects. It is also well-known that pupil dilation during cognitive tasks is a measure of subject attention state. Here we present results from six narcoleptics and six controls, a total of 360 experimental records in which pupillograms were made during cognitive tests, which indicate that narcoleptics begin pupillary dilations at a smaller diameter, begin dilating earlier poststimulus, attain higher pupillary diameter velocities, yet achieve the same equilibrium dilation diameter as controls. These findings are derived from statistical tests performed on the parameters of a nonlinear regression model of pupillary cognitive dilation as a function of time. In our experiments, the standard 1-s interdigit time between cognitive stimuli was increased to 2.3 s, which yielded pupillographic time records showing that the process of short-term memory overload sets in gradually at about four memory digits for controls and three memory digits for narcoleptics. We suggest our results can be partially explained by a narcoleptic stimulus-encoding deficit, which limits the time available for subjects to rehearse cognitive tasks. However, we also report the unexpected finding that the inferred encoding deficit is a transient one in that repeated tasks at the same memory load elicit a near normal naroleptic pupillary dilation.

Cognitive Deficits in Schizophrenia: Focus on Neuronal Nicotinic Acetylcholine Receptors and Smoking

PubMed Central

Lasalde-Dominicci, Jose

2015-01-01

Patients with schizophrenia present with deficits in specific areas of cognition. These are quantifiable by neuropsychological testing and can be clinically observable as negative signs. Concomitantly, they self-administer nicotine in the form of cigarette smoking. Nicotine dependence is more prevalent in this patient population when compared to other psychiatric conditions or to non-mentally ill people. The target for nicotine is the neuronal nicotinic acetylcholine receptor (nAChR). There is ample evidence that these receptors are involved in normal cognitive operations within the brain. This review describes neuronal nAChR structure and function, focusing on both cholinergic agonist-induced nAChR desensitization and nAChR up-regulation. The several mechanisms proposed for the nAChR up-regulation are examined in detail. Desensitization and up-regulation of nAChRs may be relevant to the physiopathology of schizophrenia. The participation of several subtypes of neuronal nAChRs in the cognitive processing of non-mentally ill persons and schizophrenic patients is reviewed. The role of smoking is then examined as a possible cognitive remediator in this psychiatric condition. Finally, pharmacological strategies focused on neuronal nAChRs are discussed as possible therapeutic avenues that may ameliorate the cognitive deficits of schizophrenia. PMID:17554626

Development of a cognitive-behavioral intervention program to treat anxiety and social deficits in teens with high-functioning autism.

PubMed

White, Susan W; Albano, Anne Marie; Johnson, Cynthia R; Kasari, Connie; Ollendick, Thomas; Klin, Ami; Oswald, Donald; Scahill, Lawrence

2010-03-01

Anxiety is a common co-occurring problem among young people with autism spectrum disorders (ASD). Characterized by deficits in social interaction, communication problems, and stereotyped behavior and restricted interests, this group of disorders is more prevalent than previously realized. When present, anxiety may compound the social deficits of young people with ASD. Given the additional disability and common co-occurrence of anxiety in ASD, we developed a manual-based cognitive-behavioral treatment program to target anxiety symptoms as well as social skill deficits in adolescents with ASD [Multimodal Anxiety and Social Skills Intervention: MASSI]. In this paper, we describe the foundation, content, and development of MASSI. We also summarize data on treatment feasibility based on a pilot study that implemented the intervention.

The weak coherence account: detail-focused cognitive style in autism spectrum disorders.

PubMed

Happé, Francesca; Frith, Uta

2006-01-01

"Weak central coherence" refers to the detail-focused processing style proposed to characterise autism spectrum disorders (ASD). The original suggestion of a core deficit in central processing resulting in failure to extract global form/meaning, has been challenged in three ways. First, it may represent an outcome of superiority in local processing. Second, it may be a processing bias, rather than deficit. Third, weak coherence may occur alongside, rather than explain, deficits in social cognition. A review of over 50 empirical studies of coherence suggests robust findings of local bias in ASD, with mixed findings regarding weak global processing. Local bias appears not to be a mere side-effect of executive dysfunction, and may be independent of theory of mind deficits. Possible computational and neural models are discussed.

Prefrontal Cortex and Social Cognition in Mouse and Man

PubMed Central

Bicks, Lucy K.; Koike, Hiroyuki; Akbarian, Schahram; Morishita, Hirofumi

2015-01-01

Social cognition is a complex process that requires the integration of a wide variety of behaviors, including salience, reward-seeking, motivation, knowledge of self and others, and flexibly adjusting behavior in social groups. Not surprisingly, social cognition represents a sensitive domain commonly disrupted in the pathology of a variety of psychiatric disorders including Autism Spectrum Disorder (ASD) and Schizophrenia (SCZ). Here, we discuss convergent research from animal models to human disease that implicates the prefrontal cortex (PFC) as a key regulator in social cognition, suggesting that disruptions in prefrontal microcircuitry play an essential role in the pathophysiology of psychiatric disorders with shared social deficits. We take a translational perspective of social cognition, and review three key behaviors that are essential to normal social processing in rodents and humans, including social motivation, social recognition, and dominance hierarchy. A shared prefrontal circuitry may underlie these behaviors. Social cognition deficits in animal models of neurodevelopmental disorders like ASD and SCZ have been linked to an altered balance of excitation and inhibition (E/I ratio) within the cortex generally, and PFC specifically. A clear picture of the mechanisms by which altered E/I ratio in the PFC might lead to disruptions of social cognition across a variety of behaviors is not well understood. Future studies should explore how disrupted developmental trajectory of prefrontal microcircuitry could lead to altered E/I balance and subsequent deficits in the social domain. PMID:26635701

Pattern of social cognition deficits in individuals with borderline personality disorder.

