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Sample records for hypokalemic periodic paralysis

  1. Hypokalemic periodic paralysis

    MedlinePlus

    ... that may be due to this condition include: Kidney stones (a side effect of acetazolamide) Irregular heartbeat during ... 2016:chap 99. Read More Breathing difficulty Carbohydrates Kidney stones Potassium test Thyrotoxic periodic paralysis Weakness Update Date ...

  2. [Hypokalemic periodic paralysis. A case report].

    PubMed

    Areta-Higuera, J D; Algaba-Montes, M; Oviedo-García, A Á

    2014-01-01

    Periodic paralysis is a rare disorder that causes episodes of severe muscle weakness that can be confused with other diseases, including epilepsy or myasthenia gravis. Hyperkalemic and hypokalemic paralysis are included within these diseases, the latter being divided into periodic paralysis (familial, thyrotoxic or sporadic) and non-periodic paralysis. In this regard, we present a case of familial hypokalemic periodic paralysis in an eighteen year-old female who was diagnosed with epilepsy in childhood, as well as a subclinical hypothyroidism (for which she received replacement therapy) months ago. The diagnosis was made by the anamnesis and the confirmation of hypokalemia. PMID:24360869

  3. Sjögren's syndrome presenting as hypokalemic periodic paralysis.

    PubMed

    Dowd, J E; Lipsky, P E

    1993-12-01

    We describe a 21-year-old Hispanic woman who presented with hypokalemic paralysis as the initial manifestation of Sjögren's syndrome (SS). Our review of the English literature revealed 12 previously reported cases of SS and renal tubular acidosis (RTA). Paralysis often preceded the sicca complex in those patients. Renal function in the patients with hypokalemic paralysis was reduced compared with that in patients who had primary SS and RTA but no history of hypokalemic paralysis (P < 0.002). Hypokalemic periodic paralysis is a rare manifestation of SS. It is seen more often in patients with primary SS, may precede the classic sicca complex, and may serve as a clinical marker for more severe renal disease in patients who have primary SS and RTA. PMID:8250993

  4. Dihydropyridine receptor mutations cause hypokalemic periodic paralysis

    SciTech Connect

    Ptacek, L.J.; Leppert, M.F.; Tawil, R.

    1994-09-01

    Hypokalemic periodic paralysis (hypoKPP) is an autosomal dominant skeletal muscle disorder manifested by episodic weakness associated with low serum potassium. Genetic linkage analysis has localized the hypoKPP gene to chromosome 1q31-q32 near a dihydropyridine receptor (DHP) gene. This receptor functions as a voltage-gated calcium channel and is also critical for excitation-contraction coupling in a voltage-sensitive and calcium-independent manner. We have characterized patient-specific DHP receptor mutations in 11 probands of 33 independent hypoKPP kindreds that occur at one of two adjacent nucleotides within the same codon and predict substitution of a highly conserved arginine in the S4 segment of domain 4 with either histidine or glycine. In one kindred, the mutation arose de novo. Taken together, these data establish the DHP receptor as the hypoKPP gene. We are unaware of any other human diseases presently known to result from DHP receptor mutations.

  5. Renal tubular acidosis complicated with hypokalemic periodic paralysis.

    PubMed

    Chang, Y C; Huang, C C; Chiou, Y Y; Yu, C Y

    1995-07-01

    Three Chinese girls with hypokalemic periodic paralysis secondary to different types of renal tubular acidosis are presented. One girl has primary distal renal tubular acidosis complicated with nephrocalcinosis. Another has primary Sjögren syndrome with distal renal tubular acidosis, which occurs rarely with hypokalemic periodic paralysis in children. The third has an isolated proximal renal tubular acidosis complicated with multiple organ abnormalities, unilateral carotid artery stenosis, respiratory failure, and consciousness disturbance. The diagnostic evaluation and emergent and prophylactic treatment for these three types of renal tubular acidosis are discussed. PMID:7575850

  6. Thyrotoxic hypokalemic periodic paralysis: An overlooked pathology in western countries.

    PubMed

    Pompeo, Arsenio; Nepa, Amleto; Maddestra, Maurizio; Feliziani, Vincenzo; Genovesi, Nicola

    2007-09-01

    Thyrotoxic hypokalemic periodic paralysis (THPP) is a complication of hyperthyroidism that is mostly diagnosed in Asian populations; consequently, it can be difficult to recognize in western populations. THPP represents an endocrine emergency that can result in respiratory insufficiency, cardiac arrhythmias, and death. Its differential diagnosis from the other more common forms of hypokalemic paralysis is important to avoid inappropriate therapy. Here, we discuss the main pathogenetic hypotheses, clinical features, and therapies of this disease. We also report an example of THPP management in our primary care unit. PMID:17693226

  7. Interictal conduction slowing in muscle fibers in hypokalemic periodic paralysis.

    PubMed

    Troni, W; Doriguzzi, C; Mongini, T

    1983-11-01

    Conduction velocity in muscle fibers of the short head of biceps brachii was reduced between attacks in all the affected members of a family suffering from hypokalemic periodic paralysis. This finding represents a further evidence of a primary alteration of sarcolemmal function in this disease. Interictal conduction slowing in muscle fibers is consistent with the prevailing pathophysiologic hypothesis, which considers an increased membrane permeability to sodium ions as the fundamental defect underlying all forms of familial periodic paralysis. PMID:6685247

  8. [Hypokalemic periodic paralysis provoked by "Ambene"].

    PubMed

    Wessel, K; Schumm, F; Peiffer, J; Schlote, W

    1985-12-01

    The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems. PMID:2936967

  9. [Primary hypokalemic periodic paralysis. Presentation of 18 cases].

    PubMed

    Ariza-Andraca, C R; Frati-Munari, A C; Ceron, E; Chavez de los Rios, J M; Martinez-Mata, J

    1993-01-01

    The clinical features of 16 males and 2 females with hypokalemic periodic paralysis (HPP) are presented. Five patients had familial HPP, 4 thyrotoxic HPP and 9 sporadic disease. The age of onset ranged from 6 to 42 years. Clinical pictures varied from paraparesis to severe quadriplegia. The disease onset was earlier in familial HPP (p < 0.05) while sporadic cases showed the most severe, albeit shorter paralysis (p < 0.05). On admission, serum potassium levels ranged from 1.5 to 3.3 mEq/L; they did not correlate with the severity of paralysis. Glucose-insulin provocation test was positive in 5/5 patients. Oral potassium chloride and amiloride were useful to prevent paralysis. Contrasting with reports from USA and Europe, in México, HPP is not exceptional, and should be considered in the differential diagnosis of acute paralysis. PMID:7926395

  10. Recurrent Hypokalemic Periodic Paralysis Unmasks Sjogren Syndrome without Sicca Symptoms.

    PubMed

    Hung, Yao-Min; Huang, Neng-Chyan; Wann, Shue-Ren; Chang, Yun-Te; Wang, Jyh-Seng

    2015-04-01

    Hypokalemic Periodic Paralysis (HPP) may occur as a rare complication of Sjogren Syndrome (SS) and Renal Tubular Acidosis (RTA). A 64-year male patient came with HPP, and was later diagnosed with distal RTA. The patient, who had no xerostomia and xerophthalmia, was diagnosed with primary SS from serologic and histologic findings of minor salivary gland biopsy. The patient recovered after potassium replacement therapy. Renal biopsy was also performed and revealed evidence of tubulointerstitial nephritis. Corticosteroids were administered and there was no recurrence of HPP during a 4-year follow-up period. The case highlights the significance of acute hypokalemia management in emergency department as it can unmask SS even if the SS is not associated with sicca symptoms. Hypokalemic paralysis associated with normal anion gap metabolic acidosis should prompt toward the diagnosis of SS. PMID:25933458

  11. [Thyrotoxic hypokalemic periodic paralysis: report of one case].

    PubMed

    Frantchez, Victoria; Valiño, José; Carracelas, Analía; Dufrechou, Carlos

    2010-11-01

    Thyrotoxic hypokalemic periodic paralysis is characterized by attacks of generalized weakness associated to hypokalemia in patients with hyperthyroidism. We report a 25-year-old man with a history of spontaneously relapsing episodes of muscular weakness, who consulted for a rapidly evolving upper and lower limb paresis. Hypokalemia associated to a primary hyperthyroidism was detected. Treatment with antithyroid Drugs and potassium supplementation reverted symptoms and the episodes of acute muscular weakness did not reappear. PMID:21279257

  12. [Thyrotoxic hypokalemic periodic paralysis in patients of African descent].

    PubMed

    Maia, Morgana Lima e; Trevisam, Paula Grasiele Carvalho; Minicucci, Marcos; Mazeto, Glaucia M F S; Azevedo, Paula S

    2014-10-01

    Thyrotoxic hypokalemic periodic paralysis (THPP) is an endocrine emergency marked by recurrent attacks of muscle weakness associated with hypokalemia and thyrotoxicosis. Asiatic male patients are most often affected. On the other hand, African descents rarely present this disease. The case described shows an afrodescendant patient with hypokalemia and tetraparesis, whose diagnosis of hyperthyroidism was considered during this crisis. The THPP, although rare, is potentially lethal. Therefore, in cases of flaccid paresis crisis this diagnosis should always be considered, especially if associated with hypokalemia. In this situation, if no previous diagnosis of hyperthyroidism, this should also be regarded. PMID:25372590

  13. The R900S mutation in CACNA1S associated with hypokalemic periodic paralysis.

    PubMed

    Ke, Qing; He, Fangping; Lu, Lingping; Yu, Ping; Jiang, Yajian; Weng, Chen; Huang, Hui; Yi, Xin; Qi, Ming

    2015-12-01

    Primary hypokalemic periodic paralysis is an autosomal dominant skeletal muscle channelopathy. In the present study, we investigated the genotype and phenotype of a Chinese hypokalemic periodic paralysis family. We used whole-exome next-generation sequencing to identify a mutation in the calcium channel, voltage-dependent, L type, alpha subunit gene (CACNA1S), R900S, which is a rare mutation associated with hypokalemic periodic paralysis. We first present a clinical description of hypokalemic periodic paralysis patients harboring CACNA1SR900S mutations: they were non-responsive to acetazolamide, but combined treatment with triamterene and potassium supplements decreased the frequency of muscle weakness attacks. All male carriers of the R900S mutation experienced such attacks, but all three female carriers were asymptomatic. This study provides further evidence for the phenotypic variation and pharmacogenomics of hypokalemic periodic paralysis. PMID:26433613

  14. Thyrotoxic hypokalemic periodic paralysis in an African male: a case report.

    PubMed

    Belayneh, Dereje K; Kellerth, Thomas

    2015-02-01

    Thyrotoxic hypokalemic periodic paralysis is a rare manifestation of thyrotoxicosis and is rarely reported in non-Asian populations. A 26-year-old Ethiopian male who presented with recurrent flaccid tetraparesis, hypokalemia, and hyperthyroidism is reported here. Thyroid function should be routinely checked in patients with acute or recurrent hypokalemic paralysis. PMID:25767707

  15. Hypokalemic periodic paralysis. A single fiber electromyographic study.

    PubMed

    De Grandis, D; Fiaschi, A; Tomelleri, G; Orrico, D

    1978-06-01

    The neurophysiological findings obtained with standard electromyography (EMG) and single fiber EMG (SFEMG) in a case of hypokalemic periodic paralysis (HoPP) are reported. During the period between paralytic attacks the only abnormalities consisted of scanty fibrillation potentials and, with SFEMG, a fiber density increase. In the first stage of an induced paralytic attack the most striking feature was decrease in fiber density, slight increase in jitter with several blocks. These results indicate a failure of the membrane surface to propagate an action potential. In some fibers the block is likely to be permanent, thus explaining the decrease in fiber density. The jitter increase is due to a slight abnormality at the synaptic site or to a variation in the propagation velocity of the muscle fiber. PMID:690662

  16. Episodic weakness and vacuolar myopathy in hypokalemic periodic paralysis.

    PubMed

    Basali, Diana; Prayson, Richard A

    2015-11-01

    We report a 50-year-old woman who presented with a 20 year history of gradually progressive lower extremity weakness, characterized by knee buckling with occasional falls and foot dragging. She also experienced difficulty in lifting her arms above her shoulders. The primary periodic paralyses are rare disorders caused by dysfunctional ion channels in skeletal muscle. The hypokalemic type is generally an autosomal dominant condition, due to missense mutations in the alpha subunits of the skeletal muscle L-type calcium channel genes, CACN1AS, or the skeletal muscle sodium channel gene, SCN4A. The affected patients typically present with episodic weakness. For our patient, the consumption of foods high in carbohydrates seemed to precipitate the episodes of weakness. Her family history was significant for six blood relatives, including three sons and three relatives on the paternal side, who had experienced similar symptoms. A biopsy of the left rectus femoralis muscle showed vacuolar myopathic changes in the scattered muscle fibers, accompanied by occasional degenerating and regenerating muscle fibers. There was no evidence of inflammation on the biopsy. The vacuoles were often associated with increased acid phosphatase staining. An electron microscopic examination showed that the vacuolar changes were due to T-tubule dilation, a characteristic of hypokalemic periodic paralysis. Other metabolic etiologies of vacuolar myopathy, such as acid phosphatase (lysosomal) associated acid maltase deficiency (a glycogen storage disease), need to be considered in the differential diagnosis. PMID:26190219

  17. Practical aspects in the management of hypokalemic periodic paralysis

    PubMed Central

    Levitt, Jacob O

    2008-01-01

    Management considerations in hypokalemic periodic paralysis include accurate diagnosis, potassium dosage for acute attacks, choice of diuretic for prophylaxis, identification of triggers, creating a safe physical environment, peri-operative measures, and issues in pregnancy. A positive genetic test in the context of symptoms is the gold standard for diagnosis. Potassium chloride is the favored potassium salt given at 0.5–1.0 mEq/kg for acute attacks. The oral route is favored, but if necessary, a mannitol solvent can be used for intravenous administration. Avoidance of or potassium prophylaxis for common triggers, such as rest after exercise, high carbohydrate meals, and sodium, can prevent attacks. Chronically, acetazolamide, dichlorphenamide, or potassium-sparing diuretics decrease attack frequency and severity but are of little value acutely. Potassium, water, and a telephone should always be at a patient's bedside, regardless of the presence of weakness. Perioperatively, the patient's clinical status should be checked frequently. Firm data on the management of periodic paralysis during pregnancy is lacking. Patient support can be found at . PMID:18426576

  18. Cardiac arrhythmias in hypokalemic periodic paralysis: Hypokalemia as only cause?

    PubMed

    Stunnenberg, Bas C; Deinum, Jaap; Links, Thera P; Wilde, Arthur A; Franssen, Hessel; Drost, Gea

    2014-09-01

    It is unknown how often cardiac arrhythmias occur in hypokalemic periodic paralysis (HypoPP) and if they are caused by hypokalemia alone or other factors. This systematic review shows that cardiac arrhythmias were reported in 27 HypoPP patients. Cases were confirmed genetically (13 with an R528H mutation in CACNA1S, 1 an R669H mutation in SCN4A) or had a convincing clinical diagnosis of HypoPP (13 genetically undetermined) if reported prior to the availability of genetic testing. Arrhythmias occurred during severe hypokalemia (11 patients), between attacks at normokalemia (4 patients), were treatment-dependent (2 patients), or unspecified (10 patients). Nine patients died from arrhythmia. Convincing evidence for a pro-arrhythmogenic factor other than hypokalemia is still lacking. The role of cardiac expression of defective skeletal muscle channels in the heart of HypoPP patients remains unclear. Clinicians should be aware of and prevent treatment-induced cardiac arrhythmia in HypoPP. PMID:25088161

  19. Secondary Sjogren's syndrome presenting with hypokalemic periodic paralysis.

    PubMed

    Dormohammadi Toosi, Taraneh; Naderi, Neda; Movassaghi, Shafieh; Seradj, Mehran Heydari; Khalvat, Ali; Shahbazi, Fatemeh

    2014-11-01

    Renal tubular acidosis (RTA) may develop in a large population of patients with Sjogren's syndrome (SS), but most of the subjects are asymptomatic. Here, we report a patient with known rheumatoid arthritis and symptoms of xerostomia, xerophthalmia and periodic paralysis. SS should be considered as a cause of RTA. The treatment of the underlying disorder may ameliorate the symptoms. PMID:25988057

  20. Secondary Sjogren's syndrome presenting with hypokalemic periodic paralysis

    PubMed Central

    Dormohammadi Toosi, Taraneh; Naderi, Neda; Movassaghi, Shafieh; Seradj, Mehran Heydari; Khalvat, Ali; Shahbazi, Fatemeh

    2014-01-01

    Renal tubular acidosis (RTA) may develop in a large population of patients with Sjogren's syndrome (SS), but most of the subjects are asymptomatic. Here, we report a patient with known rheumatoid arthritis and symptoms of xerostomia, xerophthalmia and periodic paralysis. SS should be considered as a cause of RTA. The treatment of the underlying disorder may ameliorate the symptoms. PMID:25988057

  1. A 20-year-old Chinese man with recurrent hypokalemic periodic paralysis and delayed diagnosis.

    PubMed

    Naqi, Muniba; Bhatt, Vijaya Raj; Pant, Shradha; Shrestha, Rajesh; Tadros, Michael; Murukutla, Srujitha; Rothman, Jeffrey

    2012-01-01

    Periodic paralysis in the setting of hypokalemia can be the result of several underlying conditions, requiring systematic evaluation. Thyrotoxic periodic paralysis (TPP), a curable cause of hypokalemic periodic paralysis, can often be the first manifestation of thyrotoxicosis. Because the signs and symptoms of thyrotoxicosis can be subtle and clouded by the clinical distress of the patient, the diagnosis of the underlying metabolic disorder can be overlooked. The authors report a case of TPP in a young Chinese man in whom the diagnosis of thyrotoxicosis was initially missed. This case illustrates the lack of awareness of TPP among many physicians, delay in the diagnosis of TPP and the importance of performing thyroid function testing in all cases of periodic paralysis. PMID:22665461

  2. Mutation analysis of CACNA1S and SCN4A in patients with hypokalemic periodic paralysis.

    PubMed

    Wang, Xiao-Ying; Ren, Bing-Wen; Yong, Zeng-Hua; Xu, Hong-Yan; Fu, Qiu-Xia; Yao, He-Bin

    2015-10-01

    Mutations in CACNA1S (calcium channel, voltage‑dependent, L type, alpha 1S subunit) and SCN4A (sodium channel, voltage‑gated, type IV, alpha subunit) are associated with hypokalemic periodic paralysis (HPP). The aim of the current study was to investigate CACNA1S and SCN4A mutations in patients with HPP. Mutations in CACNA1S and SCN4A were detected in three familial hypokalemic periodic paralysis (FHPP) pedigrees and in two thyrotoxic hypokalemic periodic paralysis (THPP) pedigrees using polymerase chain reaction, DNA sequencing and sequence alignment with GenBank data. A single base mutation from cytosine to guanine at site 1582 was identified in exon 11 of CACNA1S in one FHPP pedigree, resulting in an arginine to glycine (R528G) substitution. A single base mutation from thymine to cytosine at site 2012 was identified in exon 12 of SCN4A in one THPP pedigree, resulting in a phenylalanine to serine (F671S) substitution. No mutations in CACNA1S or SCN4A were identified in the remaining three pedigrees. The present study indicated that CACNA1S and SCN4A mutations are relatively rare in patients with HPP, and further studies are required to determine whether these mutation‑associated substitutions are representative of patients with HPP. PMID:26252573

  3. Enhancement of K+ conductance improves in vitro the contraction force of skeletal muscle in hypokalemic periodic paralysis.

    PubMed

    Grafe, P; Quasthoff, S; Strupp, M; Lehmann-Horn, F

    1990-05-01

    An abnormal ratio between Na+ and K+ conductances seems to be the cause for the depolarization and paralysis of skeletal muscle in primary hypokalemic periodic paralysis. Recently we have shown that the "K+ channel opener" cromakalim hyperpolarizes mammalian skeletal muscle fibers. Now we have studied the effects of this drug on the twitch force of muscle biopsies from normal and diseased human skeletal muscle. Cromakalim had little effect on the twitch force of normal muscle whereas it strongly improved the contraction force of fibers from patients suffering from hypokalemic periodic paralysis. Recordings of intracellular K+ and Cl- activities in human muscle and isolated rat soleus muscle support the view that cromakalim enhances the membrane K+ conductance (gK+). These data indicate that "K+ channel openers" may have a beneficial effect in primary hypokalemic periodic paralysis. PMID:2345562

  4. Muscle fiber conduction velocity in the diagnosis of sporadic hypokalemic periodic paralysis.

    PubMed

    Brouwer, O F; Zwarts, M J; Links, T P; Wintzen, A R

    1992-01-01

    A 6-year-old girl presented with episodes of profound muscle weakness since the age of 2 years. On the basis of decreased ictal serum potassium level and lack of metabolic disorder, primary hypokalemic periodic paralysis (HPP) was diagnosed. Both parents and 3 sibs were unaffected clinically. In all of them asymptomatic heterozygosity was very unlikely by the finding of normal muscle fiber conduction velocities, whereas in the patient interictal muscle fiber conduction velocity was lowered. Determination of muscle fiber conduction velocity can be helpful in documenting sporadic occurrence of HPP. PMID:1324813

  5. Idiopathic Generalized Epilepsy and Hypokalemic Periodic Paralysis in a Family of South Indian Descent

    PubMed Central

    Subramanian, Muthiah; Senthil, N.; Sujatha, S.

    2015-01-01

    Inherited channelopathies are a heterogeneous group of disorders resulting from dysfunction of ion channels in cellular membranes. They may manifest as diseases affecting skeletal muscle contraction, the conduction system of the heart, nervous system function, and vision syndromes. We describe a family of South Indian descent with hypokalemic periodic paralysis in which four members also have idiopathic generalized epilepsy. Hypokalemic periodic paralysis is a genetically heterogeneous channelopathy that has been linked to mutations in genes encoding three ion channels CACNIAS, SCN4A, and KCNJ2 predominantly. Although data on specific gene in idiopathic generalized epilepsy is relatively scarce, mutations of voltage gated sodium channel subunit genes (CACNB4) and nonsense mutations in voltage gated calcium channels (CACNA1A) have been linked to idiopathic generalized epilepsy in two families. We speculate that gene mutations altering the ability of the beta subunit to interact with the alpha subunit of the CaV1.1 channel and mutations in the pore-forming potassium channel subunit may be possible explanations for the combined manifestation of both diseases. Functional analysis of voltage gated calcium channel and other ion channels mutations may provide additional support and insight for the causal role of these mutations. The understanding of mutations in ion-channel genes will lead to improved diagnosis and treatment of such inherited channelopathies. PMID:25893123

  6. Idiopathic generalized epilepsy and hypokalemic periodic paralysis in a family of South Indian descent.

    PubMed

    Subramanian, Muthiah; Senthil, N; Sujatha, S

    2015-01-01

    Inherited channelopathies are a heterogeneous group of disorders resulting from dysfunction of ion channels in cellular membranes. They may manifest as diseases affecting skeletal muscle contraction, the conduction system of the heart, nervous system function, and vision syndromes. We describe a family of South Indian descent with hypokalemic periodic paralysis in which four members also have idiopathic generalized epilepsy. Hypokalemic periodic paralysis is a genetically heterogeneous channelopathy that has been linked to mutations in genes encoding three ion channels CACNIAS, SCN4A, and KCNJ2 predominantly. Although data on specific gene in idiopathic generalized epilepsy is relatively scarce, mutations of voltage gated sodium channel subunit genes (CACNB4) and nonsense mutations in voltage gated calcium channels (CACNA1A) have been linked to idiopathic generalized epilepsy in two families. We speculate that gene mutations altering the ability of the beta subunit to interact with the alpha subunit of the CaV1.1 channel and mutations in the pore-forming potassium channel subunit may be possible explanations for the combined manifestation of both diseases. Functional analysis of voltage gated calcium channel and other ion channels mutations may provide additional support and insight for the causal role of these mutations. The understanding of mutations in ion-channel genes will lead to improved diagnosis and treatment of such inherited channelopathies. PMID:25893123

  7. Weakness in the Emergency Department: Hypokalemic Periodic Paralysis Induced By Strenuous Physical Activity.

    PubMed

    Dogan, Nurettin Ozgur; Avcu, Nazire; Yaka, Elif; Isikkent, Ali; Durmus, Ugur

    2015-06-01

    Hypokalemic periodic paralysis is a rare but serious disorder that is typically caused by a channelopathy. Thyrotoxicosis, heavy exercise, high carbohydrate meal and some drugs can trigger channelopathy in genetically predisposed individuals. A 33-year-old male patient presented to the emergency department with weakness in the lower extremities. He stated that he had done heavy physical activity during the previous week. The patient exhibited motor weakness in the lower extremities (2/5 strength) during the physical examination. Initial laboratory tests showed a potassium level of 1.89 mEq/L. The initial electrocardiogram demonstrated T wave inversion and prominent U waves. The patient was treated in the emergency department with oral and intravenous potassium. The physical and ECG symptoms resolved within 16 hours of potassium supplementation and biochemical tests showed normal serum potassium levels. The patient was discharged shortly after the resolution of the symptoms. Weakness is an important but nonspecific symptom that may be brought on by a number of underlying physiological processes. Hypokalemic periodic paralysis is a rare disease that may be triggered by heavy physical activity and presents with recurrent admissions due to weakness. PMID:27336072

  8. Hypokalemic periodic paralysis; two different genes responsible for similar clinical manifestations.

    PubMed

    Kim, Hunmin; Hwang, Hee; Cheong, Hae Il; Park, Hye Won

    2011-11-01

    Primary hypokalemic periodic paralysis (HOKPP) is an autosomal dominant disorder manifesting as recurrent periodic flaccid paralysis and concomitant hypokalemia. HOKPP is divided into type 1 and type 2 based on the causative gene. Although 2 different ion channels have been identified as the molecular genetic cause of HOKPP, the clinical manifestations between the 2 groups are similar. We report the cases of 2 patients with HOKPP who both presented with typical clinical manifestations, but with mutations in 2 different genes (CACNA1Sp.Arg528His and SCN4A p.Arg672His). Despite the similar clinical manifestations, there were differences in the response to acetazolamide treatment between certain genotypes of SCN4A mutations and CACNA1S mutations. We identified p.Arg672His in the SCN4A gene of patient 2 immediately after the first attack through a molecular genetic testing strategy. Molecular genetic diagnosis is important for genetic counseling and selecting preventive treatment. PMID:22253645

  9. Hypokalemic periodic paralysis in Sjogren's syndrome secondary to distal renal tubular acidosis.

    PubMed

    Yılmaz, Hakkı; Kaya, Mustafa; Özbek, Mustafa; ÜUreten, Kemal; Safa Yıldırım, İ

    2013-07-01

    We report a 53-year-old Turkish female presented with progressive weakness and mild dyspnea. Laboratory results demonstrated severe hypokalemia with hyperchloremic metabolic acidosis. The urinary anion gap was positive in the presence of acidemia, thus she was diagnosed with hypokalemic paralysis from a severe distal renal tubular acidosis (RTA). Immunologic work-up showed a strongly positive ANA of 1:3,200 and positive antibodies to SSA and SSB. Schirmer's test was abnormal. Autoimmune and other tests revealed Sjögren syndrome as the underlying cause of the distal renal tubular acidosis. Renal involvement in Sjogren's syndrome (SS) is not uncommon and may precede sicca complaints. The pathology in most cases is a tubulointerstitial nephritis causing among other things, distal RTA, and, rarely, hypokalemic paralysis. Treatment consists of potassium repletion, alkali therapy, and corticosteroids. Primary SS could be a differential in women with acute weakness and hypokalemia. PMID:22212410

  10. Hypokalemic paralysis in a professional bodybuilder.

    PubMed

    Mayr, Florian B; Domanovits, Hans; Laggner, Anton N

    2012-09-01

    Severe hypokalemia is a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis. On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest. There may also be decreased motility of smooth muscle, manifesting with ileus or urinary retention. Rarely, severe hypokalemia may result in rhabdomyolysis. Other manifestations of severe hypokalemia include alteration of cardiac tissue excitability and conduction. Hypokalemia can produce electrocardiographic changes such as U waves, T-wave flattening, and arrhythmias, especially if the patient is taking digoxin. Common causes of hypokalemia include extrarenal potassium losses (vomiting and diarrhea) and renal potassium losses (eg, hyperaldosteronism, renal tubular acidosis, severe hyperglycemia, potassium-depleting diuretics) as well as hypokalemia due to potassium shifts (eg, insulin administration, catecholamine excess, familial periodic hypokalemic paralysis, thyrotoxic hypokalemic paralysis). Although the extent of diuretic misuse in professional bodybuilding is unknown, it may be regarded as substantial. Hence, diuretics must always be considered as a cause of hypokalemic paralysis in bodybuilders. PMID:21871759

  11. A case of periodic hypokalemic paralysis in a patient with celiac disease.

    PubMed

    Ranjan, Amitabh; Debata, Pradeep K

    2014-06-01

    A 4-year-old male child presented with recurrent episodes of diarrhoea for 6-months, each episode associated with weakness of all four limbs and documented hypokalemia who on examination had some pallor, short stature, flaccid quadriparesis with absent DTR. The patient responded clinically and biochemically to potassium supplement. TTG and Intestinal biopsy confirmed celiac disease. Patient was put on gluten free diet and patient is doing well with no recurrence. We present a case of Recurrent hypokalemic paralysis with previously unsuspected celiac disease who was not in celiac crisis. PMID:25121038

  12. Reversible electrophysiological abnormalities in hypokalemic paralysis: Case report of two cases.

    PubMed

    Sharma, C M; Nath, Kunal; Parekh, Jigar

    2014-01-01

    Compound muscle action potential (CMAP) amplitude declines during a paralytic attack in patients with hypokalemic periodic paralysis (HPP). However, serial motor nerve conduction studies in hypokalemic paralysis have not been commonly reported. We report two cases with hypokalemic paralysis, who had severely reduced CMAPs in all motor nerves at presentation during the episode of quadriparesis. However, the amplitude of CMAPs increased and reached normal levels, as the serum potassium concentration and motor power returned to normal state. PMID:24753672

  13. Exclusion of linkage between hypokalemic periodic paralysis and a candidate region in 1q31-32 suggests genetic heterogeneity

    SciTech Connect

    Sillen, A.; Wadelius, C.; Gustabson, K.H.