PubMed

Anupama V; Bhola, Poornima; Thirthalli, Jagadisha; Mehta, Urvakhsh Meherwan

2018-03-01

Social cognition deficits have been implicated in the affect regulation and interpersonal difficulties seen in borderline personality disorder (BPD). The study examined patterns of social cognition abilities, using self-report and task-based measures, among individuals diagnosed with BPD. The sample included a clinical group of 20 patients diagnosed with BPD and 20 age and gender-matched control group participants from the community with no psychiatric diagnosis. The measures included the Mentalization Questionnaire, the Reading the Mind in the Eyes Test and the Social Cognition Rating Tool in Indian Setting. Results indicated that the clinical group had lower self-reported mentalizing ability. Facial emotion recognition ability was significantly lower for the clinical group, particularly for photographs of the eye region with positive and neutral valences. The clinical group had significantly higher personalizing bias, and greater difficulties in social perception. The two groups did not differ on first and second order theory of mind, recognition of faux pas and externalizing bias. The results point to the links between social cognition deficits and interpersonal difficulties among persons with BPD. Implications include the need for pre-therapy assessment of the magnitude and patterns of social cognition difficulties in BPD, the development of culturally and ecologically valid assessments and the evaluation of interventions for social cognition vulnerabilities among individuals with BPD. Copyright © 2018 Elsevier B.V. All rights reserved.

A continuum of executive function deficits in early subcortical vascular cognitive impairment: A systematic review and meta-analysis

PubMed Central

Sudo, Felipe Kenji; Amado, Patricia; Alves, Gilberto Sousa; Laks, Jerson; Engelhardt, Eliasz

2017-01-01

ABSTRACT. Background. Subcortical Vascular Cognitive Impairment (SVCI) is a clinical continuum of vascular-related cognitive impairment, including Vascular Mild Cognitive Impairment (VaMCI) and Vascular Dementia. Deficits in Executive Function (EF) are hallmarks of the disorder, but the best methods to assess this function have yet to be determined. The insidious and almost predictable course of SVCI and the multidimensional concept of EF suggest that a temporal dissociation of impairments in EF domains exists early in the disorder. Objective: This study aims to review and analyze data from the literature about performance of VaMCI patients on the most used EF tests through a meta-analytic approach. Methods: Medline, Web of Knowledge and PsycINFO were searched, using the terms: “vascular mild cognitive impairment” OR “vascular cognitive impairment no dementia” OR “vascular mild neurocognitive disorder” AND “dysexecutive” OR “executive function”. Meta-analyses were conducted for each of the selected tests, using random-effect models. Results: Systematic review showed major discrepancies among the results of the studies included. Meta-analyses evidenced poorer performance on the Trail-Making Test part B and the Stroop color test by VaMCI patients compared to controls. Conclusion: A continuum of EF impairments has been proposed in SVCI. Early deficits appear to occur in cognitive flexibility and inhibitory control. PMID:29354217

Cognitive Variability in Adults with ADHD and AS: Disentangling the Roles of Executive Functions and Social Cognition

ERIC Educational Resources Information Center

Gonzalez-Gadea, Maria Luz; Baez, Sandra; Torralva, Teresa; Castellanos, Francisco Xavier; Rattazzi, Alexia; Bein, Victoria; Rogg, Katharina; Manes, Facundo; Ibanez, Agustin

2013-01-01

Attention-deficit/hyperactivity disorder (ADHD) and Asperger's Syndrome (AS) share a heterogeneous cognitive profile. Studies assessing executive functions (EF) and social cognition in both groups have found preserved and impaired performances. These inconsistent findings would be partially explained by the cognitive variability reported in these…

[Use of "the Middlesex Elderly Assessment of Mental State" scale in the assessment of cognitive functioning in patients with aneurysmal subarachnoid haemorrhage].

PubMed

Chyza, Karolina Julia; Polityńska, Barbara; Kochanowicz, Jan; Lewko, Janusz

2007-03-01

It is now well established that cognitive deficits are a frequent consequence of aneurysmal subarachnoid haemorrhage (SAH). The cognitive status in the acute phase of the illness may provide valuable prognostic information in relation to the effects of the proposed treatment and long-term functioning of the patient. A prerequisite for this task is the identification of instruments that might prove useful in the diagnosis of neuropsychological deficits in patients with SAH. For these purposes we used The Middlesex Elderly Assessment of Mental State (MEAMS) in order to assess the cognitive deficits consequent upon SAH. To assess the cognitive functioning of patients undergoing treatment for SAH of aneurysmal origin in the acute stage of the illness, using a modified form of the MEAMS. 49 patients participated in the study, none of whom had a previous history of neurological or psychiatric illness. The age of the patients ranged between 23-70 years. 35 (71%) patients received surgical treatment (clipping of the aneurysm neck) and in 14 (29%) the aneurysm was embolised. The patients were assessed on two occasions: the first on admission to the Neurosurgery department following the SAH, and on the second, following treatment to secure the aneurysm. A modified version of the MEAMS in two parallel versions was used in the assessment. The results obtained were evaluated with reference to a control group. A range of cognitive impairments was identified with the aid of the MEAMS in patients undergoing treatment for aneurysmal SAH. These included deficits in visual and auditory memory, executive, perceptual and visuo-spatial functions together with the tendency to perseverate. In those patients who underwent surgery, deficits were observed in the following areas: disorientation in relation to self, time and place; perceptual, memory and visuo-spatial impairments. The results obtained indicate that the Middlesex Elderly Assessment of Mental State, in the form used in the present study appears to be a sensitive and useful instrument for the screening of cognitive impairments in patients following SAH, in the acute stages of the illness.

The alteration of autophagy and apoptosis in the hippocampus of rats with natural aging-dependent cognitive deficits.