    1994-09-01

    Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant disease with attacks of paralysis of varying severity. The attacks occur at intervals of days to years in otherwise healthy people combined with hypokalemia during attacks. The paralysis attacks are precipitated by a number of different factors, like carbohydrate-rich meals, cold, exercise and mental stress. Recently linkage for HOKPP was shown for chromosome 1q31-32 and the disease was mapped between D1S413 and D1S249. The gene for the calcium channel alfa1-subunit (CACNL 1A3) maps to this interval and in two families no recombination was found between a polymorphism in the CACNL 1A3 gene and the disease. This gene is therefore considered to be a candidate for HOKPP. The analysis of a large Danish family excludes linkage to this region and to the CACNL 1A3 gene. In each direction from D1S413, 18.8 cM could be excluded and for D1S249, 14.9 cM. The present study clearly excludes the possibility that the gene causing HOKPP in a large Danish family is located in the region 1q31-32. This result shows that HOKPP is a heterogenous disease, with only one mapped gene so far.

  14. [Thyrotoxic hypokalemic periodic paralysis: 18 cases with different forms of thyrotoxicosis].

    PubMed

    Piraino Neuenschwander, P; Pumarino Carte, H; Bidegain González, F; Zura Jiménez, M L; Ferreiro Merino, F

    1995-05-01

    Thyrotoxic periodic paralysis (TPP) is a rare complication of thyrotoxicosis in whites but it is commonly reported in oriental populations. Eighteen males with TPP were studied from 1966 to 1993 (17 years) with a mean age of 32.8 years (range: 22-50 years). Their ancestor, traced back as possible, was hispanic in 15 and autoctonous indigens (mapuche) in three. They had one or more episodes of flaccid paralysis with complete recovery associated with thyrotoxicosis and hypokalemia (in the twelve patients who had their serum potassium determined). Two patients had respiratory compromise. Ten patients had their crisis onset after physical exertion and/or copious ingestion of carbohydrates. Only one of the patients had severe thyrotoxicosis and the diagnosis was made after the periodic paralysis in ten of them. The types of thyrotoxicosis associated with TPP were: Graves-Basedow disease in 13, subacute thyroitidis in three, and overdosage of thyroid hormone in two patients. In summary, TPP can occur in latin american populations, may be fatal, and is not always associated with Graves-Basedow disease. PMID:7617935

  15. The large-conductance calcium-activated potassium channel holds the key to the conundrum of familial hypokalemic periodic paralysis

    PubMed Central

    Kim, Sung-Jo; Kang, Sun-Yang; Yi, Jin Woong; Kim, Seung-Min

    2014-01-01

    Purpose Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant channelopathy characterized by episodic attacks of muscle weakness and hypokalemia. Mutations in the calcium channel gene, CACNA1S, or the sodium channel gene, SCN4A, have been found to be responsible for HOKPP; however, the mechanism that causes hypokalemia remains to be determined. The aim of this study was to improve the understanding of this mechanism by investigating the expression of calcium-activated potassium (KCa) channel genes in HOKPP patients. Methods We measured the intracellular calcium concentration with fura-2-acetoxymethyl ester in skeletal muscle cells of HOKPP patients and healthy individuals. We examined the mRNA and protein expression of KCa channel genes (KCNMA1, KCNN1, KCNN2, KCNN3, and KCNN4) in both cell types. Results Patient cells exhibited higher cytosolic calcium levels than normal cells. Quantitative reverse transcription polymerase chain reaction analysis showed that the mRNA levels of the KCa channel genes did not significantly differ between patient and normal cells. However, western blot analysis showed that protein levels of the KCNMA1 gene, which encodes KCa1.1 channels (also called big potassium channels), were significantly lower in the membrane fraction and higher in the cytosolic fraction of patient cells than normal cells. When patient cells were exposed to 50 mM potassium buffer, which was used to induce depolarization, the altered subcellular distribution of BK channels remained unchanged. Conclusion These findings suggest a novel mechanism for the development of hypokalemia and paralysis in HOKPP and demonstrate a connection between disease-associated mutations in calcium/sodium channels and pathogenic changes in nonmutant potassium channels. PMID:25379045

  16. Thyrotoxic hypokalemic periodic paralysis is a rare but potentially fatal emergency: case report and literature review.

    PubMed

    Gómez-Torres, Jeisa Y; Bravo-Llerena, Wilfredo E; Reyes-Ortiz, Luis M; Valderrábano-Wagner, Rodrigo J; Mariano-Mejías, Victor; Brunet-Rodríguez, Héctor; Lemos-Ramírez, Juan C

    2011-01-01

    We report a case of a 39 year-old Asian man in whom profound lower limb paralysis, along with severe hypokalemia and electrocardiographic changes, were the presenting features of Graves' disease (GD)-related thyrotoxicosis. Rapid recognition and management of the disorder were the key factors to avoid fatal hypokalemia-induced cardiac arrhythmias and promptly restore patient's capacity to ambulate. PMID:22111475

  17. Disrupted coupling of gating charge displacement to Na+ current activation for DIIS4 mutations in hypokalemic periodic paralysis.

    PubMed

    Mi, Wentao; Rybalchenko, Volodymyr; Cannon, Stephen C

    2014-08-01

    Missense mutations at arginine residues in the S4 voltage-sensor domains of NaV1.4 are an established cause of hypokalemic periodic paralysis, an inherited disorder of skeletal muscle involving recurrent episodes of weakness in conjunction with low serum K(+). Expression studies in oocytes have revealed anomalous, hyperpolarization-activated gating pore currents in mutant channels. This aberrant gating pore conductance creates a small inward current at the resting potential that is thought to contribute to susceptibility to depolarization in low K(+) during attacks of weakness. A critical component of this hypothesis is the magnitude of the gating pore conductance relative to other conductances that are active at the resting potential in mammalian muscle: large enough to favor episodes of paradoxical depolarization in low K(+), yet not so large as to permanently depolarize the fiber. To improve the estimate of the specific conductance for the gating pore in affected muscle, we sequentially measured Na(+) current through the channel pore, gating pore current, and gating charge displacement in oocytes expressing R669H, R672G, or wild-type NaV1.4 channels. The relative conductance of the gating pore to that of the pore domain pathway for Na(+) was 0.03%, which implies a specific conductance in muscle from heterozygous patients of ∼ 10 µS/cm(2) or 1% of the total resting conductance. Unexpectedly, our data also revealed a substantial decoupling between gating charge displacement and peak Na(+) current for both R669H and R672G mutant channels. This decoupling predicts a reduced Na(+) current density in affected muscle, consistent with the observations that the maximal dV/dt and peak amplitude of the action potential are reduced in fibers from patients with R672G and in a knock-in mouse model of R669H. The defective coupling between gating charge displacement and channel activation identifies a previously unappreciated mechanism that contributes to the reduced

  18. Disrupted coupling of gating charge displacement to Na+ current activation for DIIS4 mutations in hypokalemic periodic paralysis

    PubMed Central

    Mi, Wentao; Rybalchenko, Volodymyr

    2014-01-01

    Missense mutations at arginine residues in the S4 voltage-sensor domains of NaV1.4 are an established cause of hypokalemic periodic paralysis, an inherited disorder of skeletal muscle involving recurrent episodes of weakness in conjunction with low serum K+. Expression studies in oocytes have revealed anomalous, hyperpolarization-activated gating pore currents in mutant channels. This aberrant gating pore conductance creates a small inward current at the resting potential that is thought to contribute to susceptibility to depolarization in low K+ during attacks of weakness. A critical component of this hypothesis is the magnitude of the gating pore conductance relative to other conductances that are active at the resting potential in mammalian muscle: large enough to favor episodes of paradoxical depolarization in low K+, yet not so large as to permanently depolarize the fiber. To improve the estimate of the specific conductance for the gating pore in affected muscle, we sequentially measured Na+ current through the channel pore, gating pore current, and gating charge displacement in oocytes expressing R669H, R672G, or wild-type NaV1.4 channels. The relative conductance of the gating pore to that of the pore domain pathway for Na+ was 0.03%, which implies a specific conductance in muscle from heterozygous patients of ∼10 µS/cm2 or 1% of the total resting conductance. Unexpectedly, our data also revealed a substantial decoupling between gating charge displacement and peak Na+ current for both R669H and R672G mutant channels. This decoupling predicts a reduced Na+ current density in affected muscle, consistent with the observations that the maximal dV/dt and peak amplitude of the action potential are reduced in fibers from patients with R672G and in a knock-in mouse model of R669H. The defective coupling between gating charge displacement and channel activation identifies a previously unappreciated mechanism that contributes to the reduced excitability of affected

  19. Hypokalemic periodic paralysis

    MedlinePlus

    ... a vein (IV). Taking potassium supplements will not prevent attacks. Avoiding alcohol and eating a low-carbohydrate diet may help. A medicine called acetazolamide may be prescribed to prevent attacks. Your doctor may tell you to also ...

  20. Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome.

    PubMed

    Baldane, S; Ipekci, S H; Celik, S; Gundogdu, A; Kebapcilar, L

    2015-01-01

    A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic paralysis. Later on, despite the euthyroid condition and potassium chloride treatment, hypokalemia persisted. Further investigations revealed hyperreninemic hyperaldosteronism. The patient was considered to have Gitelman's syndrome (GS) and all genetic analysis was done. A c. 1145C>T, p. Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3, exon 9 was detected and GS was confirmed. PMID:25838649

  1. Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome

    PubMed Central

    Baldane, S.; Ipekci, S. H.; Celik, S.; Gundogdu, A.; Kebapcilar, L.

    2015-01-01

    A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic paralysis. Later on, despite the euthyroid condition and potassium chloride treatment, hypokalemia persisted. Further investigations revealed hyperreninemic hyperaldosteronism. The patient was considered to have Gitelman's syndrome (GS) and all genetic analysis was done. A c. 1145C>T, p. Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3, exon 9 was detected and GS was confirmed. PMID:25838649

  2. Hypokalemic periodic paralysis in primary hyperaldosteronism. Subclinical myopathy with atrophy of the type 2A muscle fibers.

    PubMed

    Bautista, J; Gil-Neciga, E; Gil-Peralta, A

    1979-01-01

    A case of a patient suffering from primary hyperaldosteronism is reported. In this case the disease is manifested clinically by periodic paralysis and hypopotasemia without permanent myopathy. The morphological study of the muscle demonstrates selective atrophy of the type 2A fibers as the most pronounced alteration. These findings suggest a chronic myopathic process. PMID:546663

  3. Confirmation of linkage of Hypokalemic periodic paralysis to chromosome 1q31-32: Further evidence supporting CACNL1A3 as a candidate gene

    SciTech Connect

    Lewis, K.; Knouff, C.; Gaskell, P.C.

    1994-09-01

    Hypokalemic periodic paralysis (HOKPP; MIM 170400) is one entity of a series of periodic paralyses characterized by episodic bouts of weakness with onset in the second to third decades. The hypokalemic form is defined by decreased serum potassium during a paralytic attack. HOKPP can occur in both familial and sporadic forms; the familal form is autosomal dominant with reduced penetrance in female gene carriers. Recently, Fontaine et al. have localized HOKPP to 1q31-32 in three multigenerational HOKPP families. The region of sub-localization includes the CACNL1A3 gene, making it a potential candidate for the genetic defect in HOKPP. We have ascertained and sampled 2 large multigenerational HOKPP pedigrees (N = 55 individuals with DNA) for linkage analysis. The families were initially screened for linkage with over 150 marker loci located throughout the genome. Analysis of the chromosome 1 markers D1S412, D1S413 and F13B gave significant evidence for linkage. The peak two-point lod score realized was Z = 4.34 at theta = 0.0 (D1S413). A sex-dependent penetrance of 80% was assumed, although varying the penetrance did not significantly alter the results. There was no evidence for heterogeneity. Multipoint analysis of the data defined the region between D1S238 and D1S245 (which contains the CACNL1A3 gene) as the most likely region (> 1000 odds) for the location of the HOKPP gene. There were no obligate recombinants among males or affected females for the CACNL1A3 (Z = 3.19, theta = 0.0), although several potential non-penetrant females were identified. These studies confirm linkage of HOPKK to chromosome 1 in an independent data set, lend further support of CACNL1A3 as a potential candidate gene, and give evidence for homogeneity in this disease.

  4. Sporadic hypokalemic paralysis caused by osmotic diuresis in diabetes mellitus.

    PubMed

    Vishnu, Venugopalan Y; Kattadimmal, Anoop; Rao, Suparna A; Kadhiravan, Tamilarasu

    2014-07-01

    A wide variety of neurological manifestations are known in patients with diabetes mellitus. We describe a 40-year-old man who presented with hypokalemic paralysis. On evaluation, we found that the cause of the hypokalemia was osmotic diuresis induced by marked hyperglycemia due to undiagnosed diabetes mellitus. The patient had an uneventful recovery with potassium replacement, followed by glycemic control with insulin. Barring a few instances of symptomatic hypokalemia in the setting of diabetic emergencies, to our knowledge uncomplicated hyperglycemia has not been reported to result in hypokalemic paralysis. PMID:24472241

  5. A case of hypokalemic paralysis in a patient with neurogenic diabetes insipidus.

    PubMed

    Nguyen, Frederic N; Kar, Jitesh K; Verduzco-Gutierrez, Monica; Zakaria, Asma

    2014-04-01

    Acute hypokalemic paralysis is characterized by muscle weakness or paralysis secondary to low serum potassium levels. Neurogenic diabetes insipidus (DI) is a condition where the patient excretes large volume of dilute urine due to low levels of antidiuretic hormone. Here, we describe a patient with neurogenic DI who developed hypokalemic paralysis without a prior history of periodic paralysis. A 30-year-old right-handed Hispanic male was admitted for refractory seizures and acute DI after developing a dental abscess. He had a history of pituitary adenoma resection at the age of 13 with subsequent pan-hypopituitarism and was noncompliant with hormonal supplementation. On hospital day 3, he developed sudden onset of quadriplegia with motor strength of 0 of 5 in the upper extremities bilaterally and 1 of 5 in both lower extremities with absent deep tendon reflexes. His routine laboratory studies revealed severe hypokalemia of 1.6 mEq/dL. Nerve Conduction Study (NCS) revealed absent compound motor action potentials (CMAPs) with normal sensory potentials. Electromyography (EMG) did not reveal any abnormal insertional or spontaneous activity. He regained full strength within 36 hours following aggressive correction of the hypokalemia. Repeat NCS showed return of CMAPs in all nerves tested and EMG revealed normal motor units and normal recruitment without myotonic discharges. In patients with central DI with polyuria, hypokalemia can result in sudden paralysis. Hypokalemic paralysis remains an important differential in an acute case of paralysis and early recognition and appropriate management is key. PMID:24707338

  6. Ion permeation and block of the gating pore in the voltage sensor of NaV1.4 channels with hypokalemic periodic paralysis mutations.

    PubMed

    Sokolov, Stanislav; Scheuer, Todd; Catterall, William A

    2010-08-01

    Hypokalemic periodic paralysis and normokalemic periodic paralysis are caused by mutations of the gating charge-carrying arginine residues in skeletal muscle Na(V)1.4 channels, which induce gating pore current through the mutant voltage sensor domains. Inward sodium currents through the gating pore of mutant R666G are only approximately 1% of central pore current, but substitution of guanidine for sodium in the extracellular solution increases their size by 13- +/- 2-fold. Ethylguanidine is permeant through the R666G gating pore at physiological membrane potentials but blocks the gating pore at hyperpolarized potentials. Guanidine is also highly permeant through the proton-selective gating pore formed by the mutant R666H. Gating pore current conducted by the R666G mutant is blocked by divalent cations such as Ba(2+) and Zn(2+) in a voltage-dependent manner. The affinity for voltage-dependent block of gating pore current by Ba(2+) and Zn(2+) is increased at more negative holding potentials. The apparent dissociation constant (K(d)) values for Zn(2+) block for test pulses to -160 mV are 650 +/- 150 microM, 360 +/- 70 microM, and 95.6 +/- 11 microM at holding potentials of 0 mV, -80 mV, and -120 mV, respectively. Gating pore current is blocked by trivalent cations, but in a nearly voltage-independent manner, with an apparent K(d) for Gd(3+) of 238 +/- 14 microM at -80 mV. To test whether these periodic paralyses might be treated by blocking gating pore current, we screened several aromatic and aliphatic guanidine derivatives and found that 1-(2,4-xylyl)guanidinium can block gating pore current in the millimolar concentration range without affecting normal Na(V)1.4 channel function. Together, our results demonstrate unique permeability of guanidine through Na(V)1.4 gating pores, define voltage-dependent and voltage-independent block by divalent and trivalent cations, respectively, and provide initial support for the concept that guanidine-based gating pore blockers

  7. A primary Sjögren's syndrome patient with distal renal tubular acidosis, who presented with symptoms of hypokalemic periodic paralysis: Report of a case study and review of the literature.

    PubMed

    Soy, Mehmet; Pamuk, Omer Nuri; Gerenli, Murat; Celik, Yahya

    2005-11-01

    Although renal tubular acidosis (RTA), secondary to autoimmune interstitial nephritis, develops in a large proportion of patients with Sjögren's syndrome (SS), most of the subjects are asymptomatic. Here, we shall present a 39-year-old female patient who came to us with hypokalemic periodic paralysis (HPP), and who was later diagnosed with distal RTA. The patient, who had xerostomia and xerophthalmia for a long period of time, was diagnosed with primary SS from serologic and histologic findings. The patient recovered by being prescribed potassium replacement therapy. Although renal biopsy was not performed, corticosteroids were administered because HPP indicated severe interstitial nephritis. HPP did not reoccur during a 2-year follow-up period. We also review cases with SS-related distal RTA and HPP. PMID:15690142

  8. Dengue-associated hypokalemic paralysis: causal or incidental?

    PubMed

    Malhotra, Hardeep Singh; Garg, Ravindra Kumar

    2014-05-15

    Dengue-associated hypokalemic paralysis is considered an important but under-emphasized neuromuscular complication of dengue virus infection. Review of the published literature reveals that 35 instances of hypokalemic paralysis associated with dengue have been recorded from the Indian subcontinent and all but two, were males. The median age of presentation is 29 years and moderate to severe grade pure motor quadriparesis is precipitated during the phase of defervescence of moderate to high-grade fever. Recovery starts within 12h of potassium supplementation and is usually complete in a couple of days. Redistribution or increased loss of potassium from the body is speculated as the pathophysiological mechanism involved in the causation of hypokalemia. It is not possible to derive the exact etiopathological correlation from the published literature either due to a lack of comprehensive reporting or inadequate work-up of the patients. Curious is the fact that only 35 patients had manifest-paralysis when more than two-thirds affected with the dengue virus exhibit hypokalemia; whether this indicates a genetically mediated channel disorder or an incidental association remains to be seen. PMID:24680561

  9. Hypokalemic paralysis secondary to tenofovir induced fanconi syndrome.

    PubMed

    Ramteke, Vishal V; Deshpande, Rushi V; Srivastava, Om; Wagh, Adinath

    2015-01-01

    Tenofovir induced fanconi syndrome (FS) presenting as hypokalemic paralysis is an extremely rare complication in patients on anti-retroviral therapy. We report a 50-year-old male with acquired immunodeficiency syndrome on tenofovir-based anti-retroviral therapy who presented with acute onset quadriparesis. On evaluation, he was found to have hypokalemia with hypophosphatemia, glucosuria and proteinuria suggesting FS. He regained normal power in limbs over next 12 h following correction of hypokalemia. Ours would be the second reported case in India. PMID:26692618

  10. Tenofovir induced Fanconi syndrome: A rare cause of hypokalemic paralysis.

    PubMed

    Venkatesan, E P; Pranesh, M B; Gnanashanmugam, G; Balasubramaniam, J

    2014-03-01

    We report a 55-year-old female who presented to the emergency department with acute onset quadriparesis. She was diagnosed to have acquired immunodeficiency syndrome 7 years ago and was on tenofovir based anti-retroviral therapy for past 10 months. As the patient also had hypophosphatemia, glucosuria and proteinuria Fanconi syndrome (FS) was suspected. She improved dramatically over next 12 h to regain normal power and also her renal functions improved over next few days. Tenofovir induced FS presenting as hypokalemic paralysis is very rare complication and is the first case reported from India. PMID:24701043

  11. Hypokalemic paralysis secondary to tenofovir induced fanconi syndrome

    PubMed Central

    Ramteke, Vishal V.; Deshpande, Rushi V.; Srivastava, Om; Wagh, Adinath

    2015-01-01

    Tenofovir induced fanconi syndrome (FS) presenting as hypokalemic paralysis is an extremely rare complication in patients on anti-retroviral therapy. We report a 50-year-old male with acquired immunodeficiency syndrome on tenofovir-based anti-retroviral therapy who presented with acute onset quadriparesis. On evaluation, he was found to have hypokalemia with hypophosphatemia, glucosuria and proteinuria suggesting FS. He regained normal power in limbs over next 12 h following correction of hypokalemia. Ours would be the second reported case in India. PMID:26692618

  12. Thyrotoxic periodic paralysis.

    PubMed

    Balakrishnan, Rojith Karanode; Chandran, Suresh Rama; Thirumalnesan, Geetha; Doraisamy, Nedumaran

    2011-07-01

    This article aims at highlighting the importance of suspecting thyrotoxicosis in cases of recurrent periodic flaccid paralysis; especially in Asian men to facilitate early diagnosis of the former condition. A case report of a 28 year old male patient with recurrent periodic flaccid paralysis has been presented. Hypokalemia secondary to thyrotoxicosis was diagnosed as the cause of the paralysis. The patient was given oral potassium intervention over 24 hours. The patient showed complete recovery after the medical intervention and was discharged after 24 hours with no residual paralysis. Thyrotoxic periodic paralysis (TPP) is a complication of thyrotoxicosis, more common amongst males in Asia. It presents as acute flaccid paralysis in a case of hyperthyroidism with associated hypokalemia. The features of thyrotoxicosis may be subtle or absent. Thus, in cases of recurrent or acute flaccid muscle paralysis, it is important to consider thyrotoxicosis as one of the possible causes, and take measures accordingly. PMID:21966655

  13. [Hypokalemic paralysis during pregnancy: a report of two cases].

    PubMed

    Hernández Pacheco, José Antonio; Estrada Altamirano, Ariel; Pérez Borbón, Guadalupe María; Torres Torres, Cutberto

    2009-12-01

    The hypokalemic paralysis is a disease characterized by the development of acute muscular weakness, associated to low levels of blood potassium (< 3.5 meq/L). Here we present two cases: in the first one, a 23 years old woman, with 15.5 weeks of gestation has a cuadriplegia associated to blood potassium level of 1.4 meq/L, diagnosed with distal tubular acidosis; she required mechanical ventilation for respiratory paralysis. The medical profile remits with potassium intravenous replacement and the pregnancy ends with a spontaneous abortion. The second case is a 15 years old woman with 26.5 weeks of pregnancy, who suffers a generalized paralysis with blood potassium of 2.7 meq/L, requiring also mechanical ventilation for respiratory paralysis; the final diagnosis was Barterr syndrome, and the medical profile remited after potassium supplement. Her pregnancy got complicated with a severe preeclampsia, enough reason for interrumpting the pregnancy at 29.1 weeks of gestation. In both cases Guilliain-Barre syndrome was ruled out. PMID:20077884

  14. Molecular basis for hyperkalemic periodic paralysis.

    PubMed

    Brown, R H

    At least one form of periodic paralysis is a direct consequence of a mutation in a skeletal muscle, voltage-sensitive sodium channel--it was observed that many individual with this disease developed low serum potassium levels during paralytic episodes. Some families had hyperkalemic paralysis with serum potassium levels of 6 or 7 mEg/L during paralytic crises. In both hypokalemic and hyperkalemic paralysis one of the precipitants is a period of rest after exertion. In hypokalemic periodic paralysis carbohydrates may initiate weakness. In both hyper- and hypokalemic forms, the disorder is inherited as an autosomal dominant trait. During hypokalemic and hyperkalemic paralysis, one might respectively anticipate muscle hyperpolarization or depolarization. Has been observed a potassium-related abnormality of sodium conductance in the pathogenesis at least of the hyperkalemic form of periodic paralysis. The fact that TTX reverses the physiological defect suggested the hypothesis that the primary problem might be a mutation in a TTX-sensitive sodium channel. The protein consists of some 2000 amino acids with characteristic intracytoplasmic and extracellular domains as well a four remarkably conserved membrane spanning domains, each composed of six transmembrane of a polymorphism of the human sodium channel with hyperkalemic paralysis. When multipoint analysis was used to test for coinheritance of the disease with both Na-2 and growth hormone polymorphisms, a lod score of 7 was obtained. That is, the ratio of the probability of linkage to non-linkage is 10 million to one. When extracellular potassium is increased to 10 mM, the affected myotubes demonstrate strikingly abnormal channel behavior characterized by prolonged open times or repetitive opens throughout the voltage step. Potassium implicate as a primary factor triggering an abnormal sodium channel gating mode and, as a result, aberrant sodium current behavior. It was estimated that, for the normal channel, the

  15. Thyrotoxic periodic paralysis

    MedlinePlus

    ... high levels of thyroid hormone in their blood ( hyperthyroidism , thyrotoxicosis). Causes This is a rare condition that ... include a family history of periodic paralysis and hyperthyroidism. Symptoms Symptoms involve attacks of muscle weakness or ...

  16. Thyrotoxic periodic paralysis: an endocrine cause of paraparesis.

    PubMed

    Munir, Atif

    2014-05-01

    Periodic paralysis is a muscle disorder that belongs to the family of diseases called channelopathies, manifested by episodes of painless muscle weakness. Periodic paralysis is classified as hypokalemic when episodes occur in association with low potassium levels. Most cases are hereditary. Acquired cases have been described in association with hyperthyroidism. Diagnosis is made on clinical and biochemical grounds. Patients may be markedly hypokalemic during the episode and respond well to potassium supplementation. Episodes can be prevented by achieving a euthyroid state. This report describes a young gentleman presenting with thyrotoxic hypokalemic paraparesis. The condition needs to be considered in the differential diagnosis of neuromuscular weakness in the context of hypokalemia by the treating physicians. PMID:24906287

  17. Thyrotoxic periodic paralysis

    SciTech Connect

    Ferreiro, J.E.; Arguelles, D.J.; Rams, H. Jr.

    1986-01-01

    A case of thyrotoxic periodic paralysis is reported in a Hispanic man with an unusual recurrence six weeks after radioactive iodine treatment. Thyrotoxic periodic paralysis has now been well characterized in the literature: it occurs primarily in Orientals with an overwhelming male preponderance and a higher association of specific HLA antigens. Clinical manifestations include onset after high carbohydrate ingestion or heavy exertion, with progressive symmetric weakness leading to flaccid paralysis of the extremities and other muscle groups, lasting several hours. If hypokalemia is present, potassium administration may help abort the attack. Although propranolol can be efficacious in preventing further episodes, the only definitive treatment is establishing a euthyroid state. The pathophysiology is still controversial, but reflects altered potassium and calcium dynamics as well as certain morphologic characteristics within the muscle unit itself.

  18. An unusual case of dengue infection presenting with hypokalemic paralysis with hypomagnesemia.

    PubMed

    Jain, Rajendra Singh; Gupta, Pankaj Kumar; Agrawal, Rakesh; Kumar, Sunil; Khandelwal, Kapil

    2015-08-01

    Neurological manifestations are unusual in dengue fever and can be due to neurotropic effect, systemic complications of dengue infection, or immune mediated. Acute hypokalemic paralysis is a rare systemic complication of dengue infection; however, hypokalemia along with hypomagnesemia has not been reported earlier. We herein report an extremely unusual and probably the first case of dengue infection in a 30-year-old male who presented to us with hypokalemic paralysis along with hypomagnesemia. This case report highlights that hypomagnesemia may be a significant complication in dengue infection. Correction of hypomagnesemia is of paramount importance to avoid refractory hypokalemia leading to severe consequences. PMID:26209406

  19. An unusual case of hypokalemic paralysis associated with primary Sjogren's syndrome.

    PubMed

    Toy, Walton C; Jasin, Hugo E

    2008-06-01

    43-year-old Caucasian female presented with progressive weakness and dyspnea. She was diagnosed with hypokalemic paralysis from a severe distal renal tubular acidosis (RTA). Immunologic work-up showed a strongly positive ANA of 1:640 and positive antibodies to SSA and SSB. Schirmer's test was normal. Renal involvement in Sjogren's syndrome (SS) is not uncommon and may precede sicca complaints. The pathology in most cases is a tubulointerstitial nephritis causing among other things, distal RTA, and, rarely, hypokalemic paralysis. Treatment consists of potassium repletion, alkali therapy and corticosteroids. Primary SS should be a differential in premenopausal women with acute weakness and hypokalemia. PMID:18564466

  20. Apparently persistent weakness after recurrent hypokalemic paralysis: a tale of two disorders.

    PubMed

    Ramachandiran, Nandhagopal

    2008-09-01

    A 19-year-old woman presented with recurrent hypokalemic paralysis, followed by apparently persistent symptoms due to coexisting osteomalacia. Distal renal tubular acidosis type 1 (dRTA1) linked the metabolic abnormalities and occurred as an extraglandular feature of Sjögren syndrome (SS). This case highlights the fact that in the setting of recurrent hypokalemia, apparently progressive weakness should be distinguished from primary hypokalemic paralysis and evaluated for dRTA1, as the metabolic alterations are potentially treatable. Further dRTA1 may precede the occurrence of sicca syndrome in SS. PMID:18708979

  1. Thyrotoxic periodic paralysis triggered by β2-adrenergic bronchodilators.

    PubMed

    Yeh, Fu-Chiang; Chiang, Wen-Fang; Wang, Chih-Chiang; Lin, Shih-Hua

    2014-05-01

    Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110 mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP. PMID:24852589

  2. Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Chronic Alcoholism

    PubMed Central

    Tsai, Ming-Hsien; Lin, Shih-Hua; Leu, Jyh-Gang; Fang, Yu-Wei

    2015-01-01

    Abstract Thyrotoxic periodic paralysis (TPP) is characterized by the presence of muscle paralysis, hypokalemia, and hyperthyroidism. We report the case of a young man with paralysis of the lower extremities, severe hypokalemia, and concurrent hyperthyroidism. TPP was suspected; therefore, treatment consisting of judicious potassium (K+) repletion and β-blocker administration was initiated. However, urinary K+ excretion rate, as well as refractoriness to treatment, was inconsistent with TPP. Chronic alcoholism was considered as an alternative cause of hypokalemia, and serum K+ was restored through vigorous K+ repletion and the addition of K+-sparing diuretics. The presence of thyrotoxicosis and hypokalemia does not always indicate a diagnosis of TPP. Exclusion of TPP can be accomplished by immediate evaluation of urinary K+ excretion, acid-base status, and the amount of potassium chloride required to correct hypokalemia at presentation. PMID:26426670

  3. Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace.