PubMed

Yu, Yang; Feng, Linjing; Li, Junnan; Lan, Xiaoxin; A, Lixiang; Lv, Xiaoyan; Zhang, Ming; Chen, Li

2017-09-15

The present study was aim to explore aging-dependent changes in hippocampal autophagy and apoptosis in a natural aging rat model from adult to old stages and to discover a suitable age for treating neurodegenerative diseases. Wistar rats at 5, 18 and 24months of age were used to mimic the adulthood, initial old, and old phases, respectively. The learning and cognitive ability of the rats was detected by the Morris water maze test. Morphological changes in the hippocampus were observed. Expressions of apoptosis and autophagy-related proteins were examined by Western blot. The adult group (5months) exhibited high levels of autophagy related p-ULK p-ULK-1/ULK-1 ratio, Beclin-1, LC3II and cell survival, maintaining normal learning and cognitive function and integrated hippocampal morphology. The initial old group (18 months) presented a reduced number of neurons and cognitive deficits, and exhibited high levels of apoptosis related Bax/Bcl-2 ratio, Caspase-3 activation and autophagy related p-ULK p-ULK-1/ULK-1 ratio, Beclin-1, LC3II compared to the adult group. The old group (24 months) exhibited a high level of apoptosis related Bax/Bcl-2 ratio, Caspase-3 activation and a low level of autophagy related p-ULK p-ULK-1/ULK-1 ratio, Beclin-1, LC3II compared to its younger group, as well as significant neuronal death and cognitive deficits. The degree of autophagy was generally consistent with its negative regulator, the PI3K/Akt/mTOR axis, in all groups. Our data suggest that cognitive deficits are first observed in the initial old stage. The levels of autophagy and apoptosis tend to be opposite in the adult and old phases. High levels of autophagy and apoptosis coexist in the initial old stage. Our study indicates that up-regulation of autophagy in the initial old phase to anti-cognitive deficits must be further evaluated. Copyright © 2017 Elsevier B.V. All rights reserved.

A longitudinal analysis of cognitive dysfunction, coping, and depression in multiple sclerosis.

PubMed

Rabinowitz, Amanda R; Arnett, Peter A

2009-09-01

Using a longitudinal design, the authors examined coping and cognitive functioning in the development of depression in individuals with multiple sclerosis (MS). Coping style was evaluated in 2 conceptually distinct roles: as moderator and mediator of the impact of cognitive dysfunction on depression. Using indices derived from the COPE (C. S. Carver, M. F. Scheier, & J. K. Weintraub, 1989), the authors operationalized coping in 3 ways-as active, avoidant, and an index accounting for relative levels of both. Coping both moderated and partially mediated the relationship between cognitive dysfunction and depression. Moderation results suggest that the relationship between cognitive dysfunction and depression is dependent on coping style-adaptive coping protects individuals from experiencing depression related to their cognitive deficits; however, when individuals use maladaptive coping, cognitive dysfunction puts them at risk for depression. Mediational results suggest that cognitive dysfunction leads to depression partially due to cognitive dysfunction's effects on coping. That is, cognitive deficits may impair individuals' ability to use adaptive coping strategies, leaving them more likely to use maladaptive strategies. Clinical and theoretical implications of these findings are discussed.

The Neuropsychology of Amphetamine and Opiate Dependence: Implications for Treatment

PubMed Central

Sahakian, Barbara J

2013-01-01

Chronic use of amphetamines and/or opiates has been associated with a wide range of cognitive deficits, involving domains of attention, inhibitory control, planning, decision-making, learning and memory. Although both amphetamine and opiate users show marked impairment in various aspects of cognitive function, the impairment profile is distinctly different according to the substance of abuse. In light of evidence showing that cognitive impairment in drug users has a negative impact on treatment engagement and efficacy, we review substance-specific deficits on executive and memory function, and discuss possibilities to address these during treatment intervention. PMID:17690986

Investigation of Cool and Hot Executive Function in ODD/CD Independently of ADHD

ERIC Educational Resources Information Center

Hobson, Christopher W.; Scott, Stephen; Rubia, Katya

2011-01-01

Background: Children with oppositional defiant disorder/conduct disorder (ODD/CD) have shown deficits in "cool" abstract-cognitive, and "hot" reward-related executive function (EF) tasks. However, it is currently unclear to what extent ODD/CD is associated with neuropsychological deficits, independently of attention deficit hyperactivity disorder…

Are Auditory and Visual Processing Deficits Related to Developmental Dyslexia?

ERIC Educational Resources Information Center

Georgiou, George K.; Papadopoulos, Timothy C.; Zarouna, Elena; Parrila, Rauno

2012-01-01

The purpose of this study was to examine if children with dyslexia learning to read a consistent orthography (Greek) experience auditory and visual processing deficits and if these deficits are associated with phonological awareness, rapid naming speed and orthographic processing. We administered measures of general cognitive ability, phonological…

The Neural Substrates of Cognitive Control Deficits in Autism Spectrum Disorders

ERIC Educational Resources Information Center

Solomon, Marjorie; Ozonoff, Sally J.; Ursu, Stefan; Ravizza, Susan; Cummings, Neil; Ly, Stanford; Carter, Cameron S.

2009-01-01

Executive function deficits are among the most frequently reported symptoms of autism spectrum disorders (ASDs), however, there have been few functional magnetic resonance imaging (fMRI) studies that investigate the neural substrates of executive function deficits in ASDs, and only one in adolescents. The current study examined cognitive…

Glycogen synthase kinase-3 inhibitors reverse deficits in long-term potentiation and cognition in Fragile X mice

PubMed Central

Franklin, Aimee V.; King, Margaret K.; Palomo, Valle; Martinez, Ana; McMahon, Lori L.; Jope, Richard S.