    PubMed

    Yun, Seong Eun; Kang, Yeojin; Bae, Eun Jin; Hwang, Kyungo; Jang, Ha Nee; Cho, Hyun Seop; Chang, Se-Ho; Park, Dong Jun

    2014-04-01

    A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8 mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3 = 130.40 ng/dL, TSH = 0.06 mIU/L, and free T4 = 1.73 ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4 mmol/L by intravenous infusion of only 40 mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient's thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea. PMID:24344747

  4. Periodic paralysis and the sodium-potassium pump.

    PubMed

    Layzer, R B

    1982-06-01

    Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium. PMID:6287910

  5. Hypokalemic paralysis as a presenting manifestation of primary Sjögren's syndrome: A report of two cases.

    PubMed

    Khandelwal, Deepak; Bhattacharya, Saptarshi; Khadgawat, Rajesh; Kaur, Satbir; Tandon, Nikhil; Ammini, Ariachery C

    2012-09-01

    Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease characterized by a progressive lymphocytic infiltration of the exocrine glands with varying degrees of systemic involvement. Overt or latent renal tubular acidosis (RTA), caused by tubulointerstitial nephropathy, is a common extraglandular manifestation of pSS. Hypokalemic paralysis is a well known, albeit rare complication of severe distal RTA from any cause. Cases of pSS manifesting for the first time as hypokalemic paralysis caused by distal RTA have been rarely reported. We herein present our experience of two cases, who presented to us for evaluation of hypokalemic paralysis and on work up found evidence of distal RTA, which on further work up found to be secondary to pSS. A high index of suspicion for pSS should be kept in all patients with hypokalemic paralysis. PMID:23087883

  6. Thyrotoxic Periodic Paralysis: An Underdiagnosed and Under-recognized Condition.

    PubMed

    Tella, Sri Harsha; Kommalapati, Anuhya

    2015-01-01

    Thyrotoxic hypokalemic periodic paralysis (TPP) is a condition characterized by the triad of acute hypokalemia without total body potassium deficit, episodic muscle paralysis, and thyrotoxicosis. We describe two cases of thyrotoxic periodic paralysis who presented to our hospital with potassium values of 1.3 MeQ/l and 1.2 MeQ/l, respectively. Surprisingly, the two patients had no documented past medical history. Based on the clinical features of high heart rate, palpitations (seen in both the patients), and exophthalmos (seen in one patient), thyrotoxic periodic paralysis was suspected. A thorough laboratory workup confirmed the diagnosis of thyrotoxicosis. Beta blockers were initiated promptly, along with intravenous potassium chloride, and the patients eventually improved symptomatically. These patients were eventually diagnosed with Graves' disease and were placed on methimazole, which prevented further attacks. Thyroid periodic paralysis (TPP) is a rare clinical manifestation of hyperthyroidism. Patients present with sudden onset paralysis associated with severe hypokalemia. The presence of paralysis and hypokalemia in a patient who has a history of hyperthyroidism should prompt the physician about thyrotoxic periodic paralysis. A high index of suspicion, prompt diagnosis, and management of the condition can prevent severe complications, such as cardiac arrhythmias. PMID:26623197

  7. Thyrotoxic Periodic Paralysis: An Underdiagnosed and Under-recognized Condition

    PubMed Central

    Kommalapati, Anuhya

    2015-01-01

    Thyrotoxic hypokalemic periodic paralysis (TPP) is a condition characterized by the triad of acute hypokalemia without total body potassium deficit, episodic muscle paralysis, and thyrotoxicosis. We describe two cases of thyrotoxic periodic paralysis who presented to our hospital with potassium values of 1.3 MeQ/l and 1.2 MeQ/l, respectively. Surprisingly, the two patients had no documented past medical history. Based on the clinical features of high heart rate, palpitations (seen in both the patients), and exophthalmos (seen in one patient), thyrotoxic periodic paralysis was suspected. A thorough laboratory workup confirmed the diagnosis of thyrotoxicosis. Beta blockers were initiated promptly, along with intravenous potassium chloride, and the patients eventually improved symptomatically. These patients were eventually diagnosed with Graves’ disease and were placed on methimazole, which prevented further attacks. Thyroid periodic paralysis (TPP) is a rare clinical manifestation of hyperthyroidism. Patients present with sudden onset paralysis associated with severe hypokalemia. The presence of paralysis and hypokalemia in a patient who has a history of hyperthyroidism should prompt the physician about thyrotoxic periodic paralysis. A high index of suspicion, prompt diagnosis, and management of the condition can prevent severe complications, such as cardiac arrhythmias. PMID:26623197

  8. Genetics Home Reference: hypokalemic periodic paralysis

    MedlinePlus

    ... by the flow of certain positively charged atoms (ions) into muscle cells. The CACNA1S and SCN4A proteins form channels that control the flow of these ions. The channel formed by the CACNA1S protein transports ...

  9. Rifampin-associated tubulointersititial nephritis and Fanconi syndrome presenting as hypokalemic paralysis

    PubMed Central

    2013-01-01

    Background Rifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin. Case presentation A 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and β2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient’s clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria. Conclusion This case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin. PMID:23320835

  10. Life-threatening hypokalemic paralysis in a young bodybuilder.

    PubMed

    Cheung, Kitty K T; So, Wing-Yee; Kong, Alice P S; Ma, Ronald C W; Chow, Francis C C

    2014-01-01

    We report a case of life-threatening hypokalemia in a 28-year-old bodybuilder who presented with sudden onset bilateral lower limbs paralysis few days after his bodybuilding competition. His electrocardiogram (ECG) showed typical u-waves due to severe hypokalemia (serum potassium 1.6 mmol/L, reference range (RR) 3.5-5.0 mmol/L). He was admitted to the intensive care unit (ICU) and was treated with potassium replacement. The patient later admitted that he had exposed himself to weight loss agents of unknown nature, purchased online, and large carbohydrate loads in preparation for the competition. He made a full recovery after a few days and discharged himself from the hospital against medical advice. The severe hypokalemia was thought to be caused by several mechanisms to be discussed in this report. With the ever rising number of new fitness centers recently, the ease of online purchasing of almost any drug, and the increasing numbers of youngsters getting into the bodybuilding arena, clinicians should be able to recognize the possible causes of sudden severe hypokalemia in these patients in order to revert the pathophysiology. PMID:24660073

  11. Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome.

    PubMed

    Chiang, Wen-Fang; Lin, Shih-Hung; Chan, Jenq-Shyong; Lin, Shih-Hua

    2014-02-01

    Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal < 0.22 mmol/mol), high plasma renin activity, but normal plasma aldosterone concentration. Abdominal sonography revealed neither renal stones nor nephrocalcinosis. Acquired causes of cBS such as autoimmune disease and drugs were all excluded. Molecular analysis of the CLCNKB gene, encoding ClC-Kb, and SLC12A3, encoding the thiazide-sensitive sodium chloride cotransporter (NCC), revealed compound heterozygous mutations in CLCNKB (L335P and G470E) inherited from her parents; her SLC12A3 was normal. These two mutations were not identified in 100 healthy subjects. Her plasma K+ concentration rose to 3 - 3.5 mmol/l after the addition of spironolactone. Inherited cBS may present with hypokalemic paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis. PMID:22854165

  12. Thyrotoxic periodic paralysis in Caucasian patients: a diagnostic challenge.

    PubMed

    Pichon, Bertrand; Lidove, Olivier; Delbot, Thierry; Aslangul, Elisabeth; Hausfater, Pierre; Papo, Thomas

    2005-09-01

    Secondary hypokalemic periodic paralysis is rare. However, when it occurs, it is usually associated with Graves' disease and it is mostly diagnosed in Asiatic male patients. In this report, we analyze the diagnostic procedure in three cases of hypokalemic periodic paralysis associated with Graves' disease, diagnosed in three different emergency care units over the last 3 years. Three Caucasian men (26, 30, and 39 years of age) came to the emergency care unit for acute tetraparesia. One of them had suffered 15 stereotypical episodes of tetraparesia during the last 2 years. Goiter was present in each case. Kalemia was 1.8, 2.1, and 3 mmol/l, respectively. Triggering events such as considerable sugar intake and physical exercise were present in two cases. In all cases, low TSH levels, high FT4 levels, and anti-TSH receptor antibodies led to the diagnosis of Graves' disease. All patients were treated with potassium supplementation and neomercazole. Outcome was good with a follow-up of 6, 9, and 24 months, respectively. Emergency care practitioners should be aware of this diagnosis, which may affect Caucasian patients presenting with transient tetraparesia in a primary care unit. PMID:16137557

  13. Hypokalemic paralysis as primary presentation of Fanconi syndrome associated with Sjögren syndrome.

    PubMed

    Wang, Chih-Chiang; Shiang, Jeng-Chuan; Huang, Wen-Te; Lin, Shih-Hua

    2010-06-01

    Hypokalemic paralysis is a rare presentation of Fanconi syndrome (FS) caused by Sjögren Syndrome (SS). We describe a 39-year-old man who manifested flaccid paralysis of 4 limbs. Laboratory investigations showed profound hypokalemia (1.6 mmol/L) with renal K wasting, hyperchloremic metabolic acidosis with positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, normoglycemic glycosuria, and abnormal serum creatinine concentration 2.2 mg/dL. A thorough survey for the cause of FS revealed that he had xerophthalmia and xerostomia accompanied by high anti-Ro antibody, positive Schirmer test, and delayed saliva excretion on sialoscintigraphy, confirming the diagnosis of SS. Potassium citrate, active vitamin D3, and high phosphate diet for his FS coupled with mycophenolate mofetil for SS resolved clinical symptoms and ameliorated renal function. Early recognition of HP due to the underlying SS-related FS with prompt therapy not only could terminate potentially life-threatening hypokalemia, but also improve renal outcome. PMID:20414123

  14. Domain III S4 in closed-state fast inactivation: insights from a periodic paralysis mutation.

    PubMed

    Groome, James R; Jurkat-Rott, Karin; Lehmann-Horn, Frank

    2014-01-01

    Heterologous expression of sodium channel mutations in hypokalemic periodic paralysis reveals 2 variants on channel dysfunction. Charge-reducing mutations of voltage sensing S4 arginine residues alter channel gating as typically studied with expression in mammalian cells. These mutations also produce leak currents through the voltage sensor module, as typically studied with expression in Xenopus oocytes. DIIIS4 mutations at R3 in the skeletal muscle sodium channel produce gating defects and omega current consistent with the phenotype of reduced excitability. Here, we confirm DIIIS4 R3C gating defects in the oocyte expression system for fast inactivation and its recovery. We provide novel data for the effects of the cysteine mutation on voltage sensor movement, to further our understanding of sodium channel defects in hypokalemic periodic paralysis. Gating charge movement and its remobilization are selectively altered by the mutation at hyperpolarized membrane potential, as expected with reduced serum potassium. PMID:25483590

  15. Domain III S4 in closed-state fast inactivation: Insights from a periodic paralysis mutation

    PubMed Central

    Groome, James R; Jurkat-Rott, Karin; Lehmann-Horn, Frank

    2014-01-01

    Heterologous expression of sodium channel mutations in hypokalemic periodic paralysis reveals 2 variants on channel dysfunction. Charge-reducing mutations of voltage sensing S4 arginine residues alter channel gating as typically studied with expression in mammalian cells. These mutations also produce leak currents through the voltage sensor module, as typically studied with expression in Xenopus oocytes. DIIIS4 mutations at R3 in the skeletal muscle sodium channel produce gating defects and omega current consistent with the phenotype of reduced excitability. Here, we confirm DIIIS4 R3C gating defects in the oocyte expression system for fast inactivation and its recovery. We provide novel data for the effects of the cysteine mutation on voltage sensor movement, to further our understanding of sodium channel defects in hypokalemic periodic paralysis. Gating charge movement and its remobilization are selectively altered by the mutation at hyperpolarized membrane potential, as expected with reduced serum potassium. PMID:25483590

  16. [Hypokalemic paralysis: the first presentation of primary Sjögren's syndrome].

    PubMed

    Martinho, Aurélia L; Capela, Andreia; Duarte, Fernanda

    2012-01-01

    The Sjögren's syndrome is a systemic autoimmune disorder characterized by chronic inflammation of the exocrine glands with extraglandular manifestations in up to 25% patients. Renal involvement occurs in 18.4-67% of cases, with tubulointerstitial nephritis being the most frequent pathology. We present the case of a 37 year-old woman admitted because of generalized grade 2 muscle weakness which developed over a week. We detected: hypokalemia, rhabdomyolysis, urinary pH 6.5, proteinuria and metabolic acidemia. The laboratory tests suggestive of distal renal tubular acidosis with hypokalaemia led to the diagnosis of lymphoplasmocytic tubulointerstitial nephritis, which was confirmed by renal biopsy, and to a clinical suspicion of Sjögren's syndrome. Primary Sjögren's syndrome was diagnosed in this patient based on the following criteria: xerophthalmia, xerostomia, sialadenitis, positive anti-SSA and anti-SSB antibodies, and absence of criteria for lupus and rheumatoid arthritis. During hospitalization, the patient developed deep vein thrombosis. Tests showed positive antiphospholipid antibodies and the diagnosis of secondary antiphospholipid syndrome was made. She was treated with potassium, bicarbonate, steroids, ramipril and warfarin. The authors wish to highlight the extraglandular manifestations and in particular the rarity of hypokalemic paralysis as the presenting manifestation of primary Sjögren's syndrome. PMID:22985924

  17. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.

    PubMed

    Stedwell, R E; Allen, K M; Binder, L S

    1992-03-01

    Acute hypokalemic paralysis is an uncommon cause of acute weakness. Morbidity and mortality associated with unrecognized disease include respiratory failure and death. Hence, it is imperative for physicians to be knowledgeable about the causes of hypokalemic paralysis, and consider them diagnostically. The hypokalemic paralyses represent a heterogeneous group of disorders with a final common pathway presenting as acute weakness and hypokalemia. Most cases are due to familial hypokalemic paralysis; however, sporadic cases are associated with diverse underlying etiologies including thyrotoxic periodic paralysis, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. The approach to the patient with hypokalemic paralysis includes a vigorous search for the underlying etiology and potassium replacement therapy. Further therapy depends on the etiology of the hypokalemia. Disposition depends on severity of symptoms, degree of hypokalemia, and chronicity of disease. PMID:1586409

  18. Concurrence of thyrotoxicosis and Gitelman's syndrome-associated hypokalemia-induced periodic paralysis.

    PubMed

    Imashuku, Shinsaku; Teramura-Ikeda, Tomoko; Kudo, Naoko; Kaneda, Shigehiro; Tajima, Toshihiro

    2012-04-01

    A 16-year-old Japanese boy with a history of truancy had been treated at a psychiatric clinic. When the patient was referred to us for hypokalemia-associated paralysis, the diagnosis of thyrotoxic hypokalemic periodic paralysis was made, common in Asian men. Subsequently, the patient was found to have persistently high plasma renin and aldos-terone levels. Thus, solute carrier family 12 member 3 gene (SLC12A3) analysis was performed. A novel missense homozygous mutation CTC->CAC at codon 858 (L858H) was found for which the patient was homozygous and his non-consanguineous parents heterozygote. These findings indicated that the patient developed hypokalemia-associated paralysis concurrently with thyrotoxicosis and Gitelman's syndrome. This case underscores the importance of careful examinations of adolescents with complaints of truancy as well as of precise determinations of the causes of hypokalemia-associated paralysis. PMID:22802996

  19. Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Chronic Alcoholism: A Case Report.

    PubMed

    Tsai, Ming-Hsien; Lin, Shih-Hua; Leu, Jyh-Gang; Fang, Yu-Wei

    2015-09-01

    Thyrotoxic periodic paralysis (TPP) is characterized by the presence of muscle paralysis, hypokalemia, and hyperthyroidism. We report the case of a young man with paralysis of the lower extremities, severe hypokalemia, and concurrent hyperthyroidism. TPP was suspected; therefore, treatment consisting of judicious potassium (K+) repletion and β-blocker administration was initiated. However, urinary K+ excretion rate, as well as refractoriness to treatment, was inconsistent with TPP. Chronic alcoholism was considered as an alternative cause of hypokalemia, and serum K+ was restored through vigorous K repletion and the addition of K+ -sparing diuretics. The presence of thyrotoxicosis and hypokalemia does not always indicate a diagnosis of TPP. Exclusion of TPP can be accomplished by immediate evaluation of urinary K+ excretion, acid-base status, and the amount of potassium chloride required to correct hypokalemia at presentation. PMID:26426670

  20. Thyrotoxic periodic paralysis and the sodium/potassium pump.

    PubMed

    Marx, A; Ruppersberg, J P; Pietrzyk, C; Rüdel, R

    1989-10-01

    The hypothesis of altered Na+/K+ transport in thyrotoxic periodic paralysis (TPP) was tested in an investigation of the K+ influx into erythrocytes from two patients with episodes of thyrotoxic muscle weakness. A patient with primary hypokalemic periodic paralysis (HPP) and three healthy volunteers served as controls. The TPP patients were of Oriental and Caucasian origin and differed in their clinical symptoms. For the Caucasian patient, the Na+ content of the erythrocytes was twice the control, for the Oriental patient it was normal. The K+ dependence of the ouabain-inhibitable K+ influx (the pump action) was also abnormal in the Caucasian patient, the flux being 70% of control at 2 mM [K+]e and normal at 4 mM [K+]e. The K+ influx was normal in the Oriental patient. By contrast, the K+ leak of the cells was normal in the Caucasian and was increased in the Oriental patient. The pump/leak ratio was thus reduced in both TPP patients. All parameters investigated were normal in the patient with primary HPP. It is concluded that the ion transport systems of muscle may be altered in TPP, but that the patho-mechanism might be different in the rare Caucasian cases and the rather more common Oriental cases. PMID:2558311

  1. Hypokalemic paraplegia in pregnancy.

    PubMed

    Kulkarni, Maitri; Tv, Srividya; Gopal, N

    2014-06-01

    Hypokalemic myopathy may range from numbness/weakness to complete paralysis. The aetiology may be congenital or acquired. It is characterized by acute muscular weakness with low levels of potassium (<3.5 meq/L). We present a case of 26-year-old multigravida at 36 weeks of gestation with gestational hypertension on treatment, who came with acute onset of pain, numbness and weakness of both legs which worsened following betamethasone injection. She was diagnosed to have Hypokalemic paralysis with potassium levels of 2.1 meq/L. The medical profile remitted promptly on intravenous potassium replacement. Pregnancy was continued till 37 weeks with oral potassium supplements, antihypertensives and regular monitoring of serum potassium levels. The pregnancy was terminated after 37 weeks in view of gestational hypertension. Postpartum period was uneventful, patient was discharged after two weeks when potassium levels and BP returned to normal. PMID:25121034

  2. Hypokalemic paralysis and osteomalacia secondary to renal tubular acidosis in a case with primary Sjögren's syndrome.

    PubMed

    Kawashima, Masanori; Amano, Tetsuki; Morita, Yoshitaka; Yamamura, Masahiro; Makino, Hirofumi

    2006-01-01

    A 39-year-old Japanese woman was admitted to our hospital for severe weakness owing to potassium deficiency caused by type 1 renal tubular acidosis (RTA1). Sicca complex, serological tests, and lip biopsy revealed that she had Sjögren's syndrome (SS). Acidosis was corrected by alkali supplement treatment. She also had an impaired renal function with proteinuria, and high absorbance on Ga scintigram was recognized in both kidneys. She was taking warfarin potassium after aortic valve substitution due to aortic regurgitation, therefore renal biopsy was not performed. Prednisone (20 mg/day) was administered for renal inflammation. One month later, she suffered severe chest wall pains with some local tender points over the costae of both sides, which was presumed to be due to pseudo-fractures based on osteomalacia. Hypokalemic paralysis and osteomalacia should be taken into consideration in the diagnosis of SS with RTA1. PMID:16622725

  3. Hypokalemic paralysis following severe vomiting in a child with intestinal obstruction due to round worms.

    PubMed

    Nagotkar, Leena; Shanbag, Preeti; Shenoy, Prithi

    2010-02-01

    Ascariasis is one of the most common helminthic infestations in humans. Massive infestation can give rise to serious complications such as intestinal obstruction. We present a 4-year-old boy, who presented with acute flaccid quadriparesis due to the hypokalemic alkalosis induced by severe vomiting. Severe vomiting was due to intestinal obstruction caused by round worms. PMID:19502600

  4. Randomized trials of dichlorphenamide in the periodic paralyses. Working Group on Periodic Paralysis.

    PubMed

    Tawil, R; McDermott, M P; Brown, R; Shapiro, B C; Ptacek, L J; McManis, P G; Dalakas, M C; Spector, S A; Mendell, J R; Hahn, A F; Griggs, R C

    2000-01-01

    Although the carbonic anhydrase inhibitors have been used in the treatment of the primary periodic paralyses (PPs), their efficacy has not been demonstrated in double-blind, placebo-controlled trials. Therefore, we tested the efficacy of dichlorphenamide (DCP; Daranide), a potent carbonic anhydrase inhibitor, in the treatment of episodic weakness in the primary PPs. We performed two multicenter, randomized, double-blind, placebo-controlled crossover trials, one involving 42 subjects with hypokalemic periodic paralysis (HypoPP) and the other involving 31 subjects with potassium-sensitive periodic paralysis (PSPP). In each trial, two 8-week treatment periods were separated by an active washout period of at least 9 weeks. The primary outcome variable in the HypoPP trial was the occurrence of an intolerable increase in attack severity or frequency (end point). The primary outcome variable in the PSPP trial was the number of attacks per week. In the HypoPP trial, there were 13 subjects who exhibited a preference (in terms of the end point) for either DCP or placebo, and 11 of these preferred DCP. In the PSPP trial, DCP significantly reduced attack rates relative to placebo. DCP also significantly reduced attack rates relative to placebo in the HypoPP subjects. We conclude that DCP is effective in the prevention of episodic weakness in both HypoPP and PSPP. PMID:10632100

  5. Systemic lupus erythematosus with distal renal tubular acidosis presenting as hypokalemic paralysis with respiratory failure.

    PubMed

    Koul, Parvaiz Ahmad; Wahid, Abdul; Shah, Bashir Ahmad

    2003-01-01

    An eighteen-year-old woman presented with hypokalemic respiratory failure. She was found to have distal renal tubular acidosis (dRTA) as the underlying cause for hypokalemia. This was treated successfully, and no apparent etiology for the dRTA was discovered. Three years later she presented with full-blown picture of systemic lupus erythematosus (SLE) together with features of persistent dRTA complicated, this time, with bilateral renal calculi and nephrocalcinosis. It is very likely that the dRTA was an early feature that preceded the other markers of SLE. The moral of this case is that patients with dRTA should be followed-up carefully as a primary cause for the dRTA may show up in-due-course and to monitor the treatment so as to prevent long-term complications of the RTA. PMID:18209445

  6. Thyrotoxic periodic paralysis in a pediatric patient.

    PubMed

    Jones, Peter; Papadimitropoulos, Laura; Tessaro, Mark O

    2014-01-01

    Thyrotoxic periodic paralysis is a reversible metabolic disorder that is characterized by acute muscle weakness and hypokalemia. It predominantly affects males of Asian descent. We describe the youngest such patient yet reported, a 13-year-old Asian male with a history of transient attacks of weakness who presented to our emergency department with weakness in his extremities and mild tachycardia. Laboratory test results initially revealed marked hypokalemia and later confirmed associated hyperthyroidism. Correction of the hypokalemia reversed the patient's weakness in the emergency department. PMID:24378858

  7. Normokalemic Thyrotoxic Periodic Paralysis with Preserved Reflexes- A Unique Case Report

    PubMed Central

    2015-01-01

    Although serum potassium levels are usually subnormal in Thyrotoxic Periodic Paralysis (TPP), but in exceptionally rare circumstances, it may be normal leading to the entity called normokalemic TPP. The diagnosis of normokalemic TPP is more often overlooked and/or delayed due to lack of awareness among the physicians and associated mild symptoms of hyperthyroidism. Here, the author describes the case of a 27-year-old male with newly diagnosed but untreated Grave’s disease and TPP who was normokalemic during the acute phase of paralysis. Hypokalemia was documented only after resolution of paralytic attacks during subsequent days of admission. The importance of the case report is to highlight upon the fact that TPP should always be considered in an “previously asymptomatic” young Asian individual with acute paralysis with or without hypokalemia , and thyroid function and serial potassium values should be evaluated for diagnosing the usual hypokalemic type or the more rarer variant normokalemic TPP. This case report also deserves mention as the patient of TPP had a notable feature of having preserved reflexes in the face of hypokalemia. PMID:25859483

  8. Normokalemic thyrotoxic periodic paralysis with preserved reflexes- a unique case report.

    PubMed

    Chakrabarti, Subrata

    2015-02-01

    Although serum potassium levels are usually subnormal in Thyrotoxic Periodic Paralysis (TPP), but in exceptionally rare circumstances, it may be normal leading to the entity called normokalemic TPP. The diagnosis of normokalemic TPP is more often overlooked and/or delayed due to lack of awareness among the physicians and associated mild symptoms of hyperthyroidism. Here, the author describes the case of a 27-year-old male with newly diagnosed but untreated Grave's disease and TPP who was normokalemic during the acute phase of paralysis. Hypokalemia was documented only after resolution of paralytic attacks during subsequent days of admission. The importance of the case report is to highlight upon the fact that TPP should always be considered in an "previously asymptomatic" young Asian individual with acute paralysis with or without hypokalemia , and thyroid function and serial potassium values should be evaluated for diagnosing the usual hypokalemic type or the more rarer variant normokalemic TPP. This case report also deserves mention as the patient of TPP had a notable feature of having preserved reflexes in the face of hypokalemia. PMID:25859483

  9. Renal tubular dysfunction presenting as recurrent hypokalemic periodic quadriparesis in systemic lupus erythematosus

    PubMed Central

    Prasad, D.; Agarwal, D.; Malhotra, V.; Beniwal, P.

    2014-01-01

    We report recurrent hypokalemic periodic quadriparesis in a 30-year-old woman. Patient had also symptoms of multiple large and small joint pain, recurrent oral ulceration, photosensitivity and hair loss that were persisting since last 6 months and investigations revealed systemic lupus erythematosus (SLE) with distal tubular acidosis. Our patient was successfully treated with oral potassium chloride, sodium bicarbonate, hydroxychloroquine and a short course of steroids. Thus, tubular dysfunction should be carefully assessed in patients with SLE. PMID:25249723

  10. Distal renal tubular acidosis, hypokalemic paralysis, nephrocalcinosis, primary hypothyroidism, growth retardation, osteomalacia and osteoporosis leading to pathological fracture: a case report.

    PubMed

    Basak, Ramen C; Sharkawi, Khairy Mostafa; Rahman, Mohammad Mizanur; Swar, Mayada Mohammad

    2011-07-01

    Renal tubular acidosis (RTA) is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acidosis (dRTA), hypokalemic paralysis, primary hypothyroidism, growth retardation, osteomalacia and osteopenia leading to stress fracture. All these features presenting in a single case (as in our case) is a rare occurrence, so far other cases of distal renal tubular acidosis (dRTA) have been reported. PMID:22043434

  11. Paralysis

    MedlinePlus

    Paralysis is the loss of muscle function in part of your body. It happens when something goes ... way messages pass between your brain and muscles. Paralysis can be complete or partial. It can occur ...

  12. Paralysis

    MedlinePlus

    ... is due to strokes or injuries such as spinal cord injury or a broken neck. Other causes of paralysis include Nerve diseases such as amyotrophic lateral sclerosis Autoimmune diseases ... used to be a cause of paralysis, but polio no longer occurs in the U.S.

  13. A rare case of thyrotoxic periodic paralysis precipitated by hydrocortisone

    PubMed Central

    Chakrabarti, Subrata

    2015-01-01

    Thyrotoxic periodic paralysis (TPP) is a rare, but serious condition characterized by acute paralytic attacks and hypokalemia in association with thyrotoxicosis. Although carbohydrate rich meals, strenuous exercise, alcohol, emotional stress are known precipitants of TPP, steroid treatment has rarely been reported to induce TPP. We report a case in which a patient with previously untreated Grave's disease developed TPP following administration of Intravenous hydrocortisone for control of severe anaphylaxis, which to best of our knowledge is very rare. PMID:25810683

  14. Potassium chloride supplementation alone may not improve hypokalemia in thyrotoxic hypokalemic periodic paralysis.

    PubMed

    Yu, Tsuan-Shih; Tseng, Chin-Feng; Chuang, Ying-Yen; Yeung, Lai-King; Lu, Kuo-Cheng

    2007-04-01

    This article reports a 29-year-old man who came to the Emergency Department because of sudden onset of bilateral lower extremity weakness and inability to walk after intake of a high carbohydrate meal and alcohol. He was found to have severe hypokalemia, with K(+) level at 1.7 mmol/L. However, after administration of potassium chloride (KCl), 10 mEq/h intravenous (i.v.) drip for 4 h, follow-up serum potassium was even lower at 1.5 mmol/L and the patient complained of persistent weakness. Twenty mg of propranolol, a non-selective beta-blocker, was given orally and a dramatic improvement of muscle power to grade 5 was noted after 30 min of administration. On the fifth day after discharge, he had another episode of bilateral lower extremity weakness after ingesting a mouthful of alcohol. Muscle power recovered completely after i.v. drip of KCl, 20 mEq. Laboratory data revealed an underlying primary hyperthyroidism for which he was given anti-thyroid agents and beta-blockers. PMID:17394988

  15. Molecular cloning of ion channels in Felis catus that are related to periodic paralyses in man: a contribution to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis

    PubMed Central

    Zapata, Marlyn; Kunii, Ilda S.; Paninka, Rolf M.; Simões, Denise M. N.; Castillo, Víctor A.; Reche, Archivaldo; Maciel, Rui M. B.; Dias da Silva, Magnus R.

    2014-01-01

    ABSTRACT Neck ventroflexion in cats has different causes; however, the most common is the hypokalemia associated with flaccid paralysis secondary to chronic renal failure. In humans, the most common causes of acute flaccid paralysis are hypokalemia precipitated by thyrotoxicosis and familial forms linked to mutations in sodium, potassium, and calcium channel genes. Here, we describe the sequencing and analysis of skeletal muscle ion channels in Felis catus that could be related to periodic paralyses in humans, contributing to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis. We studied genomic DNA from eleven cats, including five animals that were hyperthyroid with hypokalemia, although only one presented with muscle weakness, and six healthy control domestic cats. We identified the ion channel ortholog genes KCNJ2, KCNJ12, KCNJ14, CACNA1S and SCN4A in the Felis catus genome, together with several polymorphic variants. Upon comparative alignment with other genomes, we found that Felis catus provides evidence for a high genomic conservation of ion channel sequences. Although we hypothesized that neck ventroflexion in cats could be associated with a thyrotoxic or familial periodic paralysis channel mutation, we did not identify any previously detected human channel mutation in the hyperthyroid cat presenting hypokalemia. However, based on the small number of affected cats in this study, we cannot yet rule out this molecular mechanism. Notwithstanding, hyperthyroidism should still be considered as a differential diagnosis in hypokalemic feline paralysis. PMID:25063199

  16. Molecular cloning of ion channels in Felis catus that are related to periodic paralyses in man: a contribution to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis.

    PubMed

    Zapata, Marlyn; Kunii, Ilda S; Paninka, Rolf M; Simões, Denise M N; Castillo, Víctor A; Reche, Archivaldo; Maciel, Rui M B; Dias da Silva, Magnus R

    2014-01-01

    Neck ventroflexion in cats has different causes; however, the most common is the hypokalemia associated with flaccid paralysis secondary to chronic renal failure. In humans, the most common causes of acute flaccid paralysis are hypokalemia precipitated by thyrotoxicosis and familial forms linked to mutations in sodium, potassium, and calcium channel genes. Here, we describe the sequencing and analysis of skeletal muscle ion channels in Felis catus that could be related to periodic paralyses in humans, contributing to the understanding of the genetic susceptibility to feline neck ventroflexion and paralysis. We studied genomic DNA from eleven cats, including five animals that were hyperthyroid with hypokalemia, although only one presented with muscle weakness, and six healthy control domestic cats. We identified the ion channel ortholog genes KCNJ2, KCNJ12, KCNJ14, CACNA1S and SCN4A in the Felis catus genome, together with several polymorphic variants. Upon comparative alignment with other genomes, we found that Felis catus provides evidence for a high genomic conservation of ion channel sequences. Although we hypothesized that neck ventroflexion in cats could be associated with a thyrotoxic or familial periodic paralysis channel mutation, we did not identify any previously detected human channel mutation in the hyperthyroid cat presenting hypokalemia. However, based on the small number of affected cats in this study, we cannot yet rule out this molecular mechanism. Notwithstanding, hyperthyroidism should still be considered as a differential diagnosis in hypokalemic feline paralysis. PMID:25063199

  17. Size of quadriceps femoris may contribute to thyrotoxic periodic paralysis.

    PubMed

    Tang, Zi-Wei; He, Ying; Yao, Yu; Qiu, Li; Tian, Hao-Ming

    2015-12-01

    Thyrotoxic periodic paralysis (TPP) frequently occurs on male individuals at their third and forth decades. The major site of involvement is the proximal muscles of lower limbs. Increasing evidence has shown that the occurrence of TPP is determined by multiple factors. We hypothesized that apart from hormonal fluctuations, skeletal muscle itself may explain for the age and sex variance as well. Our study was established to explore whether the size of lower limb skeletal muscles were related to TPP. We conducted a clinical experiment including 43 patients diagnosed with TPP (Group 1) and 39 pure hyperthyroidism individuals (Group 2). Current age, body mass index (BMI), thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), average girth of bilateral upper arm and thigh, physical activity level (PAL) were measured. We also adopted B mode ultrasound to quantify the muscle thickness (MT) of the major muscle involved in the disease, the quadriceps femoris (QF, including rectus femoris, RF; vastus intermedius, VI; vastus medialis, VM and vastus lateralis, VL). Patients were matched in TSH, FT4 and FT3. PAL was also statistically identical between groups. Age, BMI, thigh girth, the average of bilateral MT of QF were statistically different. After adjusting for age, BMI and girth, Group 1 still presented with larger MT of QF than Group 2, regardless of their current thyroid hormone level. There indeed exists an independent relationship between muscle thickness and TPP. PMID:26519100

  18. Hypokalaemic Periodic Paralysis in a Patient with Subclinical Hyperthyroidism: A Rare Case

    PubMed Central

    Shaikh, Mohammed Aslam; Gummadi, Thejaswi

    2016-01-01

    Thyrotoxic Periodic Paralysis (TPP) is an uncommon disorder. Though many cases of hypokalaemic periodic paralysis are reported in overt hyperthyroidism, hypokalaemic paralysis in subclinical hyperthyroidism is very rare. Subclinical hyperthyroidism is characterised by circulating TSH levels below reference range and normal thyroid hormone levels. We describe a case of 32-year-old Asian male who presented to the emergency department with acute onset weakness and hypokalaemia with no previous history of thyroid disorder or any signs and symptoms suggestive of hyperthyroidism. He was subsequently diagnosed with Graves’ disease with subclinical hyperthyroidism. PMID:26894115

  19. A thyrotropin-secreting pituitary adenoma as a cause of thyrotoxic periodic paralysis.

    PubMed

    Alings, A M; Fliers, E; de Herder, W W; Hofland, L J; Sluiter, H E; Links, T P; van der Hoeven, J H; Wiersinga, W M

    1998-11-01

    We describe a patient with thyrotoxic periodic paralysis (TPP) caused by a thyrotropin-secreting pituitary adenoma. The diagnosis TPP was based on the combination of episodes of reversible hypokalaemic paralysis, hyperthyroidism and electrophysiological findings. A thyrotropin-secreting pituitary adenoma was diagnosed on the basis of endocrinological function tests and MRI of the pituitary gland. Before transsphenoidal resection of the adenoma, treatment with octreotide restored euthyroidism both clinically and biochemically. Immunocytochemistry of the pituitary adenoma was positive for TSH exclusively. Incubation with octreotide or quinagolide induced decreased TSH and alpha-subunit production by the cultured adenoma cells, in agreement with the pre-operative in vivo data. This paper is the first to describe in vivo and in vitro characteristics of a thyrotropin-secreting pituitary adenoma in a patient presenting with periodic paralysis. PMID:9854688

  20. Hypokalemic vacuolar myopathy of chronic alcoholism. A histological and histochemical study.

    PubMed

    Khurana, R; Kalyanaraman, K

    1977-04-01

    Recent reports have emphasized the occurrence of a myopathy in chronic alcoholism associated with hypokalemia. This report of hypokalemic myopathy in a chronic alcoholic, emphasizes the primary myopathic nature of the condition and attributes it to a possible non-specific effect of the hypokalemia on skeletal muscle. It is pointed out, that histological and histochemical changes of muscle in this type of myopathy are indistinguishable from other types of hypokalemic myopathies like periodic paralysis. It is conjectured that in alcoholic myopathy, the underlying disorder might be related to a primary disturbance of potassium metabolism, though in most cases, serum potassium is normal. It is likely that studies aimed at studying total body potassium content and turnover in alcoholic myopathy would help in understanding its pathogenesis and possible relationship to disturbed potassium metabolism. PMID:849704

  1. Thyrotoxic periodic paralysis associated with transient thyrotoxicosis due to painless thyroiditis.

    PubMed

    Oh, Sang Bo; Ahn, Jinhee; Oh, Min Young; Choi, Bo Gwang; Kang, Ji Hyun; Jeon, Yun Kyung; Kim, Sang Soo; Kim, Bo Hyun; Kim, Yong Ki; Kim, In Joo

    2012-07-01

    Thyrotoxic periodic paralysis (TPP) is a rare manifestation of hyperthyroidism characterized by muscle weakness and hypokalemia. All ethnicities can be affected, but TPP typically presents in men of Asian descent. The most common cause of TPP in thyrotoxicosis is Graves' disease. However, TPP can occur with any form of thyrotoxicosis. Up to our knowledge, very few cases ever reported the relationship between TPP and painless thyroiditis. We herein report a 25-yr-old Korean man who suffered from flaccid paralysis of the lower extremities and numbness of hands. The patient was subsequently diagnosed as having TPP associated with transient thyrotoxicosis due to painless thyroiditis. The paralytic attack did not recur after improving the thyroid function. Therefore, it is necessary that early diagnosis of TPP due to transient thyrotoxicosis is made to administer definite treatment and prevent recurrent paralysis. PMID:22787383

  2. A rare cause of acute flaccid paralysis: Human coronaviruses.

    PubMed

    Turgay, Cokyaman; Emine, Tekin; Ozlem, Koken; Muhammet, S Paksu; Haydar, A Tasdemir

    2015-01-01

    Acute flaccid paralysis (AFP) is a life-threatening clinical entity characterized by weakness in the whole body muscles often accompanied by respiratory and bulbar paralysis. The most common cause is Gullian-Barre syndrome, but infections, spinal cord diseases, neuromuscular diseases such as myasthenia gravis, drugs and toxins, periodic hypokalemic paralysis, electrolyte disturbances, and botulism should be considered as in the differential diagnosis. Human coronaviruses (HCoVs) cause common cold, upper and lower respiratory tract disease, but in the literature presentation with the lower respiratory tract infection and AFP has not been reported previously. In this study, pediatric case admitted with lower respiratory tract infection and AFP, who detected for HCoV 229E and OC43 co-infection by the real-time polymerase chain reaction, has been reported for the first time. PMID:26557177

  3. A rare cause of acute flaccid paralysis: Human coronaviruses

    PubMed Central

    Turgay, Cokyaman; Emine, Tekin; Ozlem, Koken; Muhammet, S. Paksu; Haydar, A. Tasdemir

    2015-01-01

    Acute flaccid paralysis (AFP) is a life-threatening clinical entity characterized by weakness in the whole body muscles often accompanied by respiratory and bulbar paralysis. The most common cause is Gullian–Barre syndrome, but infections, spinal cord diseases, neuromuscular diseases such as myasthenia gravis, drugs and toxins, periodic hypokalemic paralysis, electrolyte disturbances, and botulism should be considered as in the differential diagnosis. Human coronaviruses (HCoVs) cause common cold, upper and lower respiratory tract disease, but in the literature presentation with the lower respiratory tract infection and AFP has not been reported previously. In this study, pediatric case admitted with lower respiratory tract infection and AFP, who detected for HCoV 229E and OC43 co-infection by the real-time polymerase chain reaction, has been reported for the first time. PMID:26557177

  4. Hypokalaemic periodic paralysis in rural northern India--most have secondary causes.

    PubMed

    Kumar, Vinod; Armstrong, Lois; Seshadri, M S; Finny, Philip

    2014-01-01

    Hypokalaemic periodic paralysis (HPP) is a life-threatening condition. Our aim was to study the clinical profile and laboratory parameters of HPP patients and to develop an algorithm to determine the causes of HPP. 84 patients presented with HPP over a 3 year period. 58 (69.0%) were found to have renal tubular acidosis (RTA). The other causes were idiopathic HPP (8 (9.5%)), acute gastroenteritis (4 (4.8%)), suspected primary hyperaldosteronism and familial HPP (2 each (2.4%)) and suspected Gitelman/Bartter Syndrome and thyrotoxic periodic paralysis (1 each (1.2%)). The number of cases peaks in the hot season. Over a third of the patients (35.7%) had recurrent episodes. 80% had secondary HPP and therefore a biochemical evaluation is mandatory. A simple algorithm was developed. Both health professionals and patients need further education regarding this problem in order to improve diagnosis and treatment and to improve compliance. PMID:24275360

  5. Hypokalemic quadriparesis: an unusual manifestation of leptospirosis.

    PubMed

    K, Mahendran; R, Kannan; D V, Lal; G, Rajiv; K, Rajendran

    2014-01-01

    We report a 46-year-old male who presented with fever and flaccid weakness of all four limbs due to Leptospirosis associated hypokalemia. Acute hypokalemic quadriparesis is an uncommon presentation of leptospirosis, not yet widely recognised. Renal potassium wasting occurs in Leptospirosis and subsequently, the development of hypokalemia leads to paralysis. The patient had kaliuresis due to leptospirosis which improved with antibiotics and potassium replacement. PMID:24596761

  6. Thyrotoxic hypokalaemic periodic paralysis: a rare presentation of Graves' disease in a Hispanic patient.

    PubMed

    Matta, Abhishek; Koppala, Jahnavi; Gossman, William

    2014-01-01

    A 26-year-old Hispanic man with no significant medical history presented to our emergency room with gradual onset weakness of his lower extremities. He was haemodynamically stable and examination revealed loss of motor function in his lower limbs up to the level of hips. Laboratory data revealed hypokalaemia. The patient was started on potassium supplementation and he recovered his muscle strength. Differential diagnosis included familial hypokalaemic periodic paralysis and thyrotoxic periodic paralysis (TPP). Further investigations revealed a low thyroid-stimulating hormone and high free thyroxine levels. Radio iodine 123 scan revealed an enhanced homogeneous uptake in the thyroid suggesting Graves' disease. Thyroid stimulating antibodies were also found to be elevated. The patient was started on methimazole and propranolol and he never had another attack of TPP even at 1 year follow-up. PMID:24717588

  7. Hypokalaemic paralysis.

    PubMed

    Ahlawat, S K; Sachdev, A

    1999-04-01

    Hypokalaemic paralysis is a relatively uncommon but potentially life-threatening clinical syndrome. If recognised and treated appropriately, patients recover without any clinical sequellae. The syndrome of hypokalaemic paralysis represents a heterogeneous group of disorders characterised clinically by hypokalaemia and acute systemic weakness. Most cases are due to familial or primary hypokalaemic periodic paralysis; sporadic cases are associated with numerous other conditions including barium poisoning, hyperthyroidism, renal disorders, certain endocrinopathies and gastrointestinal potassium losses. The age of onset, race, family history, medications, and underlying disease states can help in identifying the cause of hypokalaemic paralysis. Initial therapy of the patient with hypokalaemic paralysis includes potassium replacement and search for underlying aetiology. Further management depends on the aetiology of hypokalaemia, severity of symptoms, and duration of disease. This review presents the differential diagnosis for hypokalaemic paralysis and discusses management of the syndrome. PMID:10715756

  8. Novel mutations in human and mouse SCN4A implicate AMPK in myotonia and periodic paralysis

    PubMed Central

    Corrochano, Silvia; Männikkö, Roope; Joyce, Peter I.; McGoldrick, Philip; Lassi, Glenda; Raja Rayan, Dipa L.; Blanco, Gonzalo; Quinn, Colin; Liavas, Andrianos; Lionikas, Arimantas; Amior, Neta; Dick, James; Healy, Estelle G.; Stewart, Michelle; Carter, Sarah; Hutchinson, Marie; Bentley, Liz; Fratta, Pietro; Cortese, Andrea; Cox, Roger; Brown, Steve D. M.; Tucci, Valter; Wackerhage, Henning; Amato, Anthony A.; Greensmith, Linda; Koltzenburg, Martin; Hanna, Michael G.; Acevedo-Arozena, Abraham

    2014-01-01

    Mutations in the skeletal muscle channel (SCN4A), encoding the Nav1.4 voltage-gated sodium channel, are causative of a variety of muscle channelopathies, including non-dystrophic myotonias and periodic paralysis. The effects of many of these mutations on channel function have been characterized both in vitro and in vivo. However, little is known about the consequences of SCN4A mutations downstream from their impact on the electrophysiology of the Nav1.4 channel. Here we report the discovery of a novel SCN4A mutation (c.1762A>G; p.I588V) in a patient with myotonia and periodic paralysis, located within the S1 segment of the second domain of the Nav1.4 channel. Using N-ethyl-N-nitrosourea mutagenesis, we generated and characterized a mouse model (named draggen), carrying the equivalent point mutation (c.1744A>G; p.I582V) to that found in the patient with periodic paralysis and myotonia. Draggen mice have myotonia and suffer from intermittent hind-limb immobility attacks. In-depth characterization of draggen mice uncovered novel systemic metabolic abnormalities in Scn4a mouse models and provided novel insights into disease mechanisms. We discovered metabolic alterations leading to lean mice, as well as abnormal AMP-activated protein kinase activation, which were associated with the immobility attacks and may provide a novel potential therapeutic target. PMID:25348630

  9. Thyrotoxic Periodic Paralysis in Long Standing Graves' Disease: An Unusual Presentation with Normokalemia

    PubMed Central

    Kannan, Lakshmi; Kim, Young Nam

    2015-01-01

    Context: Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of hyperthyroidism that is underdiagnosed and frequently missed. It is relatively common in Asian men with Graves' disease. TPP attacks are frequently associated with hypokalemia. Case Report: Here we report a non-Asian female patient with Graves' disease, who presented with flaccid paralysis associated with an episode of subacute thyroiditis (SAT). Interestingly, she was found to have low normal potassium levels in the serum during the initial attack despite which she continues to require low dose potassium supplementation to prevent recurrent TPP attacks. Unique features in our patient include her gender, ethnicity, time lag between initial diagnosis of Graves' disease, and the development of TPP and borderline low potassium levels, with the continuous need for prophylactic potassium supplementation. Conclusion: It is important to be aware of this complication of hyperthyroidism that has a dramatic yet variable presentation, but is readily amenable to therapy. PMID:25839004

  10. Hypokalaemic thyrotoxic periodic paralysis in an Asian man in the United Kingdom.

    PubMed

    Sinharay, R

    2004-01-01

    A large number of ethnic Chinese and other oriental populations are living in the West because of the modern day migration of people. Hypokalaemic periodic paralysis attributable to thyrotoxicosis is a common presentation in an Asian emergency department. It is uncommon in the white communities. There is a difference in the genetic type in the different racial groups. Thyrotoxic features are often masked or absent. Life may be threatened because of severe hypokalaemia and therefore a prompt diagnosis of this condition in the certain ethnic group presenting with weakness and hypokalaemia is essential. Thyroid function studies are mandatory in these cases. PMID:14734400

  11. A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis

    PubMed Central

    Habbout, Karima; Poulin, Hugo; Rivier, François; Giuliano, Serena; Sternberg, Damien; Fontaine, Bertrand; Eymard, Bruno; Morales, Raul Juntas; Echenne, Bernard; King, Louise; Hanna, Michael G.; Männikkö, Roope; Chahine, Mohamed; Nicole, Sophie

    2016-01-01

    Objective: To determine the molecular basis of a complex phenotype of congenital muscle weakness observed in an isolated but consanguineous patient. Methods: The proband was evaluated clinically and neurophysiologically over a period of 15 years. Genetic testing of candidate genes was performed. Functional characterization of the candidate mutation was done in mammalian cell background using whole cell patch clamp technique. Results: The proband had fatigable muscle weakness characteristic of congenital myasthenic syndrome with acute and reversible attacks of most severe muscle weakness as observed in periodic paralysis. We identified a novel homozygous SCN4A mutation (p.R1454W) linked to this recessively inherited phenotype. The p.R1454W substitution induced an important enhancement of fast and slow inactivation, a slower recovery for these inactivated states, and a frequency-dependent regulation of Nav1.4 channels in the heterologous expression system. Conclusion: We identified a novel loss-of-function mutation of Nav1.4 that leads to a recessive phenotype combining clinical symptoms and signs of congenital myasthenic syndrome and periodic paralysis, probably by decreasing channel availability for muscle action potential genesis at the neuromuscular junction and propagation along the sarcolemma. PMID:26659129

  12. Paralysis as a Presenting Symptom of Hyperthyroidism in an Active Duty Soldier.

    PubMed

    Jennette, John; Tauferner, Dustin

    2015-01-01

    Thyrotoxic periodic paralysis (TPP) is an endocrine disorder presenting with proximal motor weakness, typically greatest in the lower extremities, hypokalemia, and signs or laboratory findings consistent with hyperthyroidism. The incidence of TPP is highest in Asian males. This is a case report of a 30-year-old male active duty Soldier who presented to the emergency department complaining of several recent episodes of lower extremity paralysis. The patient underwent a workup which included serum and cerebrospinal fluid studies, and was found to be hypokalemic and hyperthyroid. Following consultation with neurology, the patient was admitted to the medicine service and treated for thyrotoxic periodic paralysis with potassium replacement and treatment of his hyperthyroidism. Since achieving a euthyroid state, he has had no recurrences of TPP. This disease should be considered in patients presenting with symmetric motor weakness and hypokalemia, whether or not symptoms of hyperthyroidism are elicited during the review of systems. PMID:26606408

  13. Rare KCNJ18 variants do not explain hypokalaemic periodic paralysis in 263 unrelated patients

    PubMed Central

    Kuhn, Marius; Jurkat-Rott, Karin; Lehmann-Horn, Frank

    2016-01-01

    Objective To examine rare KCNJ18 variations recently reported to cause sporadic and thyrotoxic hypokalaemic periodic paralysis (TPP). Methods We sequenced KCNJ18 in 474 controls (400 Caucasians, 74 male Asians) and 263 unrelated patients with periodic paralysis (PP), including 30 patients with TPP without mutations in established PP genes. Results In 10 patients without TPP, we identified 9 heterozygous, novel variations (c.–3G>A, L15S, R81C, E273X, T309I, I340T, N365S, G394R, R401W) and a questionable heterozygous causative R399X stop variant. Studies on 40 relatives of these 10 patients showed that none of the variants were de novo in the patients and that R399X occurred in 3 non-affected relatives. Most affected amino acids lacked conservation and several clinically affected relatives did not carry the patient’s variant. T309I, however, could be pathogenic under the pre-requisite of strongly reduced penetrance in females. Of the controls, 17 revealed 12 novel rare variants including the heterozygous E273X stop variant in three individuals. Conclusions Our study shows many different, rare KCNJ18 alterations in patients as well as controls. Only perhaps one meets the requirements of a disease-causing mutation. Therefore, KCNJ18 alterations are seldom pathogenic. Additional studies are required before patients with PP can be genetically diagnosed on the basis of a KCNJ18 variant alone. PMID:25882930

  14. A case of thyrotoxic periodic paralysis as initial manifestation of Graves' disease in a 16-year-old Korean adolescent

    PubMed Central

    Jung, Se Yong; Song, Kyung Chul; Shin, Jae Il; Chae, Hyun Wook; Kim, Ho-Seong

    2014-01-01

    Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism, with recurrent muscle paralysis and hypokalemia that are caused by an intracellular shift of potassium. TPP is relatively common in Asian males, but is extremely rare in children and adolescents, even for those of Asian descent. We describe a 16-year-old Korean adolescent presenting with a two-week history of episodic leg weakness in the morning. He showed sinus tachycardia, lower leg weakness, and hypokalemia. Thyroid function test showed hyperthyroidism, and thyroid ultrasonography revealed a diffuse enlarged thyroid with increased vascularity, consistent with Graves' disease. He was treated with β-adrenergic blocker and antithyroid drugs. He has been symptom free for one year, as his hyperthyroidism has been controlled well with antithyroid drugs. TPP should be considered in children and adolescents with acute paralysis of the lower extremities and hypokalemia. PMID:25346923

  15. Evaluating the Efficacy of Primary Treatment for Graves' Disease Complicated by Thyrotoxic Periodic Paralysis

    PubMed Central

    Chang, Rita Yuk-Kwan; Lang, Brian Hung-Hin; Chan, Ai Chen; Wong, Kai Pun

    2014-01-01

    Objective. Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of Graves' disease (GD). The present study compared the long-term efficacy of antithyroid drugs (ATD), radioactive iodine (RAI), and surgery in GD/TPP. Methods. Sixteen patients with GD/TPP were followed over a 14-year period. ATD was generally prescribed upfront for 12–18 months before RAI or surgery was considered. Outcomes such as thyrotoxic or TPP relapses were compared between the three modalities. Results. Eight (50.0%) patients had ATD alone, 4 (25.0%) had RAI, and 4 (25.0%) had surgery as primary treatment. Despite being able to withdraw ATD in all 8 patients for 37.5 (22–247) months, all subsequently developed thyrotoxic relapses and 4 (50.0%) had ≥1 TPP relapses. Of the four patients who had RAI, two (50%) developed thyrotoxic relapse after 12 and 29 months, respectively, and two (50.0%) became hypothyroid. The median required RAI dose to render hypothyroidism was 550 (350–700) MBq. Of the 4 patients who underwent surgery, none developed relapses but all became hypothyroid. Conclusion. To minimize future relapses, more definitive primary treatment such as RAI or surgery is preferred over ATD alone. If RAI is chosen over surgery, a higher dose (>550 MBq) is recommended. PMID:25147568

  16. Primary gradient defect distal renal tubular acidosis presenting as hypokalaemic periodic paralysis.

    PubMed

    Koul, P A; Wahid, A; Bhat, F A

    2005-07-01

    A 45 year old man presented with recurrent hypokalaemic paralysis. Laboratory investigations revealed renal tubular acidosis as the cause of the hypokalaemia, and dynamic tubular studies suggested a gradient defect as the underlying cause. The patient had associated dextrocardia. To our knowledge, this is the first report of this condition. PMID:15983101

  17. Hypokalemic quadriparesis in dengue

    PubMed Central

    Mishra, Vikas; Harbada, Rishit; Sharma, Akhilesh; Mishra, Meenakshi

    2015-01-01

    Dengue infection is the leading cause of illness and death in tropical and subtropical regions of the world. The common complications associated with dengue fever are usual hematological abnormalities, shock, and organ failure. The neurological complications of dengue are uncommon. However, evidence of dengue virus neurotropism and complications has been slowly but surely rising as seen from increased literature on this subject over the last decade. We report an uncommon case of hypokalemic quadriparesis with dengue that had a favorable outcome. PMID:25949983

  18. Hypokalemic quadriparesis in dengue.

    PubMed

    Mishra, Vikas; Harbada, Rishit; Sharma, Akhilesh; Mishra, Meenakshi

    2015-01-01

    Dengue infection is the leading cause of illness and death in tropical and subtropical regions of the world. The common complications associated with dengue fever are usual hematological abnormalities, shock, and organ failure. The neurological complications of dengue are uncommon. However, evidence of dengue virus neurotropism and complications has been slowly but surely rising as seen from increased literature on this subject over the last decade. We report an uncommon case of hypokalemic quadriparesis with dengue that had a favorable outcome. PMID:25949983

  19. Hypokalemic rhabdomyolysis: an unusual presentation of Sjogren's syndrome

    PubMed Central

    Cherif, Eya; Ben Hassine, Lamia; Kechaou, Ines; Khalfallah, Narjess

    2013-01-01

    Hypokalaemic rhabdomyolysis represents a medical emergency requiring rapid diagnosis and appropriate aetiological treatment. Renal tubular acidosis is a common cause of hypokalemia which can be idiopathic or secondary to systemic disorders such as Sjogren's syndrome. It can remain asymptomatic or manifest with metabolic abnormalities including hypokalemia paralysis, hypocalcaemia and hyperchloremic metabolic acidosis. Rhabdomyolysis presenting with severe hypokalemia as the first manifestation of Sjogren's syndrome is rare. We report a case of a 59-year-old woman who presented to our department with severe weakness of all limbs. Laboratory examination demonstrated hypokalemic rhabdomyolysis caused by distal renal tubular acidosis. Investigations revealed Sjogren's syndrome as the underlying cause of the metabolic disorders. PMID:24165505

  20. Familial hyperkalemic periodic paralysis caused by a de novo mutation in the sodium channel gene SCN4A

    PubMed Central

    Han, Ji-Yeon

    2011-01-01

    Familial hyperkalemic periodic paralysis (HYPP) is an autosomaldominant channelopathy characterized by transient and recurrent episodes of paralysis with concomitant hyperkalemia. Mutations in the skeletal muscle voltage-gated sodium channel gene SCN4A have been reported to be responsible for this disease. Here, we report the case of a 16-year-old girl with HYPP whose mutational analysis revealed a heterozygous c.2111C>T substitution in the SCN4A gene leading to a Thr704Met mutation in the protein sequence. The parents were clinically unaffected and did not have a mutation in the SCN4A gene. A de novo SCN4A mutation for familial HYPP has not previously been reported. The patient did not respond to acetazolamide, but showed a marked improvement in paralytic symptoms upon treatment with hydrochlorothiazide. The findings in this case indicate that a de novo mutation needs to be considered when an isolated family member is found to have a HYPP phenotype. PMID:22253644

  1. Facial paralysis

    MedlinePlus

    ... otherwise healthy, facial paralysis is often due to Bell palsy . This is a condition in which the facial ... speech, or occupational therapist. If facial paralysis from Bell palsy lasts for more than 6 to 12 months, ...

  2. An additional child case of an aldosterone-producing adenoma with an atypical presentation of peripheral paralysis due to hypokalemia.