2013-01-01

Background Identifying feasible therapeutic interventions is crucial for ameliorating the intellectual disability and other afflictions of Fragile X Syndrome (FXS), the most common inherited cause of intellectual disability and autism. Hippocampal glycogen synthase kinase-3 (GSK3) is hyperactive in the mouse model of FXS (FX mice), and hyperactive GSK3 promotes locomotor hyperactivity and audiogenic seizure susceptibility in FX mice, raising the possibility that specific GSK3 inhibitors may improve cognitive processes. Methods We tested if specific GSK3 inhibitors improve deficits in N-methyl-D-aspartate receptor (NMDAR)-dependent long term potentiation (LTP) at medial perforant path synapses onto dentate granule cells (MPP-DGC) and dentate gyrus-dependent cognitive behavioral tasks. Results GSK3 inhibitors completely rescued deficits in LTP at MPP-DGC synapses in FX mice. Furthermore, synaptosomes from the dentate gyrus of FX mice displayed decreased inhibitory serine-phosphorylation of GSK3β compared with wild-type littermates. The potential therapeutic utility of GSK3 inhibitors was further tested on dentate gyrus-dependent congnitive behaviors. In vivo administration of GSK3 inhibitors completely reversed impairments in several cognitive tasks in FX mice, including novel object detection, coordinate and categorical spatial processing, and temporal ordering for visual objects. Conclusions These findings establish that synaptic plasticity and cognitive deficits in FX mice can be improved by intervention with inhibitors of GSK3, which may prove therapeutically beneficial in FXS. PMID:24041505

Cognitive-motor interference during fine and gross motor tasks in children with Developmental Coordination Disorder (DCD).

PubMed

Schott, Nadja; El-Rajab, Inaam; Klotzbier, Thomas

2016-10-01

While typically developing children produce relatively automatized postural control processes, children with DCD seem to exhibit an automatization deficit. Dual tasks with various cognitive loads seem to be an effective way to assess the automatic deficit hypothesis. The aims of the study were: (1) to examine the effect of a concurrent cognitive task on fine and gross motor tasks in children with DCD, and (2) to determine whether the effect varied with different difficulty levels of the concurrent task. We examined dual-task performance (Trail-Making-Test, Trail-Walking-Test) in 20 children with DCD and 39 typically developing children. Based on the idea of the Trail-Making-Test, participants walked along a fixed pathway, following a prescribed path, delineated by target markers of (1) increasing sequential numbers, and (2) increasing sequential numbers and letters. The motor and cognitive dual-task effects (DTE) were calculated for each task. Regardless of the cognitive task, children with DCD performed equally well in fine and gross motor tasks, and were slower in the dual task conditions than under single task-conditions, compared with children without DCD. Increased cognitive task complexity resulted in slow trail walking as well as slower trail tracing. The motor interference for the gross motor tasks was least for the simplest conditions and greatest for the complex conditions and was more pronounced in children with DCD. Cognitive interference was low irrespective of the motor task. Children with DCD show a different approach to allocation of cognitive resources, and have difficulties making motor skills automatic. The latter notion is consistent with impaired cerebellar function and the "automatization deficit hypothesis", suggesting that any deficit in the automatization process will appear if conscious monitoring of the motor skill is made more difficult by integrating another task requiring attentional resources. Copyright © 2016 Elsevier Ltd. All rights reserved.

Apathy and noradrenaline: silent partners to mild cognitive impairment in Parkinson's disease?

PubMed

Loued-Khenissi, Leyla; Preuschoff, Kerstin

2015-08-01

Mild cognitive impairment (MCI) is a comorbid factor in Parkinson's disease. The aim of this review is to examine the recent neuroimaging findings in the search for Parkinson's disease MCI (PD-MCI) biomarkers to gain insight on whether MCI and specific cognitive deficits in Parkinson's disease implicate striatal dopamine or another system. The evidence implicates a diffuse pathophysiology in PD-MCI rather than acute dopaminergic involvement. On the one hand, performance in specific cognitive domains, notably in set-shifting and learning, appears to vary with dopaminergic status. On the other hand, motivational states in Parkinson's disease along with their behavioral and physiological indices suggest a noradrenergic contribution to cognitive deficits in Parkinson's disease. Finally, Parkinson's disease's pattern of neurodegeneration offers an avenue for continued research in nigrostriatal dopamine's role in distinct behaviors, as well as the specification of dorsal and ventral striatal functions. The search for PD-MCI biomarkers has employed an array of neuroimaging techniques, but still yields divergent findings. This may be due in part to MCI's broad definition, encompassing heterogeneous cognitive domains, only some of which are affected in Parkinson's disease. Most domains falling under the MCI umbrella include fronto-dependent executive functions, whereas others, notably learning, rely on the basal ganglia. Given the deterioration of the nigrostriatal dopaminergic system in Parkinson's disease, it has been the prime target of PD-MCI investigation. By testing well defined cognitive deficits in Parkinson's disease, distinct functions can be attributed to specific neural systems, overcoming conflicting results on PD-MCI. Apart from dopamine, other systems such as the neurovascular or noradrenergic systems are affected in Parkinson's disease. These factors may be at the basis of specific facets of PD-MCI for which dopaminergic involvement has not been conclusive. Finally, the impact of both dopaminergic and noradrenergic deficiency on motivational states in Parkinson's disease is examined in light of a plausible link between apathy and cognitive deficits.

Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer’s Disease

PubMed Central

Cunnane, Stephen C.; Courchesne-Loyer, Alexandre; Vandenberghe, Camille; St-Pierre, Valérie; Fortier, Mélanie; Hennebelle, Marie; Croteau, Etienne; Bocti, Christian; Fulop, Tamas; Castellano, Christian-Alexandre

2016-01-01

We propose that brain energy deficit is an important pre-symptomatic feature of Alzheimer’s disease (AD) that requires closer attention in the development of AD therapeutics. Our rationale is fourfold: (i) Glucose uptake is lower in the frontal cortex of people >65 years-old despite cognitive scores that are normal for age. (ii) The regional deficit in brain glucose uptake is present in adults <40 years-old who have genetic or lifestyle risk factors for AD but in whom cognitive decline has not yet started. Examples include young adult carriers of presenilin-1 or apolipoprotein E4, and young adults with mild insulin resistance or with a maternal family history of AD. (iii) Regional brain glucose uptake is impaired in AD and mild cognitive impairment (MCI), but brain uptake of ketones (beta-hydroxybutyrate and acetoacetate), remains the same in AD and MCI as in cognitively healthy age-matched controls. These observations point to a brain fuel deficit which appears to be specific to glucose, precedes cognitive decline associated with AD, and becomes more severe as MCI progresses toward AD. Since glucose is the brain’s main fuel, we suggest that gradual brain glucose exhaustion is contributing significantly to the onset or progression of AD. (iv) Interventions that raise ketone availability to the brain improve cognitive outcomes in both MCI and AD as well as in acute experimental hypoglycemia. Ketones are the brain’s main alternative fuel to glucose and brain ketone uptake is still normal in MCI and in early AD, which would help explain why ketogenic interventions improve some cognitive outcomes in MCI and AD. We suggest that the brain energy deficit needs to be overcome in order to successfully develop more effective therapeutics for AD. At present, oral ketogenic supplements are the most promising means of achieving this goal. PMID:27458340

Cognitive Effects of Stimulant, Guanfacine, and Combined Treatment in Child and Adolescent Attention-Deficit/Hyperactivity Disorder.