    PubMed

    Dinleyici, E C; Dogruel, N; Acikalin, M F; Tokar, B; Oztelcan, B; Ilhan, H

    2007-11-01

    Aldosterone-producing adenoma, which is characterized by hypertension, hypokalemia, and elevated aldosterone levels with suppressed plasma renin activity, is a rare condition during childhood and is also potentially curable. To the best of our knowledge, nearly 25 cases of childhood aldosterone-secreting adenoma have been reported in the literature to date. Here we describe a 13-yr-old girl with primary hyperaldosteronism secondary to aldosterone-secreting adenoma. The patient was admitted to our hospital with the neuromuscular complaints of muscle weakness and inability to walk due to hypokalemia. She had been misdiagnosed as having hypokalemic periodic paralysis 2 months before admission and her symptoms had radically improved with potassium supplementation. However, her blood pressure levels had increased and her symptoms reappeared 2 days prior to being observed during hospitalization in our institution. Laboratory examinations revealed hypokalemia (2.1 mEq/l), and increased serum aldosterone levels with suppressed plasma renin activity. Abdominal ultrasonography and abdominal magnetic resonance imaging revealed left adrenal mass. Laparoscopic adrenalectomy was performed and histopathological examinations showed benign adrenal adenoma. Serum aldosterone levels and blood pressure levels returned to normal after surgical intervention. This case demonstrates the importance of a systemic evaluation including blood pressure monitorization of children with hypokalemia as intermittent hypertension episodes may be seen; cases without hypertension may be misdiagnosed as rheumatological or neurological disorders such as hypokalemic periodic paralysis, as in our case. PMID:18075291

  3. I lost weight, but I became weak and cannot walk--a case of nutraceutical (T3)-induced thyrotoxic periodic paralysis.

    PubMed

    Panikkath, Ragesh; Nugent, Kenneth

    2014-01-01

    Thyrotoxic periodic paralysis (TPP) is a rare reversible cause of paralysis and cramping. TPP is usually precipitated by common causes of thyrotoxicosis such as Grave disease or multinodular goiter. TPP precipitated by exogenous triiodothyronine (T3) intake is an extremely rare occurrence with only 3 cases reported to date. We now report a 24-year-old healthy manual laborer who developed quadriparesis during a period of rest after heavy exertion and carbohydrate intake. He had severe hypokalemia (potassium level 1.9 mmole/L). Correction of his hypokalemia reversed the paralysis without rebound hyperkalemia. After a detailed history review, he reported that he had been consuming nutraceuticals containing T3 for 1 month to lose weight, and laboratory studies confirmed factitious T3 toxicosis. There was no evidence of renal or gastrointestinal potassium wasting. This episode of TPP was the first manifestation of thyrotoxicosis in this patient, and avoidance of T3 intake prevented more episodes. PMID:23567793

  4. Mice with an NaV1.4 sodium channel null allele have latent myasthenia, without susceptibility to periodic paralysis.

    PubMed

    Wu, Fenfen; Mi, Wentao; Fu, Yu; Struyk, Arie; Cannon, Stephen C

    2016-06-01

    Over 60 mutations of SCN4A encoding the NaV1.4 sodium channel of skeletal muscle have been identified in patients with myotonia, periodic paralysis, myasthenia, or congenital myopathy. Most mutations are missense with gain-of-function defects that cause susceptibility to myotonia or periodic paralysis. Loss-of-function from enhanced inactivation or null alleles is rare and has been associated with myasthenia and congenital myopathy, while a mix of loss and gain of function changes has an uncertain relation to hypokalaemic periodic paralysis. To better define the functional consequences for a loss-of-function, we generated NaV1.4 null mice by deletion of exon 12. Heterozygous null mice have latent myasthenia and a right shift of the force-stimulus relation, without evidence of periodic paralysis. Sodium current density was half that of wild-type muscle and no compensation by retained expression of the foetal NaV1.5 isoform was detected. Mice null for NaV1.4 did not survive beyond the second postnatal day. This mouse model shows remarkable preservation of muscle function and viability for haploinsufficiency of NaV1.4, as has been reported in humans, with a propensity for pseudo-myasthenia caused by a marginal Na(+) current density to support sustained high-frequency action potentials in muscle. PMID:27048647

  5. NaV1.4 mutations cause hypokalaemic periodic paralysis by disrupting IIIS4 movement during recovery.

    PubMed

    Groome, James R; Lehmann-Horn, Frank; Fan, Chunxiang; Wolf, Markus; Winston, Vern; Merlini, Luciano; Jurkat-Rott, Karin

    2014-04-01

    Hypokalaemic periodic paralysis is typically associated with mutations of voltage sensor residues in calcium or sodium channels of skeletal muscle. To date, causative sodium channel mutations have been studied only for the two outermost arginine residues in S4 voltage sensor segments of domains I to III. These mutations produce depolarization of skeletal muscle fibres in response to reduced extracellular potassium, owing to an inward cation-selective gating pore current activated by hyperpolarization. Here, we describe mutations of the third arginine, R3, in the domain III voltage sensor i.e. an R1135H mutation which was found in two patients in separate families and a novel R1135C mutation identified in a third patient in another family. Muscle fibres from a patient harbouring the R1135H mutation showed increased depolarization tendency at normal and reduced extracellular potassium compatible with the diagnosis. Additionally, amplitude and rise time of action potentials were reduced compared with controls, even for holding potentials at which all NaV1.4 are fully recovered from inactivation. These findings may be because of an outward omega current activated at positive potentials. Expression of R1135H/C in mammalian cells indicates further gating defects that include significantly enhanced entry into inactivation and prolonged recovery that may additionally contribute to action potential inhibition at the physiological resting potential. After S4 immobilization in the outward position, mutant channels produce an inward omega current that most likely depolarizes the resting potential and produces the hypokalaemia-induced weakness. Gating current recordings reveal that mutations at R3 inhibit S4 deactivation before recovery, and molecular dynamics simulations suggest that this defect is caused by disrupted interactions of domain III S2 countercharges with S4 arginines R2 to R4 during repolarization of the membrane. This work reveals a novel mechanism of disrupted S

  6. Transient compartment-like syndrome and normokalaemic periodic paralysis due to a Cav1.1 mutation

    PubMed Central

    Fan, Chunxiang; Lehmann-Horn, Frank; Weber, Marc-André; Bednarz, Marcin; Groome, James R.; Jonsson, Malin K. B.

    2013-01-01

    We studied a two-generation family presenting with conditions that included progressive permanent weakness, myopathic myopathy, exercise-induced contracture before normokalaemic periodic paralysis or, if localized to the tibial anterior muscle group, transient compartment-like syndrome (painful acute oedema with neuronal compression and drop foot). 23Na and 1H magnetic resonance imaging displayed myoplasmic sodium overload, and oedema. We identified a novel familial Cav1.1 calcium channel mutation, R1242G, localized to the third positive charge of the domain IV voltage sensor. Functional expression of R1242G in the muscular dysgenesis mouse cell line GLT revealed a 28% reduced central pore inward current and a −20 mV shift of the steady-state inactivation curve. Both changes may be at least partially explained by an outward omega (gating pore) current at positive potentials. Moreover, this outward omega current of 27.5 nS/nF may cause the reduction of the overshoot by 13 mV and slowing of the upstroke of action potentials by 36% that are associated with muscle hypoexcitability (permanent weakness and myopathic myopathy). In addition to the outward omega current, we identified an inward omega pore current of 95 nS/nF at negative membrane potentials after long depolarizing pulses that shifts the R1242G residue above the omega pore constriction. A simulation reveals that the inward current might depolarize the fibre sufficiently to trigger calcium release in the absence of an action potential and therefore cause an electrically silent depolarization-induced muscle contracture. Additionally, evidence of the inward current can be found in 23Na magnetic resonance imaging-detected sodium accumulation and 1H magnetic resonance imaging-detected oedema. We hypothesize that the episodes are normokalaemic because of depolarization-induced compensatory outward potassium flux through both delayed rectifiers and omega pore. We conclude that the position of the R1242G residue

  7. Thyrotoxic Periodic Paralysis and Polymorphisms of the ADRB2, AR, and GABRA3 Genes in Men with Graves Disease

    PubMed Central

    Sim, Soyoung; Lim, Seonhee; Kim, Mijin; Kwon, Hyemi; Jeon, Min Ji; Kim, Won Gu; Shong, Young Kee; Kim, Won Bae

    2016-01-01

    Background Thyrotoxic periodic paralysis (TPP) is a rare complication of thyrotoxicosis characterized by acute attacks of muscle weakness and hypokalemia. Recently, variation in several genes was suggested to be associated with TPP. This study evaluated the genetic predisposition to TPP in terms of the β2-adrenergic receptor (ADRB2), androgen receptor (AR), and γ-aminobutyric acid receptor α3 subunit (GABRA3) genes. Methods This study enrolled 48 men with Graves disease (GD) and TPP, and 48 GD patients without TPP. We compared the frequencies of candidate polymorphisms between the two groups. Results The frequency of the Gly16/Gly16 genotype in ADRB2 was not significantly associated with TPP (P=0.32). More CAG repeats (≥26) in the AR gene were not correlated with TPP (odds ratio [OR], 2.46; 95% confidence interval [CI], 0.81 to 8.09; P=0.08). The allele frequency of the TT genotype in the GABRA3 gene was not associated with TPP (OR, 1.83; 95% CI, 0.54 to 6.74; P=0.41). Conclusion The polymorphisms in the ADRB2, AR, and GABRA3 genes could not explain the genetic susceptibility to TPP in Korean men with GD. PMID:26676335

  8. Todd's Paralysis

    MedlinePlus

    ... don't know what causes Todd's paralysis. Current theories propose biological processes in the brain that involve ... All NINDS-prepared information is in the public domain and may be freely copied. Credit to the ...

  9. Thyrotoxic periodic paralysis

    MedlinePlus

    ... hormone levels A family history of the disorder Low potassium levels during attacks Symptoms that come and go ... episodes Diagnosis involves ruling out disorders associated with low potassium. The health care provider may try to trigger ...

  10. Hyperkalemic periodic paralysis

    MedlinePlus

    ... be normal or high. During an attack, muscle reflexes are decreased or absent. And muscles go limp rather than staying stiff. Muscle groups near the body, such as the shoulders and hips, are involved ...

  11. Hyperkalemic periodic paralysis

    MedlinePlus

    ... and sometimes a higher than normal level of potassium in the blood. The medical name for high potassium level is hyperkalemia . HyperPP is one of a ... with the way the body controls sodium and potassium levels in cells. Risk factors include having other ...

  12. A case of acquired Gitelman syndrome presenting as hypokalemic paralysis

    PubMed Central

    Kulkarni, M.; Kadri, P.; Pinto, R.

    2015-01-01

    We report a case of a young female patient who presented with weakness of upper and lower limbs. On evaluation, she had hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. Anti-Ro (SSA) antibody was positive. She had an acquired Gitelman syndrome due to primary Sjögren's syndrome (SS). SS presenting with features of Gitelman syndrome is very rare. PMID:26199478

  13. A case of acquired Gitelman syndrome presenting as hypokalemic paralysis.

    PubMed

    Kulkarni, M; Kadri, P; Pinto, R

    2015-01-01

    We report a case of a young female patient who presented with weakness of upper and lower limbs. On evaluation, she had hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. Anti-Ro (SSA) antibody was positive. She had an acquired Gitelman syndrome due to primary Sjögren's syndrome (SS). SS presenting with features of Gitelman syndrome is very rare. PMID:26199478

  14. Severe hypokalemic paralysis as a manifestation of a mitochondrial disorder.

    PubMed

    Finsterer, Josef; Lässer, Stefan

    2013-01-01

    Mitochondrial disorder (MtD) is usually a multisystem disease due to impaired mitochondrial energy production. Severe hypokalemia resulting in muscle weakness and rhabdomyolysis has not been reported as a phenotypic feature of MtD. Here we describe a 60-year-old male patient who developed myalgias followed by generalized muscle weakness a few days before admission. Symptoms were attributed to severe hypokalemia that occurred after the patient had discontinued spironolactone, a competitive antagonist of the aldosterone receptor, four months earlier on his own judgment. Spironolactone was given for 10 years to treat suspected primary hyperaldosteronism (Conn's syndrome). He presented with myopathic face, bilateral ptosis, hypertelorism, brachydactylia, weakness of the axial and limb muscles, and bilateral leg edema. Hypertelorism and brachydactylia are known as physical traits of MtD. Laboratory investigations revealed hypokalemia of 1.7 mmol/l and elevated serum levels of creatine kinase (2,772 U/l). Electrocardiogram showed sinus rhythm, left bundle-branch-block, repolarization abnormalities, and prolonged QTc (571 ms), which is associated with a propensity to ventricular arrhythmias. Diagnostic work-up revealed bilateral adenomas of the suprarenal glands. Conn's syndrome was regarded as a manifestation of MtD, since MtDs are frequently associated with endocrine abnormalities. The patient also presented with occasional double vision, ptosis, renal insufficiency, bilateral renal cysts, hypertriglyceridemia, arterial hypertension, and hypertrophic cardiomyopathy. Taken together, we have made the diagnosis of MtD. In conclusion, MtD may be associated with adrenal adenomas, which may cause severe symptomatic hypokalemia, manifesting as generalized weakness and myalgias due to rhabdomyolysis. Endocrine involvement may be a phenotypic feature of MtD. PMID:23985882

  15. Hypokalemic paralysis due to primary hyperaldosteronism simulating Gitelman's syndrome.

    PubMed

    Kasifoglu, Timucin; Akalin, Aysen; Cansu, Dondu Uskudar; Korkmaz, Cengiz

    2009-03-01

    Some diseases, such as Gitelman's syndrome, Bartter's syndrome, and primary hyperaldosteronism (Conn's syndrome), may bear some similar clinical and laboratory findings. Their treatment modalities being different from one another, the need for a scrupulous diagnostic evaluation arises as far as clinical practice is concerned. In this report, we present a patient with Conn's syndrome who was initially considered to have Gitelman's syndrome due to displaying a few overlapping features of both diseases. We also give an account of the hardships encountered during the diagnostic evaluation. PMID:19237821

  16. Institutional Paralysis

    ERIC Educational Resources Information Center

    Yarmolinsky, Adam

    1975-01-01

    Institutional paralysis of higher education is the result of the disjunction between faculty and administration; the disjunction between substantive planning and bugetary decision-making; the disjunction between departmental structures and functional areas of university concern; and the disjunction between the theory of direct democracy and its…

  17. INFANTILE PARALYSIS

    PubMed Central

    1917-01-01

    At the recent Forty-fourth Annual Meetings of the American Public Health Association, Cincinnati, Ohio, there was held a Round Table Discussion on Infantile Paralysis, in which health authorities throughout the country took part. This discussion was held under the auspices of the Section on Public Health Administration. Dr. George W. Goler, Health Officer of Rochester, N. Y., Chairman of this Section, presided. We take great pleasure in being able to reproduce for readers of the Journal what took place at this most important session. PMID:18009618

  18. [A case of primary aldosteronism presenting hypokalemic myopathy induced by benidipine hydrochloride; a dihydropyridine calcium channel blocker].

    PubMed

    Sugawara, H; Shiraiwa, H; Otsuka, M; Ueki, A

    2000-05-01

    We report a 46-year-old man with primary aldosteronism presenting hypokalemia, periodic paralysis and hypokalemic myopathy whose clinical course paralleled with the dosage of benidipine hydrochloride, a dihydropyridine calcium channel blocker (DHP-CCB), administered for the treatment of hypertension. To see relations between DHP-CCB and episodes of motor weakness in patients with primary aldosteronism, we surveyed retrospectively the history of motor weakness and anti-hypertensive drugs in 14 consecutive cases with primary aldosteronism in our institute. Five patients out of 11 cases (45.5%) who had received DHP-CCB experienced muscle weakness, however, the rest of three patients receiving other anti-hypertensive drug had not experienced weakness. Though, less attention has been paid as thiazide diuretics, it is reported that DHP-CCB also induces hypokalemia through several mechanisms. However, the occurrence of motor weakness by DHP-CCB is very rare. Our results show that primary aldosteronism should be taken into account when we encounter patients manifesting episodic motor weakness by the use of DHP-CCB. PMID:11002726

  19. A Case of Nonfatal Ventricular Arrhythmia Due to Thyrotoxic Periodic Paralysis in a Saudi Patient as an Initial Presentation of Graves’ Disease

    PubMed Central

    Hakami, Osamah; Ahmad, Maswood M.; Al Johani, Naji

    2016-01-01

    Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism characterized by recurrent muscle weakness and hypokalemia. It has been commonly reported in non-Asian populations. Four cases were reported in Saudis so far, and one had a life-threatening arrhythmia. We describe an additional case of a 28-year-old apparently healthy Saudi male patient, who presented with acute paraparesis associated with hypokalemia (K: 2.0 mmol/L), complicated by ventricular tachycardia and cardiac arrest. He was successfully resuscitated and his hypokalemia was corrected. A diagnosis of Graves’ disease associated with TPP was made. He was initially treated with carbimazole and β-blockers and then given a definitive therapy with radioactive iodine, which showed a good response. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness. A brief review of TPP and associated arrhythmia is included. PMID:26843815

  20. Hypokalemic myopathy associated with primary aldosteronism and glycyrrhizine-induced pseudoaldosteronism.

    PubMed

    Ishikawa, S; Saito, T; Okada, K; Atsumi, T; Kuzuya, T

    1985-12-01

    Enzymatic and histological features of muscular disorders associated with primary aldosteronism and glycyrrhizine-induced pseudoaldosteronism were studied. Among 10 patients with primary aldosteronism and 3 patients with pseudoaldosteronism, 5 patients were admitted to our hospital because of muscular weakness. The serum potassium (K) level was 1.86 +/- 0.21 mEq/l in a myopathy group on admission, a value significantly less than that of the 2.74 +/- 0.10 mEq/l in a non-myopathy group (p less than 0.01). Serum creatine phosphokinase (CPK), glutamate-oxyloacetate transaminase (GOT), and lactate dehydrogenase (LDH) were increased in the myopathy group compared to the non-myopathy group; serum CPK was 1412.6 +/- 902.6 vs. 22.8 +/- 5.0 mU/ml, serum GOT was 186.4 +/- 75.3 vs. 24.2 +/- 5.4 mU/ml (p less than 0.05), and serum LDH was 1133.4 +/- 377.3 vs. 387.6 +/- 42.5 mU/ml (p less than 0.05) in the groups with and without myopathy. Analysis of CPK isozymes revealed that the MM type exceeded 95%. The elevated serum CPK, GOT and LDH rapidly decreased to the normal range and muscular strength completely improved within 6 to 13 days after hospitalization, when the serum K level remained below than normal. Light microscopic finding of damaged muscle showed the diffuse necrosis and vacuolization of muscle fibers. Electron microscopic study clearly demonstrated complete dissolution of myofilaments with disappearance of sarcoplasmic reticulum and T-tubules in the necrotic muscle fibers. These results indicate that muscular lesions may occur in primary aldosteronism and pseudoaldosteronism when the serum K level is decreased to below 2.0 mEq/l. This myopathy is not periodic paralysis but hypokalemic myopathy. The mechanism by which K deficiency causes muscular damage remains unknown. PMID:3914413

  1. Sudden flaccid paralysis.

    PubMed

    Tariq, Mohammad; Peshin, Rohit; Ellis, Oliver; Grover, Karan

    2015-01-01

    Periodic thyrotoxic paralysis is a genetic condition, rare in the West and in Caucasians. Thyrotoxicosis, especially in western hospitals, is an easily overlooked cause of sudden-onset paralysis. We present a case of a 40-year-old man who awoke one morning unable to stand. He had bilateral lower limb flaccid weakness of 0/5 with reduced reflexes and equivocal plantars; upper limbs were 3/5 with reduced tone and reflexes. ECG sinus rhythm was at a rate of 88/min. PR interval was decreased and QT interval increased. Bloods showed potassium of 1.8 mEq/L (normal range 3.5-5), free T4 of 29.2 pmol/L (normal range 6.5-17) and thyroid-stimulating hormone (TSH) of <0.01 mIU/L (normal range 0.35-4.94). Random urinary potassium was 8.8 mEq/L (normal range 12.5-62.5). The patient was admitted initially to intensive therapy unit and given intravenous potassium. His symptoms resolved within 24 h. He was diagnosed with thyrotoxic periodic paralysis. He was discharged on carbimazole and propanolol, and follow-up was arranged in the endocrinology clinic. PMID:25566931

  2. Licorice-induced hypokalemic myopathy and hypokalemic renal tubular damage in anorexia nervosa.

    PubMed

    Ishikawa, S; Kato, M; Tokuda, T; Momoi, H; Sekijima, Y; Higuchi, M; Yanagisawa, N

    1999-07-01

    A patient with a history of anorexia nervosa developed licorice-induced hypokalemic myopathy. With potassium replacement, high CPK blood level and myopathic signs returned to normal. However, the patient manifested persistent hypokalemia and impaired renal function to concentrate and acidify the urine. Renal biopsy demonstrated intense degeneration and vacuolation of tubules with a normal glomerus which was consistent with hypokalemic nephropathy. Prolonged hypokalemia in anorexia nervosa is sometimes attributed to surreptitious purging or taking diuretics, but it is necessary to check the urine pH, the urine-specific gravity, and the urine potassium level in order to find underlying renal damage even after hypokalemic myopathy is treated successfully. PMID:10349593

  3. Muscle paralysis in thyrotoxicosis.

    PubMed

    Siddiqui, Fraz Anwar; Sheikh, Aisha

    2015-01-01

    Thyrotoxic periodic paralysis (TPP) is a condition characterised by muscle paralysis due to hypokalaemia usually secondary to thyrotoxicosis. We report a case of a 31-year-old man with no known comorbidities who presented to a tertiary healthcare unit with a 1-month history of difficulty in breathing, palpitations, weight loss and hoarseness of voice. On examination, his thyroid gland was palpable and fine hand tremors were present. An initial provisional diagnosis of hyperthyroidism was made. Three months after initial presentation, the patient presented in emergency with severe muscle pain and inability to stand. Laboratory results revealed hypokalaemia. All the symptoms reverted over the next few hours on administration of intravenous potassium. A diagnosis of TTP was established. After initial presentation, the patient was treated with carbimazole and propranolol. Once he was euthyroid, radioactive iodine ablation therapy (15 mCi) was carried out as definitive therapy, after which the patient's symptoms resolved; he is currently doing fine on levothyroxine replacement and there has been no recurrence of muscle paralysis. PMID:26025973

  4. Dengue infection presenting as acute hypokalemic quadriparesis.

    PubMed

    Gupta, N; Garg, A; Chhabra, P

    2014-01-01

    Dengue infection is one of the most common viral hemorrhagic fevers seen in the tropical countries, including India. Its presentation varies from an acute self-resolving febrile illness to life-threatening hemorrhagic shock and multiorgan dysfunction leading to death. Neurological presentations are uncommon and limited to case reports only. Most common neurological manifestations being encephalitis, acute inflammatory demyelinating polyradiculoneuropathy, transverse myelitis, and acute disseminated encephalomyelitis.Hypokalemic quadriparesis as a presenting feature of dengue is extremely rare. Here, we report this case of a 33-year-old female, who presented with hypokalemic quadriparesis and was subsequently diagnosed as dengue infection. PMID:25121379

  5. Living with Paralysis

    MedlinePlus

    ... are available to answer your questions. Call toll-free 1-800-539-7309 Mon-Fri, 9am-5pm ... are people living with or impacted by paralysis. Free services and downloads > Paralysis Resource Guide Our free ...

  6. Isolated sleep paralysis.

    PubMed

    Sawant, Neena S; Parkar, Shubhangi R; Tambe, Ravindra

    2005-10-01

    Sleep paralysis (SP) is a cardinal symptom of narcolepsy. However, little is available in the literature about isolated sleep paralysis. This report discusses the case of a patient with isolated sleep paralysis who progressed from mild to severe SP over 8 years. He also restarted drinking alcohol to be able to fall asleep and allay his anxiety symptoms. The patient was taught relaxation techniques and he showed complete remission of the symptoms of SP on follow up after 8 months. PMID:20711316

  7. Chronic hypokalemic nephropathy: a clinical study.

    PubMed

    Bock, K D; Cremer, W; Werner, U

    1978-01-01

    Description of 23 patients (21 women, 2 men) with an average age of 36.6 (19--68) years, who were hypokalemic during 6.5 years on the average (range 1/2--16 years). The cause of the potassium depletion was malnutrition (anorexia nervosa, vomiting) and/or abuse of laxatives and/or diuretics. With increasing duration of potassium depletion renal function deteriorated; in two cases terminal renal failure developed. Histology of the kidneys (9 cases) showed the picture of chronic abacterial interstitial nephritis. Urinalysis was negative or non-specific. The blood pressure levels were normal or low, hypertensive values being exceptional. Aside of hypokalemia a tendency to hyponatriemia, hypochloremia and metabolic alcalosis was observed, the latter turning into hypokalemic normochloremic acidosis with advancing renal insufficiency. Plasma renin activity and aldosterone concentration or excretion frequently were elevated, but no close correlation was found between these parameters or with the blood pressure. Bacterial infection of the urinary tract occured, if at all, in the late phase and seems to be complication rather than the cause of the kidney disease. The discussion of other possible pathogenetic factors leads to the conclusion that the term "chronic kaliopenic nephropathy" is justified. Some diagnostic and therapeutic consequences are mentioned. PMID:732256

  8. Stats About Paralysis

    MedlinePlus

    ... of advocacy to collectively combat the drivers of inequality and eradicate the obstacles to freedom faced by ... impact of paralysis across the nation, from a health, societal, and financial perspective, we are creating a ...

  9. Isolated sleep paralysis

    MedlinePlus

    ... from sleep. It is not associated with another sleep disorder. ... Sleep paralysis can be a symptom of narcolepsy . But if you do not have other symptoms of narcolepsy, there is usually no need to have sleep studies done.

  10. Isolated sleep paralysis

    MedlinePlus

    ... from sleep. It is not associated with another sleep disorder. Symptoms Episodes of isolated sleep paralysis last from ... A.M. Editorial team. Related MedlinePlus Health Topics Sleep Disorders Browse the Encyclopedia A.D.A.M., Inc. ...

  11. Surgical Treatment of Laryngeal Paralysis.

    PubMed

    Monnet, Eric

    2016-07-01

    Unilateral arytenoid lateralization is the most commonly used technique to treat laryngeal paralysis. It is important not to overabduct the arytenoid cartilage during the unilateral lateralization to minimize exposure of the rima glottides. Dogs with laryngeal paralysis treated with unilateral lateralization have a good long-term prognosis. Idiopathic polyneuropathy is the most common cause of laryngeal paralysis in dogs. PMID:26947115

  12. [Hypokalemic pareses secondary to renal tubular acidosis].

    PubMed

    Gøransson, L G; Apeland, T; Omdal, R

    2000-01-30

    A 24 year old woman presented with flaccid paralysis, severe hypokalaemia and hyperchloremia, metabolic acidosis. Immunological tests and labial glandular biopsy indicated primary Sjögren's syndrome as the underlying cause of her distal renal tubular acidosis. The patient recovered after alkali and potassium substitution and was put on oral treatment with potassium citrate. PMID:10827521

  13. Sleep paralysis and hallucinosis.

    PubMed

    Stores, Gregory

    1998-01-01

    Background: Sleep paralysis is one of the many conditions of which visual hallucinations can be a part but has received relatively little attention. It can be associated with other dramatic symptoms of a psychotic nature likely to cause diagnostic uncertainty. Methods and results: These points are illustrated by the case of a young man with a severe bipolar affective disorder who independently developed terrifying visual, auditory and somatic hallucinatory episodes at sleep onset, associated with a sense of evil influence and presence. The episodes were not obviously related to his psychiatric disorder. Past diagnoses included nightmares and night terrors. Review provided no convincing evidence of various other sleep disorders nor physical conditions in which hallucinatory experiences can occur. A diagnosis of predormital isolated sleep paralysis was made and appropriate treatment recommended. Conclusions: Sleep paralysis, common in the general population, can be associated with dramatic auxiliary symptoms suggestive of a psychotic state. Less common forms are either part of the narcolepsy syndrome or (rarely) they are familial in type. Interestingly, sleep paralysis (especially breathing difficulty) features prominently in the folklore of various countries. PMID:11568409

  14. The Price of Paralysis

    ERIC Educational Resources Information Center

    Thweatt, Steven C.

    2009-01-01

    There are situations in which people feel that it is perfectly acceptable to take no action at all, given a certain set of circumstances. Not only is this a generally unacceptable approach to problem solving, but this type of paralysis can have far reaching and unintended consequences. Since childhood, one has at times held out hope that if he/she…

  15. Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism.

    PubMed

    Koul, Parvaiz Ahmad; Wahid, A

    2011-09-01

    A 43- year- old woman on treatment for primary hypothyroidism presented with 1- day progressive weakness of all her limbs and history of similar episodes in the past. Clinical examination revealed grade 2 hyporeflexive weakness. Investigations revealed features of hypokalemia, metabolic acidosis, alkaline urine, and a fractional bicarbonate excretion of 3.5%, consistent with distal renal tubular acidosis. Antithyroid peroxidase and antithroglobulin antibodies were positive, suggesting an autoimmune basis for the pathogenesis of the functional tubular defect. Bicarbonate therapy resulted in a sustained clinical recovery. PMID:21912036

  16. [Hypokalemic paralysis revealing Sjögren's syndrome associated with auto-immune thyroiditis].

    PubMed

    Baaj, Mohamed; Safi, Somaya; Hassikou, Hassna; Tabache, Fatima; Mouden, Karim; Hadri, Larbi

    2010-02-01

    We report a case of 36-year-old woman, admitted for hypotonic tetraparesis. Laboratory tests revealed severe hypokalaemia, acidosis, hyperchloremia and alkaline urinary pH allowing the diagnosis of distal tubular acidosis. Additional investigations led to the diagnosis of primary Sjögren's syndrome associated with Hashimoto's thyroïditis. The evolution was favorable under potassium citrate alkalinisation, the corticosteroid therapy and hormonal substitution. Based on this observation, the pathogenesis of distal tubular acidosis during auto-immune diseases (Sjögren's syndrome, monoclonal hypergammaglobulinemia, hypothyroidism) was discussed as well as its consequences and management. PMID:19836323

  17. Visual Experiences during Paralysis

    PubMed Central

    Whitham, Emma M.; Fitzgibbon, Sean P.; Lewis, Trent W.; Pope, Kenneth J.; DeLosAngeles, Dylan; Clark, C. Richard; Lillie, Peter; Hardy, Andrew; Gandevia, Simon C.; Willoughby, John O.