PubMed

Bilder, Robert M; Loo, Sandra K; McGough, James J; Whelan, Fiona; Hellemann, Gerhard; Sugar, Catherine; Del'Homme, Melissa; Sturm, Alexandra; Cowen, Jennifer; Hanada, Grant; McCracken, James T

2016-08-01

Psychostimulants are partially effective in reducing cognitive dysfunction associated with attention-deficit/hyperactivity disorder (ADHD). Cognitive effects of guanfacine, an alternative treatment, are poorly understood. Given its distinct action on α2A receptors, guanfacine may have different or complementary effects relative to stimulants. This study tested stimulant and guanfacine monotherapies relative to combined treatment on cognitive functions important in ADHD. Children with ADHD (n = 182; aged 7-14 years) completed an 8-week, double blind, randomized, controlled trial with 3 arms: d-methylphenidate (DMPH), guanfacine (GUAN), or combination treatment with DMPH and GUAN (COMB). A nonclinical comparison group (n = 93) had baseline testing, and a subset was retested 8 weeks later (n = 38). Analyses examined treatment effects in 4 cognitive domains (working memory, response inhibition, reaction time, and reaction time variability) constructed from 20 variables. The ADHD group showed impaired working memory relative to the nonclinical comparison group (effect size = -0.53 SD unit). The treatments differed in effects on working memory but not other cognitive domains. Combination treatment improved working memory more than GUAN but was not significantly better than DMPH alone. Treatment did not fully normalize the initial deficit in ADHD relative to the comparison group. Combined treatment with DMPH and GUAN yielded greater improvements in working memory than placebo or GUAN alone, but the combined treatment was not superior to DMPH alone and did not extend to other cognitive domains. Although GUAN may be a useful add-on treatment to psychostimulants, additional strategies appear to be necessary to achieve normalization of cognitive function in ADHD. Single Versus Combination Medication Treatment for Children With Attention Deficit Hyperactivity Disorder; http://clinicaltrials.gov/; NCT00429273. Copyright © 2016 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.

Clearing the fog: a review of the effects of dietary omega-3 fatty acids and added sugars on chemotherapy-induced cognitive deficits

PubMed Central

Gaudier-Diaz, Monica M.; Weinhold, Kellie R.; DeVries, A. Courtney

2017-01-01

Cancer treatments such as chemotherapy have been an important part of extending survival in women diagnosed with breast cancer. However, chemotherapy can cause potentially toxic side effects in the brain that impair memory, verbal fluency, and processing speed in up to 30% of women treated. Women report that post-chemotherapy cognitive deficits negatively impact quality of life and may last up to ten years after treatment. Mechanisms underlying these cognitive impairments are not fully understood, but emerging evidence suggests that chemotherapy induces structural changes in the brain, produces neuroinflammation, and reduces adult hippocampal neurogenesis. Dietary approaches that modify inflammation and neurogenesis are promising strategies for reducing chemotherapy-induced cognitive deficits in breast cancer survivors. In this review, we describe the cognitive and neuronal side effects associated with commonly used chemotherapy treatments for breast cancer, and we focus on the often opposing actions of omega-3 fatty acids and added sugars on cognitive function, neuroinflammation, and adult hippocampal neurogenesis. Omega-3 fatty acids administered concurrently with doxorubicin chemotherapy have been shown to prevent depressive-like behaviors and reduce neuroinflammation, oxidative stress, and neural apoptosis in rodent models. In contrast, diets high in added sugars may interact with n-3 FAs to diminish their anti-inflammatory activity or act independently to increase neuroinflammation, reduce adult hippocampal neurogenesis, and promote cognitive deficits. We propose that a diet rich in long-chain, marine-derived omega-3 fatty acids and low in added sugars may be an ideal pattern for preventing or alleviating neuroinflammation and oxidative stress, thereby protecting neurons from the toxic effects of chemotherapy. Research testing this hypothesis could lead to the identification of modifiable dietary choices to reduce the long-term impact of chemotherapy on the cognitive functions that are important to quality of life in breast cancer survivors. PMID:27933449

Clearing the fog: a review of the effects of dietary omega-3 fatty acids and added sugars on chemotherapy-induced cognitive deficits.

PubMed

Orchard, Tonya S; Gaudier-Diaz, Monica M; Weinhold, Kellie R; Courtney DeVries, A