    2011-01-01

    Rationale: Paralyzed human volunteers (n = 6) participated in several studies the primary one of which required full neuromuscular paralysis while awake. After the primary experiment, while still paralyzed and awake, subjects undertook studies of humor and of attempted eye-movement. The attempted eye-movements tested a central, intentional component to one’s internal visual model and are the subject of this report. Methods: Subjects reclined in a supportive chair and were ventilated after paralysis (cisatracurium, 20 mg intravenously). In illumination, subjects were requested to focus alternately on the faces of investigators standing on the left and the right within peripheral vision. In darkness, subjects were instructed to look away from a point source of light. Subjects were to report their experiences after reversal of paralysis. Results: During attempted eye-movement in illumination, one subject had an illusion of environmental movement but four subjects perceived faces as clearly as if they were in central vision. In darkness, four subjects reported movement of the target light in the direction of attempted eye-movements and three could control the movement of the light at will. Conclusion: The hypothesis that internal visual models receive intended ocular-movement-information directly from oculomotor centers is strengthened by this evidence. PMID:22162967

  18. Whole genome and exome sequencing realignment supports the assignment of KCNJ12, KCNJ17, and KCNJ18 paralogous genes in thyrotoxic periodic paralysis locus: functional characterization of two polymorphic Kir2.6 isoforms.

    PubMed

    Paninka, Rolf M; Mazzotti, Diego R; Kizys, Marina M L; Vidi, Angela C; Rodrigues, Hélio; Silva, Silas P; Kunii, Ilda S; Furuzawa, Gilberto K; Arcisio-Miranda, Manoel; Dias-da-Silva, Magnus R

    2016-08-01

    Next-generation sequencing (NGS) has enriched the understanding of the human genome. However, homologous or repetitive sequences shared among genes frequently produce dubious alignments and can puzzle NGS mutation analysis, especially for paralogous potassium channels. Potassium inward rectifier (Kir) channels are important to establish the resting membrane potential and regulating the muscle excitability. Mutations in Kir channels cause disorders affecting the heart and skeletal muscle, such as arrhythmia and periodic paralysis. Recently, a susceptibility muscle channelopathy-thyrotoxic periodic paralysis (TPP)-has been related to Kir2.6 channel (KCNJ18 gene). Due to their high nucleotide sequence homology, variants found in the potassium channels Kir2.6 and Kir2.5 have been mistakenly attributable to Kir2.2 polymorphisms or mutations. We aimed at elucidating nucleotide misalignments by performing realignment of whole exome sequencing (WES) and whole genome sequencing (WGS) reads to specific Kir2.2, Kir2.5, and Kir2.6 cDNA sequences using BWA-MEM/GATK pipeline. WES/WGS reads correctly aligned 26.9/43.2, 37.6/31.0, and 35.4/25.8 % to Kir2.2, Kir2.5, and Kir2.6, respectively. Realignment was able to reduce over 94 % of misalignments. No putative mutations of Kir2.6 were identified for the three TPP patients included in the cohort of 36 healthy controls using either WES or WGS. We also distinguished sequences for a single Kir2.2, a single Kir2.5 sequence, and two Kir2.6 isoforms, which haplotypes were named RRAI and QHEV, based on changes at 39, 40, 56, and 249 residues. Electrophysiology records on both Kir2.6_RRAI and _QHEV showed typical rectifying currents. In our study, the reduction of misalignments allowed the elucidation of paralogous gene sequences and two distinct Kir2.6 haplotypes, and pointed the need for checking the frequency of these polymorphisms in other populations with different genetic background. PMID:27008341

  19. Clinical and neurophysiological features of tick paralysis.

    PubMed

    Grattan-Smith, P J; Morris, J G; Johnston, H M; Yiannikas, C; Malik, R; Russell, R; Ouvrier, R A

    1997-11-01

    The clinical and neurophysiological findings in six Australian children with generalized tick paralysis are described. Paralysis is usually caused by the mature female of the species Ixodes holocyclus. It most frequently occurs in the spring and summer months but can be seen at any time of year. Children aged 1-5 years are most commonly affected. The tick is usually found in the scalp, often behind the ear. The typical presentation is a prodrome followed by the development of an unsteady gait, and then ascending, symmetrical, flaccid paralysis. Early cranial nerve involvement is a feature, particularly the presence of both internal and external ophthalmoplegia. In contrast to the experience with North American ticks, worsening of paralysis in the 24-48 h following tick removal is common and the child must be carefully observed over this period. Death from respiratory failure was relatively common in the first half of the century and tick paralysis remains a potentially fatal condition. Respiratory support may be required for > 1 week but full recovery occurs. This is slow with several weeks passing before the child can walk unaided. Anti-toxin has a role in the treatment of seriously ill children but there is a high incidence of acute allergy and serum sickness. Neurophysiological studies reveal low-amplitude compound muscle action potentials with normal motor conduction velocities, normal sensory studies and normal response to repetitive stimulation. The biochemical structure of the toxin of I. holocyclus has not been fully characterized but there are many clinical, neurophysiological and experimental similarities to botulinum toxin. PMID:9397015

  20. [Rehabilitation of facial paralysis].

    PubMed

    Martin, F

    2015-10-01

    Rehabilitation takes an important part in the treatment of facial paralysis, especially when these are severe. It aims to lead the recovery of motor activity and prevent or reduce sequelae like synkinesis or spasms. It is preferable that it be proposed early in order to set up a treatment plan based on the results of the assessment, sometimes coupled with an electromyography. In case of surgery, preoperative work is recommended, especially in case of hypoglossofacial anastomosis or lengthening temporalis myoplasty (LTM). Our proposal is to present an original technique to enhance the sensorimotor loop and the cortical control of movement, especially when using botulinum toxin and after surgery. PMID:26195012

  1. A Paralysis of Social Policy?

    ERIC Educational Resources Information Center

    Blau, Joel

    1992-01-01

    Reviews paralysis of U.S. social policy. Notes that, although federal government has implemented new social programs, programs either are provided on condition of willingness to work or are modest in scope. Linking paralysis with literature on government ineffectuality, traces origins of ineffectuality of political/economic policies of past 20…

  2. A young man presenting with paralysis after vigorous exercise

    PubMed Central

    Gubran, Christopher; Narain, Rajay; Malik, Luqmaan; Saeed, Saad Aldeen

    2012-01-01

    Thyrotoxic periodic paralysis (TPP) is a rare metabolic disorder characterised by muscular weakness and paralysis in predisposed thyrotoxic patients. Although patients with TPP are almost uniformly men of Asian descent, cases have been reported in Caucasian and other ethnic populations. The rapid increase in ethnic diversity in Western and European nations has led to increase in TPP reports, where it was once considered exceedingly rare. Correcting the hypokalaemic and hyperthyroid state tends to reverse the paralysis. However, failure to recognise the condition may lead to delay in diagnosis and serious consequences including respiratory failure and death. We describe a young man who was diagnosed with hyperthyroidism who presented with acute paralysis. The clinical characteristics, pathophysiology and management of TTP are reviewed. PMID:22927268

  3. Studies on immunological paralysis

    PubMed Central

    Howard, J. G.; Zola, H.; Christie, G. H.; Courtenay, Barbara M.

    1971-01-01

    Type 3 pneumococcal polysaccharide (SIII) with average molecular weight 220,000 was depolymerized by heating aqueous solutions under pressure. The immunogenicity and tolerogenicity of fractions with molecular weights of 121,000, 31,000 and 4000 were compared with the native antigen by means of direct splenic PFC and serum haemagglutinin assays. Fall in molecular weight was accompanied by progressive reduction in both immunizing and tolerance-inducing properties. The 4000 molecular weight preparation (ten glucuronosidoglucose units) was feebly immunogenic and non-tolerogenic, although known to contain intact determinants. Depolymerization was also correlated with loss of antibody-neutralizing activity. Paralysis with SIII involves `high-zone' tolerance in the B lymphocyte population. The proposition is discussed that immunogenicity is here a necessary characteristic of the inducing antigen. PMID:4398137

  4. Whole-Body Muscle MRI in Patients with Hyperkalemic Periodic Paralysis Carrying the SCN4A Mutation T704M: Evidence for Chronic Progressive Myopathy with Selective Muscle Involvement

    PubMed Central

    Lee, Young Han; Lee, Hyung-Soo; Lee, Hyo Eun; Hahn, Seok; Nam, Tai-Seung; Choi, Young-Chul; Kim, Seung Min

    2015-01-01

    Background and Purpose Hyperkalemic periodic paralysis (hyperKPP) is a muscle sodium-ion channelopathy characterized by recurrent paralytic attacks. A proportion of affected individuals develop fixed or chronic progressive weakness that results in significant disability. However, little is known about the pathology of hyperKPP-induced fixed weakness, including the pattern of muscle involvement. The aim of this study was to characterize the patterns of muscle involvement in hyperKPP by whole-body magnetic resonance imaging (MRI). Methods We performed whole-body muscle MRI in seven hyperKPP patients carrying the T704M mutation in the SCN4A skeletal sodium-channel gene. Muscle fat infiltration, suggestive of chronic progressive myopathy, was analyzed qualitatively using a grading system and was quantified by the two-point Dixon technique. Results Whole-body muscle MRI analysis revealed muscle atrophy and fatty infiltration in hyperKPP patients, especially in older individuals. Muscle involvement followed a selective pattern, primarily affecting the posterior compartment of the lower leg and anterior thigh muscles. The muscle fat fraction increased with patient age in the anterior thigh (r=0.669, p=0.009), in the deep posterior compartment of the lower leg (r=0.617, p=0.019), and in the superficial posterior compartment of the lower leg (r=0.777, p=0.001). Conclusions Our whole-body muscle MRI findings provide evidence for chronic progressive myopathy in hyperKPP patients. The reported data suggest that a selective pattern of muscle involvement-affecting the posterior compartment of the lower leg and the anterior thigh-is characteristic of chronic progressive myopathy in hyperKPP. PMID:26256659

  5. Genetics Home Reference: hyperkalemic periodic paralysis

    MedlinePlus

    ... when the weak or paralyzed muscles release potassium ions into the bloodstream. In other cases, attacks are ... contractions is the flow of positively charged atoms (ions), including sodium, into muscle cells. The SCN4A protein ...

  6. [Tongue paralysis of neoplastic origin].

    PubMed

    Marco, M; Dalmau, J; Aguilar, M

    1989-10-01

    Tongue paralysis are often underestimated, particularly when isolated or having a chronic course. Sometimes, its early recognition may lead to the diagnosis of a tumor process, favorably modifying its course. We have retrospectively analyzed 13 cases of tongue paralysis of neoplastic etiology. In a woman, the paralysis was due to a lesion of the corticobulbar pathway whereas in the remaining 12, the alteration occurred in the hypoglossal nerve, particularly at extrabulbar intracranial and cranial base tract (10 cases). The clinical picture was due to the primary tumor in 9 patients, and due to bone or leptomeningeal metastases in the remaining four cases. In five cases, the lesion of the XII cranial nerve was essential for the diagnosis of the neoplasm or the neoplastic recurrence and in four cases, it was the only affected cranial nerve. PMID:2637769

  7. For Parents: Children and Teens with Paralysis

    MedlinePlus

    ... are available to answer your questions. Call toll-free 1-800-539-7309 Mon-Fri, 9am-5pm ... are people living with or impacted by paralysis. Free services and downloads > Paralysis Resource Guide Our free ...

  8. Hyperkalemic paralysis in primary adrenal insufficiency

    PubMed Central

    Mishra, Ajay; Pandya, Himanshu V.; Dave, Nikhil; Sapre, Chinmaye M.; Chaudhary, Sneha

    2014-01-01

    Hyperkalemic paralysis due to Addison's disease is rare, and potentially life-threatening entity presenting with flaccid motor weakness. This case under discussion highlights Hyperkalemic paralysis as initial symptomatic manifestation of primary adrenal insufficiency. PMID:25136192

  9. Isolated sleep paralysis elicited by sleep interruption.

    PubMed

    Takeuchi, T; Miyasita, A; Sasaki, Y; Inugami, M; Fukuda, K

    1992-06-01

    We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy. PMID:1621022

  10. The relationship between the Southern Oscillation Index, rainfall and the occurrence of canine tick paralysis, feline tick paralysis and canine parvovirus in Australia.

    PubMed

    Rika-Heke, Tamara; Kelman, Mark; Ward, Michael P

    2015-07-01

    The aim of this study was to describe the association between climate, weather and the occurrence of canine tick paralysis, feline tick paralysis and canine parvovirus in Australia. The Southern Oscillation Index (SOI) and monthly average rainfall (mm) data were used as indices for climate and weather, respectively. Case data were extracted from a voluntary national companion animal disease surveillance resource. Climate and weather data were obtained from the Australian Government Bureau of Meteorology. During the 4-year study period (January 2010-December 2013), a total of 4742 canine parvovirus cases and 8417 tick paralysis cases were reported. No significant (P ≥ 0.05) correlations were found between the SOI and parvovirus, canine tick paralysis or feline tick paralysis. A significant (P < 0.05) positive cross-correlation was found between parvovirus occurrence and rainfall in the same month (0.28), and significant negative cross-correlations (-0.26 to -0.36) between parvovirus occurrence and rainfall 4-6 months previously. Significant (P < 0.05) negative cross-correlations (-0.34 to -0.39) were found between canine tick paralysis occurrence and rainfall 1-3 months previously, and significant positive cross-correlations (0.29-0.47) between canine tick paralysis occurrence and rainfall 7-10 months previously. Significant positive cross-correlations (0.37-0.68) were found between cases of feline tick paralysis and rainfall 6-10 months previously. These findings may offer a useful tool for the management and prevention of tick paralysis and canine parvovirus, by providing an evidence base supporting the recommendations of veterinarians to clients thus reducing the impact of these diseases. PMID:25841899

  11. Facial nerve paralysis in children.

    PubMed

    Ciorba, Andrea; Corazzi, Virginia; Conz, Veronica; Bianchini, Chiara; Aimoni, Claudia

    2015-12-16

    Facial nerve palsy is a condition with several implications, particularly when occurring in childhood. It represents a serious clinical problem as it causes significant concerns in doctors because of its etiology, its treatment options and its outcome, as well as in little patients and their parents, because of functional and aesthetic outcomes. There are several described causes of facial nerve paralysis in children, as it can be congenital (due to delivery traumas and genetic or malformative diseases) or acquired (due to infective, inflammatory, neoplastic, traumatic or iatrogenic causes). Nonetheless, in approximately 40%-75% of the cases, the cause of unilateral facial paralysis still remains idiopathic. A careful diagnostic workout and differential diagnosis are particularly recommended in case of pediatric facial nerve palsy, in order to establish the most appropriate treatment, as the therapeutic approach differs in relation to the etiology. PMID:26677445

  12. Facial nerve paralysis in children

    PubMed Central

    Ciorba, Andrea; Corazzi, Virginia; Conz, Veronica; Bianchini, Chiara; Aimoni, Claudia

    2015-01-01

    Facial nerve palsy is a condition with several implications, particularly when occurring in childhood. It represents a serious clinical problem as it causes significant concerns in doctors because of its etiology, its treatment options and its outcome, as well as in little patients and their parents, because of functional and aesthetic outcomes. There are several described causes of facial nerve paralysis in children, as it can be congenital (due to delivery traumas and genetic or malformative diseases) or acquired (due to infective, inflammatory, neoplastic, traumatic or iatrogenic causes). Nonetheless, in approximately 40%-75% of the cases, the cause of unilateral facial paralysis still remains idiopathic. A careful diagnostic workout and differential diagnosis are particularly recommended in case of pediatric facial nerve palsy, in order to establish the most appropriate treatment, as the therapeutic approach differs in relation to the etiology. PMID:26677445

  13. [Surgical Therapy of Acquired Unilateral Diaphragmatic Paralysis: Indication and Results].

    PubMed

    Wiesemann, S; Haager, B; Passlick, B

    2016-09-01

    Unilateral elevation of the diaphragm may be due to various causes and requires further elucidation when the aetiology is unknown. Elevation of the diaphragm is often caused by diaphragmatic paralysis, either due to damage to the phrenic nerve or to the phrenic muscle. Patients typically complain of increased respiratory distress when lying down, bending or swimming. Basic diagnostic testing consists of a chest X-ray, as well as spirometry and computer tomography of the neck and chest. In many cases, no cause can be identified for the diaphragmatic paralysis. In symptomatic patients, diaphragm plication leads to fixation and thus to a reduction in the paradoxal respiratory movement of the paralysed diaphragm. In a large majority of studies, this results in significant and lasting improvement in vital capacity and respiratory distress. Spontaneous recovery of diaphragm paralysis is possible, even after several months, so a waiting period of at least 6 months should elapse before diaphragmatic plication is performed, if the clinical situation allows. The procedure can be performed minimally invasively, with low morbidity and mortality. When cutting the phrenic nerve, a nerve suture is recommended, if possible, or otherwise diaphragm plication during the procedure, especially in the case of pneumonectomy. This review provides an overview of the causes, pathophysiology, symptoms, diagnosis, therapy and results of diaphragmatic plication in acquired, unilateral diaphragmatic paralysis in adults, and suggests an algorithm for diagnostic testing and therapy. PMID:27607888

  14. Hypokalemic paralysis as a presenting manifestation of primary Sjögren's syndrome accompanied by vitamin D deficiency.

    PubMed

    Liao, Chen-Yi; Wang, Chih-Chiang; Chen, I-Hung; Shiang, Jeng-Chuan; Liu, Mei-Yu; Tsai, Ming-Kai

    2013-01-01

    Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease characterized by progressive lymphocyte infiltration of the exocrine glands. Overt or latent renal tubular acidosis (RTA) is a common extraglandular manifestation of pSS.Vitamin D deficiency is associated with autoimmune disorders; however, the potential correlation between pSS and vitamin D deficiency is rarely discussed. The current patient presented with distal RTA, hypocalcemia, and hypophosphatemia that were found to be secondary to both vitamin D deficiency and pSS. In patients diagnosed with both distal RTA and vitamin D deficiency, clinicians should consider autoimmune diseases such as pSS, as a possible underlying etiology. PMID:24126399

  15. Studies on immunological paralysis

    PubMed Central

    Miranda, J. J.; Zola, H.; Howard, J. G.

    1972-01-01

    The induction and loss of tolerance to native and depolymerized fractions of levan, a thymus-independent antigen, have been studied in (DBA/1×CBA-T6T6)F1 mice by a direct plaque-forming cell (PFC) assay. Tolerance following 1 mg native levan began to break by 80 days, whereas mice remained specifically unresponsive 150 days after 10 mg. Effects attributable to long persistence of antigen have been demonstrated. The following main features of levan tolerance were established by transfer of spleen cells to 900 R-irradiated recipients: (1) the induction period is very short—less than 24 hours. (2) No detectable immunity accompanies or precedes induction. (3) The fall in immunogenicity with reduction in molecular weight (mol. wt) of levan is not accompanied by loss of tolerogenicity. An effectively tolerogenic, non-immunogenic fraction (mol. wt<10,000) was found. (4) There is no rapid loss of tolerance following cell transfer (reactivity is only regained after 50 days), arguing against the existence of tolerant cells in this model. As these results and those from corresponding investigations with SIII and HGG all show major dissimilarities, it is considered imprudent to base generalizations concerning the nature of B cell tolerance on studies with only one type of antigen. Whether or not two different kinds of specific unresponsiveness might be implicated with these cells is discussed. PMID:4567654

  16. [The history of facial paralysis].

    PubMed

    Glicenstein, J

    2015-10-01

    Facial paralysis has been a recognized condition since Antiquity, and was mentionned by Hippocratus. In the 17th century, in 1687, the Dutch physician Stalpart Van der Wiel rendered a detailed observation. It was, however, Charles Bell who, in 1821, provided the description that specified the role of the facial nerve. Facial nerve surgery began at the end of the 19th century. Three different techniques were used successively: nerve anastomosis, (XI-VII Balance 1895, XII-VII, Korte 1903), myoplasties (Lexer 1908), and suspensions (Stein 1913). Bunnell successfully accomplished the first direct facial nerve repair in the temporal bone, in 1927, and in 1932 Balance and Duel experimented with nerve grafts. Thanks to progress in microsurgical techniques, the first faciofacial anastomosis was realized in 1970 (Smith, Scaramella), and an account of the first microneurovascular muscle transfer published in 1976 by Harii. Treatment of the eyelid paralysis was at the origin of numerous operations beginning in the 1960s; including palpebral spring (Morel Fatio 1962) silicone sling (Arion 1972), upperlid loading with gold plate (Illig 1968), magnets (Muhlbauer 1973) and transfacial nerve grafts (Anderl 1973). By the end of the 20th century, surgeons had at their disposal a wide range of valid techniques for facial nerve surgery, including modernized versions of older techniques. PMID:26088742

  17. Levothyroxine and Prednisone Causing Generalized Weakness in a Middle-Aged Man

    PubMed Central

    Word, Andrew; Davidson, Kevin; Elsayed, Essam

    2012-01-01

    Thyrotoxic induced hypokalemic periodic paralysis is a rare disorder that had been described in middle-aged men, predominantly Asians and Hispanics. This case presented with generalized weakness and hypokalemia after changing prescription for levothyroxine and starting prednisone to treat upper respiratory infection in a previously asymptomatic middle-aged Hispanic male. In this paper, we will go over the clinical presentation, mechanisms, and treatment of thyrotoxic induced hypokalemic periodic paralysis. Our objectives are to identify the classic constellation of findings in thyrotoxic periodic paralysis and to recognize the importance of considering thyrotoxic periodic paralysis among patients with hypokalemia. PMID:23119192

  18. [Facial paralysis surgery. Current concepts].

    PubMed

    Robla-Costales, David; Robla-Costales, Javier; Socolovsky, Mariano; di Masi, Gilda; Fernández, Javier; Campero, Álvaro

    2015-01-01

    Facial palsy is a relatively common condition, from which most cases recover spontaneously. However, each year, there are 127,000 new cases of irreversible facial paralysis. This condition causes aesthetic, functional and psychologically devastating effects in the patients who suffer it. Various reconstructive techniques have been described, but there is no consensus regarding their indication. While these techniques provide results that are not perfect, many of them give a very good aesthetic and functional result, promoting the psychological, social and labour reintegration of these patients. The aim of this article is to describe the indications for which each technique is used, their results and the ideal time when each one should be applied. PMID:25498528

  19. Hypokalemic quadriplegia and respiratory arrest revealing primary Sjögren's syndrome.

    PubMed

    Poux, J M; Peyronnet, P; Le Meur, Y; Favereau, J P; Charmes, J P; Leroux-Robert, C

    1992-04-01

    We report a case of hypokalemic flaccid quadriplegia with sudden respiratory arrest in a 38-year-old woman discovered to have distal renal tubular acidosis which lead to the diagnosis of primary Sjögren's syndrome. This case is compared to 8 similar cases previously described in the literature. PMID:1582057

  20. Timing of spontaneous sleep-paralysis episodes.

    PubMed

    Girard, Todd A; Cheyne, J Allan

    2006-06-01

    The objective of this prospective naturalistic field study was to determine the distribution of naturally occurring sleep-paralysis (SP) episodes over the course of nocturnal sleep and their relation to bedtimes. Regular SP experiencers (N = 348) who had previously filled out a screening assessment for SP as well as a general sleep survey were recruited. Participants reported, online over the World Wide Web, using a standard reporting form, bedtimes and subsequent latencies of spontaneous episodes of SP occurring in their homes shortly after their occurrence. The distribution of SP episodes over nights was skewed to the first 2 h following bedtime. Just over one quarter of SP episodes occurred within 1 h of bedtime, although episodes were reported throughout the night with a minor mode around the time of normal waking. SP latencies following bedtimes were moderately consistent across episodes and independent of bedtimes. Additionally, profiles of SP latencies validated self-reported hypnagogic, hypnomesic, and hypnopompic SP categories, as occurring near the beginning, middle, and end of the night/sleep period respectively. Results are consistent with the hypothesis that SP timing is controlled by mechanisms initiated at or following sleep onset. These results also suggest that SP, rather than uniquely reflecting anomalous sleep-onset rapid eye movement (REM) periods, may result from failure to maintain sleep during REM periods at any point during the sleep period. On this view, SP may sometimes reflect the maintenance of REM consciousness when waking and SP hallucinations the continuation of dream experiences into waking life. PMID:16704578

  1. Relationship between isolated sleep paralysis and geomagnetic influences: a case study.

    PubMed

    Conesa, J

    1995-06-01

    This preliminary report, of a longitudinal study, looks at the relationship between geomagnetic activity and the incidence of isolated sleep paralysis over a 23.5-mo. period. The author, who has frequently and for the last 24 years experienced isolated sleep paralysis was the subject. In addition, incidence of lucid dreaming, vivid dreams, and total dream frequency were looked at with respect to geomagnetic activity. The data were in the form of dream-recall frequency recorded in a diary. These frequency data were correlated with geomagnetic activity k-index values obtained from two observatories. A significant correlation was obtained between periods of local geomagnetic activity and the incidence of isolated sleep paralysis. Specifically, periods of relatively quiet geomagnetic activity were significantly associated with an increased incidence of episodes. PMID:7478886

  2. Isolated sleep paralysis: a web survey.

    PubMed

    Buzzi, G; Cirignotta, F

    2000-01-01

    Isolated Sleep Paralysis (SP) occurs at least once in a lifetime in 40-50% of normal subjects, while as a chronic complaint it is an uncommon and scarcely known disorder. A series of messages written by subjects who experienced at least one episode of SP, containing more or less detailed descriptions of this disorder, were collected from the Sleep Web site of the University of California in Los Angeles between January 1996 and July 1998. Two hundred and sixty-four messages fulfilling the International Classification of Sleep Disorders (ICSD) (Thorpy, 1990) minimal criteria for SP were analyzed. A wide spectrum of severity was evident, with a frequency of episodes ranging from one in a lifetime to almost every night, and a variety of emotional and hallucinatory experiences associated with SP episodes were reported. Clinical similarities between the recurrent form of isolated SP and channelopathies (in particular, periodic paralyses) are discussed. An activation of limbic system structures is suggested in order to explain some of the most common subjective experiences associated with SP. PMID:11382902

  3. Sleep paralysis in the elderly.

    PubMed

    Wing, Y K; Chiu, H; Leung, T; Ng, J

    1999-06-01

    Isolated sleep paralysis (SP) is a common sleep phenomenon that is highly colored by indigenous beliefs. In Hong Kong Chinese, the 'ghost oppression phenomenon' (GO) has been shown to be descriptively identical to SP. The prevailing concept is that the majority of cases with SP have their onset during adolescence, but the lack of any systematic study on an older population means that late-onset cases can not be excluded. In a study investigating the prevalence of mental disorders in Chinese elderly aged above 70 y in Hong Kong, we employed the revised GO questionnaire to study the prevalence of SP in this group of elderly as well. One hundred and fifty-eight subjects were finally analyzed for the study. Almost 18% (95% C.I. 11.77%, 23.68%) of the subjects reported experiences of GO. Their description of the features of GO showed striking similarity to those of SP. There was a clear bimodal distribution of onset of GO with peaks during adolescence and after age 60 y. At least one-third of the cases were late onset. In concordance with the rapid eye movement (REM)/wakefulness dissociation hypothesis of SP, those elderly with GO+ experiences also had more frequent nocturnal sleep disturbances. A family history was reported in 10% of subjects. PMID:10389097

  4. SURGICAL MANAGEMENT OF VOCAL CORD PARALYSIS: THE NEED FOR CAREFUL PATIENT SELECTION

    PubMed Central

    Kokong, DD; Adoga, AA; Bakari, A; Okundia, PO; Onakoya, PA; Nwaorgu, OGB

    2015-01-01

    Background Vocal cord paralysis is one of the challenging laryngeal clinical entities confronting the Laryngologist and indeed, the Phono-surgeon. The ability to maintain an effective balance between voice and airway function to ensure good quality of life requires expertise. This study is therefore designed to highlight our experience on surgical management of vocal cord paralysis. Method Clinical notes of all patients that met the inclusion criteria for this study on vocal cord paralysis over a ten-year period were analysed. Data was generated from patients’ case files retrieved using standard codes according to the International Classification of Diseases (ICD-10). Results From the 7,941 new ENT cases seen, 26 patients had vocal cord paralysis (VCP) giving a prevalence of 0.3%. The male to female ratio was 1: 4.2 with a mean age of 45.7years ± 6.3. Their ages ranged from 21–80 years. Thyroidectomy was the main causal factor in 46.2% while idiopathic causes was documented in 23.1%. Twenty-three patients (88.5%) had unilateral VCP from which 21(91.3%) were abductor paralysis. The ratio of Left: Right VCP was 3:1. All the 3 bilateral cases were abductor paralysis. Neurotropic agents only, were effective in cases of unilateral VCP. However, in those with bilateral paralysis, two had tracheostomy only, while the third had a laryngo-fissure, arytenoidoplasty and endo-laryngeal stenting in addition. All were successfully decannulated with good voice quality. Conclusion With these observations, we suggest the choice of appropriate surgical technique, timing and careful patient selection in order to preserve voice, curtail operative sequelae and achieve good quality of life (QoL) which is the overall management strategy, be borne in mind. PMID:26709328

  5. Massive Retinal Pigment Epithelial Detachment Following Acute Hypokalemic Quadriparesis in Dengue Fever

    PubMed Central

    Goel, Neha; Bhambhwani, Vishaal; Jain, Pooja; Ghosh, Basudeb

    2016-01-01

    Purpose: To describe an unusual retinal manifestation of dengue fever in an endemic region. Case Report: A 35 year old male presenting with acute onset decreased vision in his right eye, was found to have a massive retinal pigment epithelial detachment (PED) extending up to the vascular arcades. He had been diagnosed with acute hypokalemic quadriparesis in dengue fever in the preceding week, which had resolved following treatment. The patient was managed conservatively. At three months follow up, there was spontaneous flattening of the PEDs with improvement in visual acuity. Conclusion: Dengue fever complicated by acute hypokalemic quadriparesis can be associated with PED, which can be large. The condition resolves spontaneously and bears a good prognosis.

  6. Ulnar nerve paralysis after forearm bone fracture.

    PubMed

    Schwartsmann, Carlos Roberto; Ruschel, Paulo Henrique; Huyer, Rodrigo Guimarães

    2016-01-01

    Paralysis or nerve injury associated with fractures of forearm bones fracture is rare and is more common in exposed fractures with large soft-tissue injuries. Ulnar nerve paralysis is a rare condition associated with closed fractures of the forearm. In most cases, the cause of paralysis is nerve contusion, which evolves with neuropraxia. However, nerve lacerations and entrapment at the fracture site always need to be borne in mind. This becomes more important when neuropraxia appears or worsens after reduction of a closed fracture of the forearm has been completed. The importance of diagnosing this injury and differentiating its features lies in the fact that, depending on the type of lesion, different types of management will be chosen. PMID:27517030

  7. Screening of cases of acute flaccid paralysis for poliomyelitis eradication: ways to improve specificity.

    PubMed Central

    Andrus, J. K.; de Quadros, C.; Olivé, J. M.; Hull, H. F.