2017-02-01

Cancer treatments such as chemotherapy have been an important part of extending survival in women diagnosed with breast cancer. However, chemotherapy can cause potentially toxic side effects in the brain that impair memory, verbal fluency, and processing speed in up to 30% of women treated. Women report that post-chemotherapy cognitive deficits negatively impact quality of life and may last up to ten years after treatment. Mechanisms underlying these cognitive impairments are not fully understood, but emerging evidence suggests that chemotherapy induces structural changes in the brain, produces neuroinflammation, and reduces adult hippocampal neurogenesis. Dietary approaches that modify inflammation and neurogenesis are promising strategies for reducing chemotherapy-induced cognitive deficits in breast cancer survivors. In this review, we describe the cognitive and neuronal side effects associated with commonly used chemotherapy treatments for breast cancer, and we focus on the often opposing actions of omega-3 fatty acids and added sugars on cognitive function, neuroinflammation, and adult hippocampal neurogenesis. Omega-3 fatty acids administered concurrently with doxorubicin chemotherapy have been shown to prevent depressive-like behaviors and reduce neuroinflammation, oxidative stress, and neural apoptosis in rodent models. In contrast, diets high in added sugars may interact with n-3 FAs to diminish their anti-inflammatory activity or act independently to increase neuroinflammation, reduce adult hippocampal neurogenesis, and promote cognitive deficits. We propose that a diet rich in long-chain, marine-derived omega-3 fatty acids and low in added sugars may be an ideal pattern for preventing or alleviating neuroinflammation and oxidative stress, thereby protecting neurons from the toxic effects of chemotherapy. Research testing this hypothesis could lead to the identification of modifiable dietary choices to reduce the long-term impact of chemotherapy on the cognitive functions that are important to quality of life in breast cancer survivors.

Executive control deficits in substance-dependent individuals: a comparison of alcohol, cocaine, and methamphetamine and of men and women.

PubMed

van der Plas, Ellen A A; Crone, Eveline A; van den Wildenberg, Wery P M; Tranel, Daniel; Bechara, Antoine

2009-08-01

Substance dependence is associated with executive function deficits, but the nature of these executive defects and the effect that different drugs and sex have on these defects have not been fully clarified. Therefore, we compared the performance of alcohol- (n = 33; 18 women), cocaine- (n = 27; 14 women), and methamphetamine-dependent individuals (n = 38; 25 women) with sex-matched healthy comparisons (n = 36; 17 women) on complex decision making as measured with the Iowa Gambling Task, working memory, cognitive flexibility, and response inhibition. Cocaine- and methamphetamine-dependent individuals were impaired on complex decision making, working memory, and cognitive flexibility, but not on response inhibition. The deficits in working memory and cognitive flexibility were milder than the decision-making deficits and did not change as a function of memory load or task switching. Interestingly, decision making was significantly more impaired in women addicted to cocaine or methamphetamine than in men addicted to these drugs. Together, these findings suggest that drug of choice and sex have different effects on executive functioning, which, if replicated, may help tailor intervention.

Ameliorating effects of preadolescent aniracetam treatment on prenatal ethanol-induced impairment in AMPA receptor activity.

PubMed

Wijayawardhane, Nayana; Shonesy, Brian C; Vaithianathan, Thirumalini; Pandiella, Noemi; Vaglenova, Julia; Breese, Charles R; Dityatev, Alexander; Suppiramaniam, Vishnu

2008-01-01

Ethanol-induced damage in the developing hippocampus may result in cognitive deficits such as those observed in fetal alcohol spectrum disorder (FASD). Cognitive deficits in FASD are partially mediated by alterations in glutamatergic synaptic transmission. Recently, we reported that synaptic transmission mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is impaired following fetal ethanol exposure. This finding led us to develop a rational approach for the treatment of alcohol-related cognitive deficits using aniracetam, an allosteric AMPAR modulator. In the present study, 28 to 34-day-old rats exposed to ethanol in utero were treated with aniracetam, and subsequently exhibited persistent improvement in mEPSC amplitude, frequency, and decay time. Furthermore, these animals expressed positive changes in synaptic single channel properties, suggesting that aniracetam ameliorates prenatal ethanol-induced deficits through modifications at the single channel level. Specifically, single channel open probability, conductance, mean open and closed times, and the number and burst duration were positively affected. Our findings emphasize the utility of compounds which slow the rate of deactivation and desensitization of AMPARs such as aniracetam.

Theory of mind and verbal working memory deficits in parents of autistic children.

PubMed

Gokcen, Sezen; Bora, Emre; Erermis, Serpil; Kesikci, Hande; Aydin, Cahide

2009-03-31

The objective of this study was to investigate the potential values of executive function and social cognition deficits as endophenotypes of autism. While theory of mind (ToM) is generally accepted as a unitary concept, some have suggested that ToM may be separated into two components (mental state reasoning and decoding). In this study, both aspects of ToM and verbal working memory abilities were investigated with relatively demanding tasks. The authors used a neurocognitive battery to compare the executive function and social cognition skills of 76 parents of autistic probands with 41 parents of healthy children. Both groups were matched for IQ, age and gender. Index parents had verbal working memory deficits. They had also low performance on a mental state reasoning task. Index parents had difficulties in reasoning about others' emotions. In contrast to findings in the control group, low performance of mental state reasoning ability was not associated with working memory deficit in index parents. Social cognition and working memory impairments may represent potential endophenotypes, related to an underlying vulnerability for autistic spectrum disorders.

Impaired Midline Theta Power and Connectivity During Proactive Cognitive Control in Schizophrenia.

PubMed

Ryman, Sephira G; Cavanagh, James F; Wertz, Christopher J; Shaff, Nicholas A; Dodd, Andrew B; Stevens, Brigitte; Ling, Josef; Yeo, Ronald A; Hanlon, Faith M; Bustillo, Juan; Stromberg, Shannon F; Lin, Denise S; Abrams, Swala; Mayer, Andrew R

2018-05-25

Disrupted proactive cognitive control, a form of early selection and active goal maintenance, is hypothesized to underlie the broad cognitive deficits observed in patients with schizophrenia (SPs). Current research suggests that the disrupted activation within and connectivity between regions of the cognitive control network contribute to disrupted proactive cognitive control; however, no study has examined these mechanisms using an AX Continuous Performance Test task in schizophrenia. Twenty-six SPs (17 male subjects; mean age 34.46 ± 8.77 years) and 28 healthy control participants (HCs; 16 male subjects; mean age 31.43 ± 7.23 years) underwent an electroencephalogram while performing the AX Continuous Performance Test. To examine the extent of activation and level of connectivity within the cognitive control network, power, intertrial phase clustering, and intersite phase clustering metrics were calculated and analyzed. SPs exhibited expected general decrements in behavioral performance relative to HCs and a more selective deficit in conditions requiring proactive cognitive control. Additionally, SPs exhibited deficits in midline theta power and connectivity during proactive cognitive control trials. Specifically, HCs exhibited significantly greater theta power for B cues relative to A cues, whereas SPs exhibited no significant differences between A- and B-cue theta power. Additionally, differential theta connectivity patterns were observed in SPs and HCs. Behavioral measures of proactive cognitive control predicted functional outcomes in SPs. This study suggests that low-frequency midline theta activity is selectively disrupted during proactive cognitive control in SPs. The disrupted midline theta activity may reflect a failure of SPs to proactively recruit cognitive control processes. Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Cognitive deficit in methamphetamine users relative to childhood academic performance: link to cortical thickness.

PubMed

Dean, Andy C; Morales, Angelica M; Hellemann, Gerhard; London, Edythe D

2018-04-20

Individuals with cognitive problems may be predisposed to develop substance use disorders; therefore, differences in cognitive function between methamphetamine users and control participants may be attributable to premorbid factors rather than methamphetamine use. The goal of this study was to clarify the extent to which this is the case. Childhood academic transcripts were obtained for 37 methamphetamine-dependent adults and 41 control participants of similar educational level and premorbid IQ. Each participant completed a comprehensive cognitive battery and received a structural magnetic resonance imaging scan. Data from control participants and linear regression were used to develop a normative model to describe the relationship between childhood academic performance and scores on the cognitive battery. Using this model, cognitive performance of methamphetamine users was predicted from their premorbid academic scores. Results indicated that methamphetamine users' childhood grade point average was significantly lower than that of the control group (p < 0.05). Further, methamphetamine users' overall cognitive performance was lower than was predicted from their grade point average prior to methamphetamine use (p = 0.001), with specific deficits in attention/concentration and memory (ps < 0.01). Memory deficits were associated with lower whole-brain cortical thickness (p < 0.05). Thus, in addition to having an apparent premorbid weakness in cognition, methamphetamine users exhibit subsequent cognitive function that is significantly lower than premorbid estimates would predict. The results support the view that chronic methamphetamine use causes a decline in cognition and/or a failure to develop normative cognitive abilities, although aside from methamphetamine use per se, other drug use and unidentified factors likely contribute to the observed effects.

Cognitive impairment in schizophrenia and affective psychoses: implications for DSM-V criteria and beyond.

PubMed

Bora, Emre; Yücel, Murat; Pantelis, Christos

2010-01-01

It has recently been suggested that the diagnostic criteria of schizophrenia should include specific reference to cognitive impairments characterizing the disorder. Arguments in support of this assertion contend that such inclusion would not only serve to increase the awareness of cognitive deficits in affected patients, among both clinicians and researchers alike, but also increase the "point of rarity" between schizophrenia and mood disorders. The aim of the current article is to examine this latter assertion in light of the recent opinion piece provided by Keefe and Fenton (Keefe RSE, Fenton WS. How should DSM-V criteria for schizophrenia include cognitive impairment? Schizophr Bull. 2007;33:912-920). Through literature review, we explore the issue of whether cognitive deficits do in fact differentiate the major psychoses. The overall results of this inquiry suggest that inclusion of cognitive impairment criteria in Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (DSM-V) would not provide a major advancement in discriminating schizophrenia from bipolar disorder and affective psychoses. Therefore, while cognitive impairment should be included in DSM-V, it should not dictate diagnostic specificity--at least not until more comprehensive evidence-based reviews of the current diagnostic system have been undertaken. Based on this evidence, we consider several alternatives for the DSM-V definition of cognitive impairment in schizophrenia, including (1) the inclusion of cognitive impairment as a specifier and (2) the definition of cognitive impairment as a dimension within a hybrid categorical-dimensional system. Given the state of current evidence, these possibilities appear to represent the most parsimonious approaches to the inclusion of cognitive deficits in the diagnostic criteria of schizophrenia and, potentially, of mood disorders.

Decreased theta power at encoding and cognitive mapping deficits in elderly individuals during a spatial memory task.

PubMed

Lithfous, Ségolène; Tromp, Delphine; Dufour, André; Pebayle, Thierry; Goutagny, Romain; Després, Olivier

2015-10-01

The purpose of this study was to investigate the role of theta activity in cognitive mapping, and to determine whether age-associated decreased theta power may account for navigational difficulties in elderly individuals. Cerebral activity was recorded using electroencephalograph in young and older individuals performing a spatial memory task that required the creation of cognitive maps. Power spectra were computed in the frontal and parietal regions and correlated with recognition performance. We found that accuracy of cognitive mapping was positively correlated with left frontal theta activity during encoding in young adults but not in older individuals. Compared with young adults, older participants were impaired in the creation of cognitive maps and showed reduced theta and alpha activity at encoding. These results suggest that encoding processes are impaired in older individual, which may explain age-related cognitive mapping deficits. Copyright © 2015 Elsevier Inc. All rights reserved.

Burn Injuries and Their Impact on Cognitive-Communication Skills in the Inpatient Rehabilitation Setting.

PubMed

Hendricks, Carla Tierney; Camara, Kristin; Violick Boole, Kathryn; Napoli, Maureen F; Goldstein, Richard; Ryan, Colleen M; Schneider, Jeffrey C

The prevalence and extent of cognitive-communication disorders and factors that have impact on outcomes are examined in the burn population within an inpatient rehabilitation facility. A retrospective data analysis was conducted on adults diagnosed with burn injury (n = 144). Descriptive statistics were used to identify the prevalence of cognitive-communication deficits on admission and discharge. The main outcomes were cognitive-communication ratings on discharge from inpatient rehabilitation as measured by the memory and problem-solving domains of the Functional Independence Measure (FIM) and composite score of the Functional Communication Measure (FCM). Medical, demographic and rehabilitation predictors of the main outcomes were assessed using regression analyses. On admission to inpatient rehabilitation, 79% of the total population presented with cognitive-communication impairments, and of them, 27% presented with persistent deficits on discharge. Admission FIM memory score, marital status, and age were significant predictors of discharge FIM memory score. Admission FIM problem-solving score, age, marital status, and prehospital living-with were significant predictors of discharge FIM problem-solving score. Admission FCM score and age were significant predictors of discharge FCM cognitive score. Persons with burn injuries are at risk for cognitive-communication impairments, which may persist after inpatient rehabilitation. FIM data obtained on admission can be used as a screening tool to identify these at-risk patients. Future work is needed to assess the efficacy of speech-language pathologist intervention for cognitive-communication deficits within the burn injury population.