    1992-01-01

    The Pan American Health Organization in 1985 adopted an initiative to eradicate poliomyelitis from the Western Hemisphere. In 1990, over 2000 cases of acute flaccid paralysis (AFP) were reported in this region, of which < 1% were determined to be caused by wild poliovirus. At present, the eradication programme uses AFP as the criterion for surveillance of children aged < 15 years; this is 100% sensitive, but not specific. To minimize unnecessary diagnostic investigations, we studied all 4333 cases of AFP reported to the programme during 1989 and 1990 in order to develop more efficient operational screening criteria for cases of AFP. Among children with AFP, the use of criteria such as age < 6 years and either presence of fever at the onset of paralysis or a < 4-day period for complete development of paralysis resulted in a sensitivity of 96% (95% C.I. 90-103%) and specificity of 49% (C.I. 47-52%). With criteria of age < 6 years and fever present at the onset of paralysis the sensitivity was 75% (C.I. 61-89%) and specificity was 73% (C.I. 71-75%). These results suggest that by screening young children with AFP who either had fever at the onset or showed a rapid progression of paralysis, the number of cases of AFP requiring investigation can be reduced by one half, with minimal compromise in the sensitivity of confirmed poliomyelitis case detection. PMID:1281445

  8. Hyperkalaemic paralysis--a bizarre presentation of renal failure.

    PubMed

    Cumberbatch, G L; Hampton, T J

    1999-05-01

    Paralysis due to hyperkalaemia is rare and the diagnosis may be overlooked in the first instance. However it is rapidly reversible and so long as electro-cardiography and serum potassium measurement are urgently done in all patients presenting with paralysis, it will not be missed. A case of hyperkalaemic paralysis is described and a review of the emergency management discussed. PMID:10353058

  9. Resolution of sleep paralysis by weak electromagnetic fields in a patient with multiple sclerosis.

    PubMed

    Sandyk, R

    1997-08-01

    Sleep paralysis refers to episodes of inability to move during the onset of sleep or more commonly upon awakening. Patients often describe the sensation of struggling to move and may experience simultaneous frightening vivid hallucinations and dreams. Sleep paralysis and other manifestations of dissociated states of wakefulness and sleep, which reflect deficient monoaminergic regulation of neural modulators of REM sleep, have been reported in patients with multiple sclerosis (MS). A 40 year old woman with remitting-progressive multiple sclerosis (MS) experienced episodes of sleep paralysis since the age of 16, four years prior to the onset of her neurological symptoms. Episodes of sleep paralysis, which manifested at a frequency of about once a week, occurred only upon awakening in the morning and were considered by the patient as a most terrifying experience. Periods of mental stress, sleep deprivation, physical fatigue and exacerbation of MS symptoms appeared to enhance the occurrence of sleep paralysis. In July of 1992 the patient began experimental treatment with AC pulsed applications of picotesla intensity electromagnetic fields (EMFs) of 5Hz frequency which were applied extracerebrally 1-2 times per week. During the course of treatment with EMFs the patient made a dramatic recovery of symptoms with improvement in vision, mobility, balance, bladder control, fatigue and short term memory. In addition, her baseline pattern reversal visual evoked potential studies, which showed abnormally prolonged latencies in both eyes, normalized 3 weeks after the initiation of magnetic therapy and remained normal more than 2.5 years later. Since the introduction of magnetic therapy episodes of sleep paralysis gradually diminished and abated completely over the past 3 years. This report suggests that MS may be associated with deficient REM sleep inhibitory neural mechanisms leading to sleep paralysis secondary to the intrusion of REM sleep atonia and dream imagery into the

  10. Abdominal muscle paralysis associated with herpes zoster.

    PubMed

    Gottschau, P; Trojaborg, W

    1991-10-01

    We describe a 77-year-old women with cutaneous herpes zoster in the area of the right T9-T11 dermatomes complicated by abdominal muscle paralysis. Four months after onset of paralysis, stimulation of appropriate intercostal nerves failed to evoke responses from the corresponding segments of the rectus abdominis muscle. Three months later EMG of these muscle segments revealed profuse denervation activity and spontaneous long-lasting burst of high frequency discharges. Magnetic stimulation applied transcranially and peripherally at T10 evoked responses from the left, but not from the right paralytic rectus abdominis muscle. Electric stimulation of right T10 elicited a markedly delayed, prolonged and polyphasic response in the transverse abdominis muscle and EMG revealed polyphasia and increased motor unit potential duration in muscle segments underlying herpes zoster eruption. One and a half years after onset, the paralysis of the rectus abdominis muscle was still present. A survey of the literature concerning this rare type of zoster paralysis is presented. PMID:1837649

  11. Cultural variation in the clinical presentation of sleep paralysis.

    PubMed

    de Jong, Joop T V M

    2005-03-01

    Sleep paralysis is one of the lesser-known and more benign forms of parasomnias. The primary or idiopathic form, also called isolated sleep paralysis, is illustrated by showing how patients from different cultures weave the phenomenology of sleep paralysis into their clinical narratives. Clinical case examples are presented of patients from Guinea Bissau, the Netherlands, Morocco, and Surinam with different types of psychopathology, but all accompanied by sleep paralysis. Depending on the meaning given to and etiological interpretations of the sleep paralysis, which is largely culturally determined, patients react to the event in specific ways. PMID:15881269

  12. Focal and abnormally persistent paralysis associated with congenital paramyotonia

    PubMed Central

    Magot, Armelle; David, Albert; Sternberg, Damien; Péréon, Yann

    2014-01-01

    Mutations of the skeletal muscle voltage-gated sodium channel (NaV1.4) are an established cause of several clinically distinct forms of periodic paralysis and myotonia. Focal paresis has sometimes already been described. We report a case with atypical clinical manifestation comprising paramyotonia and cold-induced persistent and focal paralysis. A 27-year-old woman presented with paramyotonia congenita since her childhood. She experienced during her childhood one brief episode of generalised weakness. At the age of 27, she experienced a focal paresis lasting for several months. The known mutation p.Val1293Ile was found in the muscle sodium channel gene (SCN4A). Channel inactivation is involved in most Na+ channelopathies. Fast inactivation is known to be responsible for the myotonia phenotype. We hypothesise that the V1293I mutation may also alter the slow inactivation in specific conditions, for example, prolonged cold exposure or prolonged and intensive exercise. This observation broadens the spectrum of clinical manifestations of this sodium channel mutation. PMID:24939454

  13. Paralysie musculaire secondaire à une polymyosite

    PubMed Central

    Ennafiri, Meryem; Elotmani, Wafae; Awab, Almahdi; El Moussaoui, Rachid; El Hijri, Ahmed; Alilou, Mustapha; Azzouzi, Abderrahim

    2015-01-01

    Les polymyosites sont des maladies inflammatoires des muscles striés, d’étiologie inconnue. Le déficit musculaire, qui se résume généralement à une fatigabilité, évolue de façon bilatérale, symétrique et non sélective avec prédominance sur les muscles proximaux. L'intensité de la faiblesse musculaire est variable d'un sujet à un autre, de la simple gêne fonctionnelle à un état grabataire. Nous rapportons l'observation d'un cas de polymyosite particulièrement sévère avec paralysie musculaire complète, touchant tous les muscles de l'organisme, d’évolution favorable sous immunoglobulines intraveineuses et nous discutons les facteurs favorisant la paralysie musculaire. PMID:26185559

  14. Diagnosing limb paresis and paralysis in sheep

    PubMed Central

    Crilly, James Patrick; Rzechorzek, Nina; Scott, Philip

    2015-01-01

    Paresis and paralysis are uncommon problems in sheep but are likely to prompt farmers to seek veterinary advice. A thorough and logical approach can aid in determining the cause of the problem and highlighting the benefit of veterinary involvement. While this may not necessarily alter the prognosis for an individual animal, it can help in formulating preventive measures and avoid the costs – both in economic and in welfare terms – of misdirected treatment. Distinguishing between central and peripheral lesions is most important, as the relative prognoses are markedly different, and this can often be achieved with minimal equipment. This article describes an approach to performing a neurological examination of the ovine trunk and limbs, the ancillary tests available and the common and important causes of paresis and paralysis in sheep. PMID:26752801

  15. Miller Fisher syndrome presenting as palate paralysis.

    PubMed

    Noureldine, Mohammad Hassan A; Sweid, Ahmad; Ahdab, Rechdi

    2016-09-15

    We report a 63-year old patient who presented to our care initially with a hypernasal voice followed by ataxia, ptosis, dysphonia, and paresthesias. The patient's history, physical examination, and additional tests led to a Miller Fisher syndrome (MFS) diagnosis. Palatal paralysis as an inaugurating manifestation of MFS is quite rare and requires special attention from neurologists and otolaryngologists. Although it may present as benign as an acute change in voice, early diagnosis and prompt management may prevent further complications. PMID:27609285

  16. Literature study on clinical treatment of facial paralysis in the last 20 years using Web of Science

    PubMed Central

    Zhang, Xiaoge; Feng, Ling; Du, Liang; Zhang, Anxiang; Tang, Tian

    2012-01-01

    BACKGROUND: Facial paralysis is defined as severe or complete loss of facial muscle motor function. OBJECTIVE: The study was undertaken to explore a bibliometric approach to quantitatively assess the research on clinical treatment of facial paralysis using rehabilitation, physiotherapy and acupuncture using Web of Science from 1992 to 2011. DESIGN: Bibliometric approach. DATA RETRIEVAL: A bibliometric analysis based on the publications on Web of Science was performed using key words such as “facial paralysis”, “rehabilitation”, “physiotherapy” and “acupuncture”. INCLUSIVE CRITERIA: (1) Research articles on the clinical treatment of facial paralysis using acupuncture or physiotherapy (e.g. exercise, electro-stimulation) and other rehabilitation methods; (2) researches on human and animal fundamentals, clinical trials and case reports; (3) Article types: article, review, proceedings paper, note, letter, editorial material, discussion, book chapter. (4) Publication year: 1992–2011 inclusive. Exclusion criteria: (1) Articles on the causes and diagnosis on facial paralysis; (2) Type of articles: correction; (3) Articles from following databases: all databases related to social science and chemical databases in Web of Science. MAIN OUTCOME MEASURES: (1) Overall number of publications; (2) number of publications annually; (3) number of citations received annually; (4) top cited paper; (5) subject categories of publication; (6) the number of countries in which the article is published; (7) distribution of output in journals. RESULTS: Overall population stands at 3 543 research articles addressing the clinical treatment of facial paralysis in Web of Science during the study period. There is also a markedly increase in the number of publications on the subject “facial paralysis treatments using rehabilitation” during the first decade of the 21st century, except in 2004 and 2006 when there are perceptible drops in the number of articles published. The

  17. Vocal Cord Paralysis and its Etiologies: A Prospective Study

    PubMed Central

    Seyed Toutounchi, Seyed Javad; Eydi, Mahmood; Golzari, Samad EJ; Ghaffari, Mohammad Reza; Parvizian, Nashmil

    2014-01-01

    Introduction: Vocal cord paralysis is a common symptom of numerous diseases and it may be due to neurogenic or mechanical fixation of the cords. Paralysis of the vocal cords is just a symptom of underlying disease in some cases; so, clinical diagnosis of the underlying cause leading to paralysis of the vocal cords is important. This study evaluates the causes of vocal cord paralysis. Methods: In a prospective study, 45 patients with paralyzed vocal cord diagnosis were examined by tests such as examination of the pharynx, larynx, esophagus, thyroid, cervical, lung, and mediastinum, brain and heart by diagnostic imaging to investigate the cause vocal cord paralysis. The study was ended by diagnosing the reason of vocal cord paralysis at each stage of the examination and the clinical studies. Results: The mean duration of symptoms was 18.95±6.50 months. The reason for referral was phonation changes (97.8%) and aspiration (37.8%) in the subjects. There was bilateral paralysis in 6.82%, left paralysis in 56.82% and right in 63.36% of subjects. The type of vocal cord placement was midline in 52.8%, paramedian in 44.4% and lateral in 2.8% of the subjects. The causes of vocal cords paralysis were idiopathic paralysis (31.11%), tumors (31.11%), surgery (28.89%), trauma, brain problems, systemic disease and other causes (2.2%). Conclusion: An integrated diagnostic and treatment program is necessary for patients with vocal cord paralysis. Possibility of malignancy should be excluded before marking idiopathic reason to vocal cord paralysis. PMID:24753832

  18. The pattern of isolated sleep paralysis among Nigerian medical students.

    PubMed

    Ohaeri, J U; Odejide, A O; Ikuesan, B A; Adeyemi, J D

    1989-07-01

    In a cross-sectional study of the patterns of isolated sleep paralysis among 164 Nigerian medical students, 26.1% admitted having experienced this phenomenon. About 31% of the females and 20% of the males had had this experience. Of those with sleep paralysis, 32.6% had hypnogenic hallucinations during the episode, mainly visual. Sleep paralysis was not significantly associated with psychosocial distress or differences in personality profile. Although the rate differs across cultures, the myths associated with sleep paralysis are similar. PMID:2787863

  19. The dosage requirements for immunological paralysis by soluble proteins

    PubMed Central

    Mitchison, N. A.

    1968-01-01

    The quantitative dose requirements for induction of paralysis by BSA in mice has been the subject of further study. Parallel studies have been made with lysozyme, ovalbumin, diphtheria toxoid and ribonuclease, in which similar paralysing and immunizing procedures were used, and similar direct binding tests applied to measurement of the response. In normal adults all the antigens tested induced high-zone paralysis and concomitant immunization, but BSA alone induced low-zone paralysis. With irradiation, with courses of injection commencing at birth, and with paralysis-maintaining treatment, all the antigens tested induced paralysis in a zone quantitatively similar to the low zone detectable in normal adults with BSA. Neither irradiation, treatment with cortisol, nor thymectomy affected the rate of induction of paralysis in the low zone. On the other hand the minimum dose required for immunization varied markedly from one antigen to another. The ability of BSA to induce low-zone paralysis in normal adults can, therefore, be attributed to the failure of low doses of this antigen to immunize. The consistency of paralysis threshold, in contrast to the variability for immunization, is interpreted as evidence of an additional step of complexity involved in immunization that is not required for paralysis. PMID:5696262

  20. Facial-paralysis diagnostic system based on 3D reconstruction

    NASA Astrophysics Data System (ADS)

    Khairunnisaa, Aida; Basah, Shafriza Nisha; Yazid, Haniza; Basri, Hassrizal Hassan; Yaacob, Sazali; Chin, Lim Chee

    2015-05-01

    The diagnostic process of facial paralysis requires qualitative assessment for the classification and treatment planning. This result is inconsistent assessment that potential affect treatment planning. We developed a facial-paralysis diagnostic system based on 3D reconstruction of RGB and depth data using a standard structured-light camera - Kinect 360 - and implementation of Active Appearance Models (AAM). We also proposed a quantitative assessment for facial paralysis based on triangular model. In this paper, we report on the design and development process, including preliminary experimental results. Our preliminary experimental results demonstrate the feasibility of our quantitative assessment system to diagnose facial paralysis.

  1. Tick paralysis in Australia caused by Ixodes holocyclus Neumann

    PubMed Central

    Hall-Mendelin, S; Craig, S B; Hall, R A; O’Donoghue, P; Atwell, R B; Tulsiani, S M; Graham, G C

    2011-01-01

    Ticks are obligate haematophagous ectoparasites of various animals, including humans, and are abundant in temperate and tropical zones around the world. They are the most important vectors for the pathogens causing disease in livestock and second only to mosquitoes as vectors of pathogens causing human disease. Ticks are formidable arachnids, capable of not only transmitting the pathogens involved in some infectious diseases but also of inducing allergies and causing toxicoses and paralysis, with possible fatal outcomes for the host. This review focuses on tick paralysis, the role of the Australian paralysis tick Ixodes holocyclus, and the role of toxin molecules from this species in causing paralysis in the host. PMID:21396246

  2. Periocular Reconstruction in Patients with Facial Paralysis.

    PubMed

    Joseph, Shannon S; Joseph, Andrew W; Douglas, Raymond S; Massry, Guy G

    2016-04-01

    Facial paralysis can result in serious ocular consequences. All patients with orbicularis oculi weakness in the setting of facial nerve injury should undergo a thorough ophthalmologic evaluation. The main goal of management in these patients is to protect the ocular surface and preserve visual function. Patients with expected recovery of facial nerve function may only require temporary and conservative measures to protect the ocular surface. Patients with prolonged or unlikely recovery of facial nerve function benefit from surgical rehabilitation of the periorbital complex. Current reconstructive procedures are most commonly intended to improve coverage of the eye but cannot restore blink. PMID:27040589

  3. Teaching about Inequality: Student Resistance, Paralysis, and Rage.

    ERIC Educational Resources Information Center

    Davis, Nancy J.

    1992-01-01

    Discusses three classroom climates that are often encountered in teaching about inequality and social stratification: resistance, paralysis, and rage. Describes resistance as denying the existence or importance of inequality. Defines paralysis as classes that see little chance of overcoming inequality. Suggests that the enraged class is unable to…

  4. Like a Deer in the Headlights: The Paralysis of Stuckness

    ERIC Educational Resources Information Center

    Anderson-Nathe, Ben

    2008-01-01

    When describing how they experience moments of not-knowing, youth workers often talk about a sense of paralysis, as though their uncertainty becomes physically constraining. This chapter describes the first of five themes associated with youth workers' experiences of not knowing what to do: the paralysis of stuckness. In addition to describing and…

  5. Neurobrucellosis developing unilateral oculomotor nerve paralysis.

    PubMed

    Işıkay, Sedat; Yılmaz, Kutluhan; Ölmez, Akgün

    2012-11-01

    Brucellosis is a zoonotic infectious disease that is common around the world. Its clinical course demonstrates great diversity as it can affect all organs and systems. However, the central nervous system is rarely affected in the pediatric population. Neurobrucellosis is most frequently observed with meningitis and has numerous complications, including meningocephalitis, myelitis, cranial nerve paralyses, radiculopathy, and neuropathy. Neurobrucellosis affects the second, third, sixth, seventh, and eighth cranial nerves. Involvement of the oculomotor nerves is a very rare complication in neurobrucellosis although several adult cases have been reported. In this article, we present the case of a 9-year-old girl who developed unilateral nerve paralysis as a secondary complication of neurobrucellosis and recovered without sequel after treatment. This case is notable because it is a very rare, the first within the pediatric population. Our article emphasizes that neurobrucellosis should be considered among the distinguishing diagnoses in every case that is admitted for nerve paralysis in regions where Brucella infection is endemic. PMID:22244219

  6. Yamamoto New Scalp Acupuncture, Applied Kinesiology, and Breathing Exercises for Facial Paralysis in a Young Boy Caused by Lyme Disease-A Case Report.

    PubMed

    Molsberger, Friedrich; Raak, C; Teuber, M

    2016-01-01

    The case study reports on the effect of pharmacological, complementary, and alternative medicine including YNSA, Applied Kinesiology, and respiratory exercises in a 9-year-old boy with facial paralysis. The boy suffered from borreliosis and one-sided facial paralysis that occurred 3.5 weeks after being bitten by a tick and persisted despite 4 weeks of medication with antibiotics. In the first treatment, muscle function as assessed by the coachman׳s test was normalized, and improvement in the facial paralysis was observed. Within 8 additional treatments over a period of 2 months, the boy showed complete recovery. The case shows a multimodal approach to facial paralysis integrating pharmacological treatment and CAM including YNSA, Applied Kinesiology, and breathing exercises. PMID:27102135

  7. The developing shoulder has a limited capacity to recover after a short duration of neonatal paralysis

    PubMed Central

    Potter, Ryan; Havlioglu, Necat; Thomopoulos, Stavros

    2014-01-01

    Mechanical stimuli are required for the proper development of the musculoskeletal system. Removal of muscle forces during fetal or early post-natal timepoints impairs the formation of bone, tendon, and their attachment (the enthesis). The goal of the current study was to examine the capacity of the shoulder to recover after a short duration of neonatal rotator cuff paralysis, a condition mimicking the clinical condition neonatal brachial plexus palsy. We asked if reapplication of muscle load to a transiently paralyzed muscle would allow for full recovery of tissue properties. CD-1 mice were injected with botulinum toxin A to paralyze the supraspinatus muscle from birth through 2 weeks and subsequently allowed to recover. The biomechanics of the enthesis was determined using tensile testing and the morphology of the shoulder joint was determined using micro computed tomography and histology. A recovery period of at least 10 weeks was required to achieve control properties, demonstrating a limited capacity of the shoulder to recover after only two weeks of muscle paralysis. Although care must be taken when extrapolating results from an animal model to the human condition, the results of the current study imply that treatment of neonatal brachial plexus palsy should be aggressive, as even short periods of paralysis could lead to long-term deficiencies in enthesis biomechanics and shoulder morphology. PMID:24831237

  8. Isolated sleep paralysis and fearful isolated sleep paralysis in outpatients with panic attacks.

    PubMed

    Sharpless, Brian A; McCarthy, Kevin S; Chambless, Dianne L; Milrod, Barbara L; Khalsa, Shabad-Ratan; Barber, Jacques P

    2010-12-01

    Isolated sleep paralysis (ISP) has received scant attention in clinical populations, and there has been little empirical consideration of the role of fear in ISP episodes. To facilitate research and clinical work in this area, the authors developed a reliable semistructured interview (the Fearful Isolated Sleep Paralysis Interview) to assess ISP and their proposed fearful ISP (FISP) episode criteria in 133 patients presenting for panic disorder treatment. Of these, 29.3% met lifetime ISP episode criteria, 20.3% met the authors' lifetime FISP episode criteria, and 12.8% met their recurrent FISP criteria. Both ISP and FISP were associated with minority status and comorbidity. However, only FISP was significantly associated with posttraumatic stress disorder, body mass, anxiety sensitivity, and mood and anxiety disorder symptomatology. PMID:20715166

  9. Recurrent Attacks of Hypokalemic Quadriparesis: An Unusual Presentation of Primary Sjögren Syndrome.

    PubMed

    Seirafian, Shiva; Shafie, Mohammad; Abedini, Amin; Pakzad, Bahram; Roomizadeh, Peyman

    2016-01-01

    We herein report the case of a 64-year old woman with recurrent attacks of hypokalemic quadriparesis which resulted from distal renal tubular acidosis (dRTA) secondary to Sjögren syndrome. The patient presented with sudden onset quadriparesis. A physical examination showed symmetric weakness of all four limbs. Severe hypokalemia (1.8 mEq/L), accompanied by normal anion gap metabolic acidosis, a positive urine anion gap and an inappropriately high urine pH pointed toward the diagnosis of dRTA. Further investigations disclosed primary Sjögren syndrome, which had not previously been recognized. On the basis of the current report and a review of the literature we suggest investigating the possibility of Sjögren syndrome in all patients with clinically unexplained dRTA. PMID:27374687

  10. Bulbar Paralysis and Facial Paralysis due to Metastatic Hepatocellular Carcinoma: A Case Report and Literature Review.

    PubMed

    Liu, Min; Liu, Shixin; Liu, Bailong; Liu, Bin; Guo, Liang; Wang, Xu; Wang, Qiang; Yang, Shuo; Dong, Lihua

    2016-01-01

    Skull-base metastasis (SBM) from hepatocellular carcinoma (HCC) is extremely rare, and multiple cranial nerve paralysis due to SBM from HCC is also rare. We report a case of bulbar and facial paralysis due to SBM from HCC. A 46-year-old Chinese man presented with a hepatic right lobe lesion that was detected during a routine physical examination. After several failed attempts to treat the primary tumor and bone metastases, neurological examination revealed left VII, IX, X, and XI cranial nerve paralysis. Computed tomography of the skull base subsequently revealed a large mass that had destroyed the left occipital and temporal bones and invaded the adjacent structure. After radiotherapy (27 Gy, 9 fractions), the patient experienced relief from his pain, and the cranial nerve dysfunction regressed. However, the patient ultimately died, due to the tumor's progression. Radiotherapy is usually the best option to relieve pain and achieve regression of cranial nerve dysfunction in cases of SBM from HCC, although early treatment is needed to achieve optimal outcomes. The present case helps expand our understanding regarding this rare metastatic pathway and indicates that improved awareness of SBM in clinical practice can help facilitate timely and appropriate treatment. PMID:26825921

  11. Bilateral traumatic facial paralysis. Case report.

    PubMed

    Undabeitia, Jose; Liu, Brian; Pendleton, Courtney; Nogues, Pere; Noboa, Roberto; Undabeitia, Jose Ignacio

    2013-01-01

    Although traumatic injury of the facial nerve is a relatively common condition in neurosurgical practice, bilateral lesions related to fracture of temporal bones are seldom seen. We report the case of a 38-year-old patient admitted to Intensive Care Unit after severe head trauma requiring ventilatory support (Glasgow Coma Scale of 7 on admission). A computed tomography (CT) scan confirmed a longitudinal fracture of the right temporal bone and a transversal fracture of the left. After successful weaning from respirator, bilateral facial paralysis was observed. The possible aetiologies for facial diplegia differ from those of unilateral injury. Due to the lack of facial asymmetry, it can be easily missed in critically ill patients, and both the high resolution CT scan and electromyographic studies can be helpful for correct diagnosis. PMID:23541180

  12. Paralysis recovery in humans and model systems

    NASA Technical Reports Server (NTRS)

    Edgerton, V. Reggie; Roy, Roland R.

    2002-01-01

    Considerable evidence now demonstrates that extensive functional and anatomical reorganization following spinal cord injury occurs in centers of the brain that have some input into spinal motor pools. This is very encouraging, given the accumulating evidence that new connections formed across spinal lesions may not be initially functionally useful. The second area of advancement in the field of paralysis recovery is in the development of effective interventions to counter axonal growth inhibition. A third area of significant progress is the development of robotic devices to quantify the performance level of motor tasks following spinal cord injury and to 'teach' the spinal cord to step and stand. Advances are being made with robotic devices for mice, rats and humans.

  13. Clinical analysis of cervical radiculopathy causing deltoid paralysis.

    PubMed

    Chang, Han; Park, Jong-Beom; Hwang, Jin-Yeun; Song, Kyung-Jin

    2003-10-01

    In general, deltoid paralysis develops in patients with cervical disc herniation (CDH) or cervical spondylotic radiculopathy (CSR) at the level of C4/5, resulting in compression of the C5 nerve root. Therefore, little attention has been paid to CDH or CSR at other levels as the possible cause of deltoid paralysis. In addition, the surgical outcomes for deltoid paralysis have not been fully described. Fourteen patients with single-level CDH or CSR, who had undergone anterior cervical decompression and fusion for deltoid paralysis, were included in this study. The severity of deltoid paralysis was classified into five grades according to manual motor power test, and the severity of radiculopathy was recorded on a visual analog scale (zero to ten points). The degree of improvement in both the severity of deltoid paralysis and radiculopathy following surgery was evaluated. Of 14 patients, one had C3/4 CDH, four had C4/5 CDH, three had C4/5 CSR, one had C5/6 CDH, and five had C5/6 CSR. Both deltoid paralysis and radiculopathy improved significantly with surgery (2.57+/-0.51 grades vs 4.14+/-0.66, P=0.001, and 7.64+/-1.65 points vs 3.21+/-0.58, P=0.001, respectively). In conclusion, the current study demonstrates that deltoid paralysis can develop due to CDH or CSR not only C4/5, but also at the levels of C3/4 and C5/6, and that surgical decompression significantly improves the degree of deltoid paralysis due to cervical radiculopathy. PMID:12734743

  14. [Deviation index of eye and mouth on peripheral facial paralysis].

    PubMed

    Li, Xue; Liao, Pin-Dong; Luo, Min; Zhu, Bin-Ye

    2011-09-01

    Differences of some points, levels and angles of the healthy and affected sides of patients with peripheral facial paralysis were picked out according to photographs. Through analysis of the index between the healthy and affected side of the patients and the difference between healthy people and patients, it is approved that those special points, levels and angles, which are called as deviation index of eye and mouth, can evaluate peripheral facial paralysis objectively and judge the degree of deviation. Therefore, it provides references for the diagnosis of facial paralysis and its degree judgement. PMID:21972641

  15. Progress in Paralysis | NIH MedlinePlus the Magazine

    MedlinePlus

    ... of this page please turn JavaScript on. Feature: Spinal Cord Stimulation Progress in Paralysis Past Issues / Summer 2014 ... 1.275 million of those cases resulted from spinal cord injury. This is five times the previous estimate. ...