A Longitudinal Operant Assessment of Cognitive and Behavioural Changes in the HdhQ111 Mouse Model of Huntington’s Disease

PubMed Central

Dunnett, Stephen B.; Brooks, Simon P.

2016-01-01

Huntington’s disease (HD) is characterised by motor symptoms which are often preceded by cognitive and behavioural changes, that can significantly contribute to disease burden for people living with HD. Numerous knock-in mouse models of HD are currently available for scientific research. However, before their use, they must be behaviourally characterised to determine their suitability in recapitulating the symptoms of the human condition. Thus, we sought to longitudinally characterise the nature, severity and time course of cognitive and behavioural changes observed in HdhQ111 heterozygous knock-in mice.To determine changes in cognition and behaviour an extensive battery of operant tests including: fixed ratio, progressive ratio, the five choice serial reaction time task and the serial implicit learning task, were applied longitudinally to HdhQ111 and wild type mice. The operant test battery was conducted at 6, 12 and 18 months of age. Significant deficits were observed in HdhQ111 animals in comparison to wild type animals in all operant tests indicating altered cognition (attentional and executive function) and motivation. However, the cognitive and behavioural deficits observed were not shown to be progressive over time in the longitudinal testing paradigm that was utilised. The results therefore demonstrate that the HdhQ111 mouse model of HD reflects some features of the cognitive and behavioural changes shown in the human condition of HD. Although, the cognitive and behavioural deficits demonstrated were not shown to be progressive over time. PMID:27701442

Cognitive predictors of balance in Parkinson's disease.

PubMed

Fernandes, Ângela; Mendes, Andreia; Rocha, Nuno; Tavares, João Manuel R S

2016-06-01

Postural instability is one of the most incapacitating symptoms of Parkinson's disease (PD) and appears to be related to cognitive deficits. This study aims to determine the cognitive factors that can predict deficits in static and dynamic balance in individuals with PD. A sociodemographic questionnaire characterized 52 individuals with PD for this work. The Trail Making Test, Rule Shift Cards Test, and Digit Span Test assessed the executive functions. The static balance was assessed using a plantar pressure platform, and dynamic balance was based on the Timed Up and Go Test. The results were statistically analysed using SPSS Statistics software through linear regression analysis. The results show that a statistically significant model based on cognitive outcomes was able to explain the variance of motor variables. Also, the explanatory value of the model tended to increase with the addition of individual and clinical variables, although the resulting model was not statistically significant The model explained 25-29% of the variability of the Timed Up and Go Test, while for the anteroposterior displacement it was 23-34%, and for the mediolateral displacement it was 24-39%. From the findings, we conclude that the cognitive performance, especially the executive functions, is a predictor of balance deficit in individuals with PD.

Cognitive rehabilitation training in patients with brain tumor-related epilepsy and cognitive deficits: a pilot study.

PubMed

Maschio, Marta; Dinapoli, Loredana; Fabi, Alessandra; Giannarelli, Diana; Cantelmi, Tonino

2015-11-01

The aim of this pilot observational study was to evaluate effect of cognitive rehabilitation training (RehabTr) on cognitive performances in patients with brain tumor-related epilepsy (BTRE) and cognitive disturbances. Medical inclusion criteria: patients (M/F) ≥ 18 years ≤ 75 with symptomatic seizures due to primary brain tumors or brain metastases in stable treatment with antiepileptic drugs; previous surgical resection or biopsy; >70 Karnofsky Performance Status; stable oncological disease. Eligible patients recruited from 100 consecutive patients with BTRE at first visit to our Center from 2011 to 2012. All recruited patients were administered battery of neuropsychological tests exploring various cognitive domains. Patients considered to have a neuropsychological deficit were those with at least one test score for a given domain indicative of impairment. Thirty patients out of 100 showed cognitive deficits, and were offered participation in RehabTr, of which 16 accepted (5 low grade glioma, 4 high grade glioma, 2 glioblastoma, 2 meningioma and 3 metastases) and 14 declined for various reasons. The RehabTr consisted of one weekly individual session of 1 h, for a total of 10 weeks, carried out by a trained psychologist. The functions trained were: memory, attention, visuo-spatial functions, language and reasoning by means of Training NeuroPsicologico (TNP(®)) software. To evaluate the effect of the RehabTr, the same battery of tests was administered directly after cognitive rehabilitation (T1), and at six-month follow-up (T2). Statistical analysis with Student T test for paired data showed that short-term verbal memory, episodic memory, fluency and long term visuo-spatial memory improved immediately after the T1 and remained stable at T2. At final follow-up all patients showed an improvement in at least one domain that had been lower than normal at baseline. Our results demonstrated a positive effect of rehabilitative training at different times, and, for these reasons, should encourage future research in this area with large, randomized clinical trials that evaluate the impact of a cognitive rehabilitation in patients with BTRE and cognitive deficits.

Exploring the Use of Cognitive Intervention for Children with Acquired Brain Injury

ERIC Educational Resources Information Center

Missiuna, Cheryl; DeMatteo, Carol; Hanna, Steven; Mandich, Angela; Law, Mary; Mahoney, William; Scott, Louise

2010-01-01

Introduction: Children with acquired brain injury (ABI) often experience cognitive, motor, and psychosocial deficits that affect participation in everyday activities. Cognitive Orientation to Daily Occupational Performance (CO-OP) is an individualized treatment that teaches cognitive strategies necessary to support successful performance.…