  16. Neonatal peripheral facial paralysis' evaluation with photogrammetry: A case report.

    PubMed

    da Fonseca Filho, Gentil Gomes; de Medeiros Cirne, Gabriele Natane; Cacho, Roberta Oliveira; de Souza, Jane Carla; Nagem, Danilo; Cacho, Enio Walker Azevedo; Moran, Cristiane Aparecida; Abreu, Bruna; Pereira, Silvana Alves

    2015-12-01

    Facial paralysis in newborns can leave functional sequelae. Determining the evolution and amount of functional losses requires consistent evaluation methods that measure, quantitatively, the evolution of clinical functionality. This paper reports an innovative method of facial assessment for the case of a child 28 days of age with unilateral facial paralysis. The child had difficulty breast feeding, and quickly responded to the physical therapy treatment. PMID:26607566

  17. Sleep paralysis, sexual abuse, and space alien abduction.

    PubMed

    McNally, Richard J; Clancy, Susan A

    2005-03-01

    Sleep paralysis accompanied by hypnopompic ('upon awakening') hallucinations is an often-frightening manifestation of discordance between the cognitive/perceptual and motor aspects of rapid eye movement (REM) sleep. Awakening sleepers become aware of an inability to move, and sometimes experience intrusion of dream mentation into waking consciousness (e.g. seeing intruders in the bedroom). In this article, we summarize two studies. In the first study, we assessed 10 individuals who reported abduction by space aliens and whose claims were linked to apparent episodes of sleep paralysis during which hypnopompic hallucinations were interpreted as alien beings. In the second study, adults reporting repressed, recovered, or continuous memories of childhood sexual abuse more often reported sleep paralysis than did a control group. Among the 31 reporting sleep paralysis, only one person linked it to abuse memories. This person was among the six recovered memory participants who reported sleep paralysis (i.e. 17% rate of interpreting it as abuse-related). People rely on personally plausible cultural narratives to interpret these otherwise baffling sleep paralysis episodes. PMID:15881271

  18. Hypokalemic quadriparesis and rhabdomyolysis as a rare presentation of distal renal tubular acidosis.

    PubMed

    Ahmad Bhat, Manzoor; Ahmad Laway, Bashir; Mustafa, Farhat; Shafi Kuchay, Mohammad; Mubarik, Idrees; Ahmad Palla, Nazir

    2014-01-01

    Distal renal tubular acidosis is a syndrome of abnormal urine acidification and is characterized by hyperchloremic metabolic acidosis, hypokalemia, hypercalciurea, nephrocalcinosis and nephrolithiasis. Despite the presence of persistent hypokalemia, acute muscular paralysis is rarely encountered in males. Here, we will report an eighteen year old male patient who presented with flaccid quadriparesis and was subsequently found to have rhabdomyolysis, severe short stature, skeletal deformities and primary distal renal tubular acidosis. PMID:25250276

  19. Tick holocyclotoxins trigger host paralysis by presynaptic inhibition.

    PubMed

    Chand, Kirat K; Lee, Kah Meng; Lavidis, Nickolas A; Rodriguez-Valle, Manuel; Ijaz, Hina; Koehbach, Johannes; Clark, Richard J; Lew-Tabor, Ala; Noakes, Peter G

    2016-01-01

    Ticks are important vectors of pathogens and secreted neurotoxins with approximately 69 out of 692 tick species having the ability to induce severe toxicoses in their hosts. The Australian paralysis tick (Ixodes holocyclus) is known to be one of the most virulent tick species producing a flaccid paralysis and fatalities caused by a family of neurotoxins known as holocyclotoxins (HTs). The paralysis mechanism of these toxins is temperature dependent and is thought to involve inhibition of acetylcholine levels at the neuromuscular junction. However, the target and mechanism of this inhibition remain uncharacterised. Here, we report that three members of the holocyclotoxin family; HT-1 (GenBank AY766147), HT-3 (GenBank KP096303) and HT-12 (GenBank KP963967) induce muscle paralysis by inhibiting the dependence of transmitter release on extracellular calcium. Previous study was conducted using extracts from tick salivary glands, while the present study is the first to use pure toxins from I. holocyclus. Our findings provide greater insight into the mechanisms by which these toxins act to induce paralysis. PMID:27389875

  20. Tick holocyclotoxins trigger host paralysis by presynaptic inhibition

    PubMed Central

    Chand, Kirat K.; Lee, Kah Meng; Lavidis, Nickolas A.; Rodriguez-Valle, Manuel; Ijaz, Hina; Koehbach, Johannes; Clark, Richard J.; Lew-Tabor, Ala; Noakes, Peter G.

    2016-01-01

    Ticks are important vectors of pathogens and secreted neurotoxins with approximately 69 out of 692 tick species having the ability to induce severe toxicoses in their hosts. The Australian paralysis tick (Ixodes holocyclus) is known to be one of the most virulent tick species producing a flaccid paralysis and fatalities caused by a family of neurotoxins known as holocyclotoxins (HTs). The paralysis mechanism of these toxins is temperature dependent and is thought to involve inhibition of acetylcholine levels at the neuromuscular junction. However, the target and mechanism of this inhibition remain uncharacterised. Here, we report that three members of the holocyclotoxin family; HT-1 (GenBank AY766147), HT-3 (GenBank KP096303) and HT-12 (GenBank KP963967) induce muscle paralysis by inhibiting the dependence of transmitter release on extracellular calcium. Previous study was conducted using extracts from tick salivary glands, while the present study is the first to use pure toxins from I. holocyclus. Our findings provide greater insight into the mechanisms by which these toxins act to induce paralysis. PMID:27389875

  1. A clinician's guide to recurrent isolated sleep paralysis.

    PubMed

    Sharpless, Brian A

    2016-01-01

    This review summarizes the empirical and clinical literature on sleep paralysis most relevant to practitioners. During episodes of sleep paralysis, the sufferer awakens to rapid eye movement sleep-based atonia combined with conscious awareness. This is usually a frightening event often accompanied by vivid, waking dreams (ie, hallucinations). When sleep paralysis occurs independently of narcolepsy and other medical conditions, it is termed "isolated" sleep paralysis. Although the more specific diagnostic syndrome of "recurrent isolated sleep paralysis" is a recognized sleep-wake disorder, it is not widely known to nonsleep specialists. This is likely due to the unusual nature of the condition, patient reluctance to disclose episodes for fear of embarrassment, and a lack of training during medical residencies and graduate education. In fact, a growing literature base has accrued on the prevalence, risk factors, and clinical impact of this condition, and a number of assessment instruments are currently available in both self-report and interview formats. After discussing these and providing suggestions for accurate diagnosis, differential diagnosis, and patient selection, the available treatment options are discussed. These consist of both pharmacological and psychotherapeutic interventions which, although promising, require more empirical support and larger, well-controlled trials. PMID:27486325

  2. An fMRI investigation of racial paralysis

    PubMed Central

    Mason, Malia F.; Vandello, Joseph A.; Biga, Andrew; Dyer, Rebecca

    2013-01-01

    We explore the existence and underlying neural mechanism of a new norm endorsed by both black and white Americans for managing interracial interactions: “racial paralysis’, the tendency to opt out of decisions involving members of different races. We show that people are more willing to make choices—such as who is more intelligent, or who is more polite—between two white individuals (same-race decisions) than between a white and a black individual (cross-race decisions), a tendency which was evident more when judgments involved traits related to black stereotypes. We use functional magnetic resonance imaging to examine the mechanisms underlying racial paralysis, to examine the mechanisms underlying racial paralysis, revealing greater recruitment of brain regions implicated in socially appropriate behavior (ventromedial prefrontal cortex), conflict detection (anterior cingulate cortex), deliberative processing (dorsolateral prefrontal cortex), and inhibition (ventrolateral prefrontal cortex). We also discuss the impact of racial paralysis on the quality of interracial relations. PMID:22267521

  3. Transtympanic Facial Nerve Paralysis: A Review of the Literature

    PubMed Central

    Schaefer, Nathan; O’Donohue, Peter; French, Heath; Griffin, Aaron; Gochee, Peter

    2015-01-01

    Summary: Facial nerve paralysis because of penetrating trauma through the external auditory canal is extremely rare, with a paucity of published literature. The objective of this study is to review the literature on transtympanic facial nerve paralysis and increase physician awareness of this uncommon injury through discussion of its clinical presentation, management and prognosis. We also aim to improve patient outcomes in those that have sustained this type of injury by suggesting an optimal management plan. In this case report, we present the case of a 46-year-old white woman who sustained a unilateral facial nerve paresis because of a garfish penetrating her tympanic membrane and causing direct damage to the tympanic portion of her facial nerve. On follow-up after 12 months, her facial nerve function has largely returned to normal. Transtympanic facial nerve paralysis is a rare injury but can have a favorable prognosis if managed effectively. PMID:26090278

  4. An instance of sleep paralysis in Moby-Dick.

    PubMed

    Herman, J

    1997-07-01

    It is suggested that picturesque medical conditions can, at times, be encountered in literary works composed prior to their clinical delineation. This is true of sleep paralysis, of which the first scientific description was given by Silas Weir Mitchell in 1876. A quarter of a century earlier, Herman Melville, in Moby-Dick, gave a precise account of a case, including the predisposing factors and sexual connotations, all in accord with modern theory. The details of Ishmael's attack of sleep paralysis, the stresses leading up to it, and the associations causing him to recall the experience are given here. PMID:9322274

  5. Neonatal vocal cord paralysis-an early presentation of hereditary neuralgic amyotrophy due to a mutation in the SEPT9 gene.

    PubMed

    Leshinsky-Silver, E; Ginzberg, M; Dabby, R; Sadeh, M; Lev, D; Lerman-Sagie, T

    2013-01-01

    Hereditary neuralgic amyotrophy is a rare autosomal dominant disorder involving recurrent episodes of painful brachial plexus neuropathies. Involvement of other nerves has been described in some families. The age of onset is from infancy to adulthood. Mutations in the SEPT9 gene were identified in approximately half of the hereditary neuralgic amyotrophy families. We evaluated a family with six affected members from three generations with a point mutation in the SEPT9 gene. One of the patients presented in the neonatal period with vocal cord paralysis necessitating intubation and prolonged ventilation. The neonatal presentation of vocal cord paralysis broadens the phenotypic spectrum of hereditary neuralgic amyotrophy. The identification of a SEPT9 mutation in a neonate with respiratory distress due to vocal cord paralysis expands the differential diagnosis in these patients. PMID:22981636

  6. Closed-loop control of spinal cord stimulation to restore hand function after paralysis

    PubMed Central

    Zimmermann, Jonas B.; Jackson, Andrew

    2014-01-01

    As yet, no cure exists for upper-limb paralysis resulting from the damage to motor pathways after spinal cord injury or stroke. Recently, neural activity from the motor cortex of paralyzed individuals has been used to control the movements of a robot arm but restoring function to patients' actual limbs remains a considerable challenge. Previously we have shown that electrical stimulation of the cervical spinal cord in anesthetized monkeys can elicit functional upper-limb movements like reaching and grasping. Here we show that stimulation can be controlled using cortical activity in awake animals to bypass disruption of the corticospinal system, restoring their ability to perform a simple upper-limb task. Monkeys were trained to grasp and pull a spring-loaded handle. After temporary paralysis of the hand was induced by reversible inactivation of primary motor cortex using muscimol, grasp-related single-unit activity from the ventral premotor cortex was converted into stimulation patterns delivered in real-time to the cervical spinal gray matter. During periods of closed-loop stimulation, task-modulated electromyogram, movement amplitude, and task success rate were improved relative to interleaved control periods without stimulation. In some sessions, single motor unit activity from weakly active muscles was also used successfully to control stimulation. These results are the first use of a neural prosthesis to improve the hand function of primates after motor cortex disruption, and demonstrate the potential for closed-loop cortical control of spinal cord stimulation to reanimate paralyzed limbs. PMID:24904251

  7. Long-term results of diaphragmatic plication in adults with unilateral diaphragm paralysis

    PubMed Central

    2010-01-01

    Background In this study we aimed to evaluate the long-term outcome of diaphragmatic plication for symptomatic unilateral diaphragm paralysis. Methods Thirteen patients who underwent unilateral diaphragmatic plication (2 patients had right, 11 left plication) between January 2003 and December 2006 were evaluated. One patient died postoperatively due to sepsis. The remaining 12 patients [9 males, 3 females; mean age 60 (36-66) years] were reevaluated with chest radiography, flouroscopy or ultrasonography, pulmonary function tests, computed tomography (CT) or magnetic resonance imaging (MRI), and the MRC/ATS dyspnea score at an average of 5.4 (4-7) years after diaphragmatic plication. Results The etiology of paralysis was trauma (9 patients), cardiac by pass surgery (3 patients), and idiopathic (1 patient). The principle symptom was progressive dyspnea with a mean duration of 32.9 (22-60) months before surgery. All patients had an elevated hemidiaphragm and paradoxical movement radiologically prior to surgery. There were partial atelectasis and reccurent infection of the lower lobe in the affected side on CT in 9 patients. Atelectasis was completely improved in 9 patients after plication. Preoperative spirometry showed a clear restrictive pattern. Mean preoperative FVC was 56.7 ± 11.6% and FEV1 65.3 ± 8.7%. FVC and FEV1 improved by 43.6 ± 30.6% (p < 0.001) and 27.3 ± 10.9% (p < 0.001) at late follow-up. MRC/ATS dyspnea scores improved 3 points in 11 patients and 1 point in 1 patient at long-term (p < 0.0001). Eight patients had returned to work at 3 months after surgery. Conclusions Diaphragmatic plication for unilateral diaphragm paralysis decreases lung compression, ensures remission of symptoms, and improves quality of life in long-term period. PMID:21078140

  8. Hysterical paralysis and premature burial: a medieval Persian case, fear and fascination in the West, and modern practice.

    PubMed

    Agutter, Paul S; Shoja, Mohammadali M; Tubbs, R Shane; Rashidi, Mohammad Reza; Khalili, Majid; Hosseini, Seyed Fazel; Ghabili, Kamyar; Cohen-Gadol, Aaron A; Loukas, Marios

    2013-04-01

    Premature burial (taphophobia) is an ancient fear, but it became especially common in 18th and 19th century Europe and may have a modern-day counterpart. Examination of a well-documented case from medieval Persia reveals the importance of funeral practices in the risk of actual premature burial and sheds light on the question of why taphophobia became so prevalent in Europe during the early industrial revolution period. The medieval Persian case was attributed to hysterical paralysis (conversion). We discuss the relationship between hysterical paralysis and premature burial more generally and show that although understanding of conversion syndrome remains incomplete, modern knowledge and practices have limited the risk of any similar tragedy today. PMID:23472788

  9. Serotoninergic agents in the treatment of isolated sleep paralysis.

    PubMed

    Snyder, S; Hams, G

    1982-09-01

    The authors report three cases of isolated sleep paralysis controlled by L-tryptophan with or without amitriptyline. Both agents increase CNS 5-hydroxytryptamine availability, whereas imipramine, which was ineffective in the one case in which it was tried, affects predominantly norepinephrine reuptake. PMID:7114320

  10. Prevalence of isolated sleep paralysis in black subjects.

    PubMed

    Bell, C C; Shakoor, B; Thompson, B; Dew, D; Hughley, E; Mays, R; Shorter-Gooden, K

    1984-05-01

    Sleep paralysis is a state of consciousness experienced while waking from sleep or falling asleep. It is characterized by an experience of being unable to move for several seconds or minutes. This study represents the first survey to measure the incidence of this disorder in a black population of healthy subjects and psychiatric patients. PMID:6737506

  11. Immobility in Mobility: Narratives of Social Class, Education, and Paralysis

    ERIC Educational Resources Information Center

    Nainby, Keith; Pea, John B.

    2003-01-01

    Social mobility carries with it a sense of loss. To be socially mobile is to move from one place, economically, culturally, personally, to another. One consequence of that loss, sometimes, is immobility--a paralysis brought on by the violent, forceful, uncertain rush of social mobility itself. The immobility of fear, the feeling stuck, the not…

  12. A clinician’s guide to recurrent isolated sleep paralysis

    PubMed Central

    Sharpless, Brian A

    2016-01-01

    This review summarizes the empirical and clinical literature on sleep paralysis most relevant to practitioners. During episodes of sleep paralysis, the sufferer awakens to rapid eye movement sleep-based atonia combined with conscious awareness. This is usually a frightening event often accompanied by vivid, waking dreams (ie, hallucinations). When sleep paralysis occurs independently of narcolepsy and other medical conditions, it is termed “isolated” sleep paralysis. Although the more specific diagnostic syndrome of “recurrent isolated sleep paralysis” is a recognized sleep–wake disorder, it is not widely known to nonsleep specialists. This is likely due to the unusual nature of the condition, patient reluctance to disclose episodes for fear of embarrassment, and a lack of training during medical residencies and graduate education. In fact, a growing literature base has accrued on the prevalence, risk factors, and clinical impact of this condition, and a number of assessment instruments are currently available in both self-report and interview formats. After discussing these and providing suggestions for accurate diagnosis, differential diagnosis, and patient selection, the available treatment options are discussed. These consist of both pharmacological and psychotherapeutic interventions which, although promising, require more empirical support and larger, well-controlled trials. PMID:27486325

  13. Marek's disease virus induced transient paralysis--a closer look

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Marek’s Disease (MD) is a lymphoproliferative disease of domestic chickens caused by a highly cell-associated alpha herpesvirus, Marek’s disease virus (MDV). Clinical signs of MD include depression, crippling, weight loss, and transient paralysis (TP). TP is a disease of the central nervous system...

  14. Clinical Efficacy of Electroneurography in Acute Facial Paralysis

    PubMed Central

    2016-01-01

    The estimated incidence of acute facial paralysis is approximately 30 patients per 100000 populations annually. Facial paralysis is an extremely frightening situation and gives extreme stress to patients because obvious disfiguring face may cause significant functional, aesthetic, and psychological disturbances. For stressful patients with acute facial paralysis, it is very important for clinicians to answer the questions like whether or not their facial function will return to normal, how much of their facial function will be recovered, and how long this is going to take. It is also important for clinicians to treat the psychological aspects by adequately explaining the prognosis, in addition to providing the appropriate medical treatment. For decades, clinicians have used various electrophysiologic tests, including the nerve excitability test, the maximal stimulation test, electroneurography, and electromyography. In particular, electroneurography is the only objective measure that is useful in early stage of acute facial paralysis. In this review article, we first discuss the pathophysiology of injured peripheral nerve. And then, we describe about various electrophysiologic tests and discuss the electroneurography extensively. PMID:27144227

  15. Acute Flaccid Paralysis: The New, The Old, and The Preventable

    PubMed Central

    Macesic, N.; Hall, V.; Mahony, A.; Hueston, L.; Ng, G.; Macdonell, R.; Hughes, A.; Fitt, G.; Grayson, M. L.

    2016-01-01

    Acute flaccid paralysis (AFP) has a changing epidemiology with ongoing polio outbreaks and emerging causes such as nonpolio enteroviruses and West Nile virus (WNV). We report a case of AFP from the Horn of Africa that was initially classified as probable polio but subsequently found to be due to WNV. PMID:26788545

  16. A rare case of paralysis in an endemic area.

    PubMed

    Yardimci, Bulent; Kazancioglu, Rumeyza

    2015-01-01

    Thyrotoxicosis mostly presents with tachycardia, tremor, weight loss and other hypermetabolism signs. However, there are other unusual signs of thyrotoxicosis such as paralysis. This unusual clinical presentation may postpone prompt diagnosis and treatment. In this case report, we present a 27-years-old woman, who presented with quadriparesis at the emergency department. PMID:26101516

  17. A rare case of paralysis in an endemic area

    PubMed Central

    Yardimci, Bulent; Kazancioglu, Rumeyza

    2015-01-01

    Thyrotoxicosis mostly presents with tachycardia, tremor, weight loss and other hypermetabolism signs. However, there are other unusual signs of thyrotoxicosis such as paralysis. This unusual clinical presentation may postpone prompt diagnosis and treatment. In this case report, we present a 27-years-old woman, who presented with quadriparesis at the emergency department. PMID:26101516

  18. Clinical Efficacy of Electroneurography in Acute Facial Paralysis.

    PubMed

    Lee, Dong-Hee

    2016-04-01

    The estimated incidence of acute facial paralysis is approximately 30 patients per 100000 populations annually. Facial paralysis is an extremely frightening situation and gives extreme stress to patients because obvious disfiguring face may cause significant functional, aesthetic, and psychological disturbances. For stressful patients with acute facial paralysis, it is very important for clinicians to answer the questions like whether or not their facial function will return to normal, how much of their facial function will be recovered, and how long this is going to take. It is also important for clinicians to treat the psychological aspects by adequately explaining the prognosis, in addition to providing the appropriate medical treatment. For decades, clinicians have used various electrophysiologic tests, including the nerve excitability test, the maximal stimulation test, electroneurography, and electromyography. In particular, electroneurography is the only objective measure that is useful in early stage of acute facial paralysis. In this review article, we first discuss the pathophysiology of injured peripheral nerve. And then, we describe about various electrophysiologic tests and discuss the electroneurography extensively. PMID:27144227

  19. Israeli acute paralysis virus associated paralysis symptoms, viral tissue distribution and Dicer-2 induction in bumblebee workers (Bombus terrestris).

    PubMed

    Wang, Haidong; Meeus, Ivan; Smagghe, Guy

    2016-08-01

    Although it is known that Israeli acute paralysis virus (IAPV) can cause bee mortality, the symptoms of paralysis and the distribution of the virus in different body tissues and their potential to respond with an increase of the siRNA antiviral immune system have not been studied. In this project we worked with Bombus terrestris, which is one of the most numerous bumblebee species in Europe and an important pollinator for wild flowers and many crops in agriculture. Besides the classic symptoms of paralysis and trembling prior to death, we report a new IAPV-related symptom, crippled/immobilized forelegs. Reverse-transcriptase quantitative PCR showed that IAPV accumulates in different body tissues (midgut, fat body, brain and ovary). The highest levels of IAPV were observed in the fat body. With fluorescence in situ hybridization (FISH) we detected IAPV in the Kenyon cells of mushroom bodies and neuropils from both antennal and optic lobes of the brain in IAPV-infected workers. Finally, we observed an induction of Dicer-2, a core gene of the RNAi antiviral immune response, in the IAPV-infected tissues of B. terrestris workers. According to our results, tissue tropism and the induction strength of Dicer-2 could not be correlated with virus-related paralysis symptoms. PMID:27230225

  20. 'A Leg to Stand On' by Oliver Sacks: a unique autobiographical account of functional paralysis.

    PubMed

    Stone, Jon; Perthen, Jo; Carson, Alan J

    2012-09-01

    Oliver Sacks, the well known neurologist and writer, published his fourth book, 'A Leg to Stand On', in 1984 following an earlier essay 'The Leg' in 1982. The book described his recovery after a fall in a remote region of Norway in which he injured his leg. Following surgery to reattach his quadriceps muscle, he experienced an emotional period in which his leg no longer felt a part of his body, and he struggled to regain his ability to walk. Sacks attributed the experience to a neurologically determined disorder of body-image and bodyego induced by peripheral injury. In the first edition of his book Sacks explicitly rejected the diagnosis of 'hysterical paralysis' as it was then understood, although he approached this diagnosis more closely in subsequent revisions. In this article we propose that, in the light of better understanding of functional neurological symptoms, Sacks' experiences deserve to be reappraised as a unique insight in to a genuinely experienced functional/psychogenic leg paralysis following injury. PMID:22872718

  1. [On the contribution of magnets in sequelae of facial paralysis. Preliminary clinical study].

    PubMed

    Fombeur, J P; Koubbi, G; Chevalier, A M; Mousset, C

    1988-01-01

    This trial was designed to evaluate the efficacy of EPOREC 1 500 magnets as an adjuvant to rehabilitation following peripheral facial paralysis. Magnetotherapy is used in many other specialties, and in particular in rheumatology. The properties of repulsion between identical poles were used to decrease the effect of sequelae in the form of contractures on the facial muscles. There were two groups of 20 patients: one group with physiotherapy only and the other with standard rehabilitation together with the use of magnets. These 40 patients had facial paralysis of various origins (trauma, excision of acoustic neuroma, Bell's palsy etc). Obviously all patients had an intact nerve. It was at the time of the development of contractures that magnets could be used in terms of evaluation of their efficacy of action on syncinesiae, contractures and spasticity. Magnets were worn at night for a mean period of six months and results were assessed in terms of disappearance of eye-mouth syncinesiae, and in terms of normality of facial tone. Improvement and total recovery without sequelae were obtained far more frequently in the group which wore magnets, encouraging us to continue along these lines. PMID:3178094

  2. High prevalence of isolated sleep paralysis: kanashibari phenomenon in Japan.

    PubMed

    Fukuda, K; Miyasita, A; Inugami, M; Ishihara, K

    1987-06-01

    In Japan, a set of experiences called kanashibari is considered identical with isolated sleep paralysis. We investigated this phenomenon by means of a questionnaire administered to 635 college students (390 men and 245 women). Of all subjects, about 40% had experienced at least one episode of kanashibari [subjects of K(+)]. Therefore, isolated sleep paralysis is apparently a more common phenomenon than is usually appreciated. About half of the subjects of K(+) reported that they had been under "physical or psychological stress" or in a "disturbed sleep and wakefulness cycle" immediately before the episode. Many subjects of K(+) experienced the first episode in adolescence. In the distribution of age of first attack, the peak occurred at an earlier age in women subjects than in men subjects. These findings suggest that two factors influence the occurrence of the phenomenon. One is exogenous physical or psychological load and the other is endogenous biological development. PMID:3629091

  3. The pattern of isolated sleep paralysis among Nigerian nursing students.

    PubMed

    Ohaeri, J U; Adelekan, M F; Odejide, A O; Ikuesan, B A

    1992-01-01

    In a cross-sectional study of the pattern of isolated sleep paralysis among the entire population of nursing students at the Neuropsychiatric Hospital in Abeokuta, Nigeria (consisting of 58 males and 37 females), 44% admitted having experienced this phenomenon. The findings largely supported the results of a similar study of Nigerian medical students, except that there was a slight male preponderance among those who had the experience. Visual hallucination was the most common perceptual problem associated with the episodes, and all the affected subjects were most distressed by the experience. Whereas sleep paralysis in this country has not been found to be significantly associated with psychosocial distress or differences in personality profile, the popular view in Africa and the United States is that it is caused by witchcraft. PMID:1602503

  4. Isolated sleep paralysis, vivid dreams and geomagnetic influences: II.

    PubMed

    Conesa, J

    1997-10-01

    This report describes a test of the hypothesis that significant changes in the ambient geomagnetic field are associated with altered normal nighttime dream patterns. Specifically, it was predicted that there would be a greater incidence of isolated sleep, paralysis or vivid dreams with abrupt rises and falls of geomagnetic activity. The author's (JC) and a second subject's (KC) daily reports of dream-recall were analyzed in the context of daily fluctuations of geomagnetic activity (K indices). Two analyses of variance indicated (i) significantly higher geomagnetic activity three days before a recorded isolated sleep paralysis event and (ii) significantly lower geomagnetic activity three days before an unusually vivid dream took place. Conversely, geomagnetic activity did not fluctuate significantly for randomly selected days. Testing a large sample over time is required for confirmation and extension of this work. PMID:9347546

  5. Recurrent largngeal nerve paralysis: a laryngographic and computed tomographic study

    SciTech Connect

    Agha, F.P.

    1983-07-01

    Vocal cord paralysis is a relatively common entity, usually resulting from a pathologic process of the vagus nerve or its recurrent larynegeal branch. It is rarely caused by intralargngeal lesions. Four teen patients with recurrent laryngeal nerve paralysis (RLNP) were evaluated by laryngography, computed tomography (CT), or both. In the evaluation of the paramedian cord, CT was limited in its ability to differentiate between tumor or RLNP as the cause of the fixed cord, but it yielded more information than laryngography on the structural abnormalities of the larynx and pre-epiglottic and paralaryngeal spaces. Laryngography revealed distinct features of RLNP and is the procedure of choice for evaluation of functional abnormalities of the larynx until further experience with faster CT scanners and dynamic scanning of the larynx is gained.

  6. Mounier-Kuhn syndrome and bilateral vocal cord paralysis.

    PubMed

    Dincer, H Erhan; Holweger, Joshua D

    2012-07-01

    Mounier-Kuhn syndrome is a rare disorder of unknown cause that is characterized by atrophy of the elastic and smooth muscle of the tracheobronchial tree leading to tracheobronchomegaly and bronchiectasis. The syndrome is likely underdiagnosed, because the patients usually present with common respiratory symptoms such as productive cough and usually labeled as chronic obstructive pulmonary disease. Diagnosis is established on the basis of radiologic findings. Association with bilateral vocal cord paralysis has not been described. Treatment is mainly supportive. Symptomatic patients may require endobronchial stenting if airway collapse is encountered. Here, we described a patient who presented with hoarseness and pneumonia. Further studies confirmed the diagnosis of Mounier-Kuhn syndrome with bilateral vocal cord paralysis. PMID:23207474

  7. Isolated Paralysis of the Adductor Pollicis: A Case Report

    PubMed Central

    De Maio, F.; Bisicchia, S.; Farsetti, P.; Ippolito, E.

    2011-01-01

    We report a case of isolated paralysis of the right adductor pollicis in a 30-year-old woman. Electromyographic study showed involvement of the deep motor branch of the ulnar nerve. A ganglion and an anomalous muscle were both ruled out clinically and by MRI as a possible cause of the paralysis. At surgical exploration, we found a fibrous band joining the pisiform and the hook of the hamate bone that compressed the deep motor branch of the ulnar nerve. The fibrous band was excised, and a neurolysis of the motor branch of the ulnar nerve was performed. At followup, eight months later, the patient had fully recovered strength of the adductor muscle. PMID:21991410

  8. A case of isolated abducens nerve paralysis in maxillofacial trauma.

    PubMed

    Keskin, Elif Seda; Keskin, Ekrem; Atik, Bekir; Koçer, Abdülkadir

    2015-01-01

    Nervus abducens is a pure motor nerve located in the pons. It retracts the eyeball laterally by stimulating rectus lateralis muscle. In case of their paralysis, diplopia and restriction in the eye movements while looking sideways, are seen. Since the same signs are seen due to the muscle entrapment in blowout fractures, its differential diagnosis has importance in terms of the treatment protocol and avoiding unnecessary operations. In this article, we present a 22-year-old male patient who was referred to our department due to the prediagnosis of blowout fracture following maxillofacial trauma. However, he was diagnosed with abducens nerve paralysis after the consultations and analysis and his restriction of movement was resolved via systemic steroid treatment instead of unnecessary operation. PMID:26981484

  9. A case of isolated abducens nerve paralysis in maxillofacial trauma

    PubMed Central

    Keskin, Elif Seda; Keskin, Ekrem; Atik, Bekir; Koçer, Abdülkadir

    2015-01-01

    Nervus abducens is a pure motor nerve located in the pons. It retracts the eyeball laterally by stimulating rectus lateralis muscle. In case of their paralysis, diplopia and restriction in the eye movements while looking sideways, are seen. Since the same signs are seen due to the muscle entrapment in blowout fractures, its differential diagnosis has importance in terms of the treatment protocol and avoiding unnecessary operations. In this article, we present a 22-year-old male patient who was referred to our department due to the prediagnosis of blowout fracture following maxillofacial trauma. However, he was diagnosed with abducens nerve paralysis after the consultations and analysis and his restriction of movement was resolved via systemic steroid treatment instead of unnecessary operation. PMID:26981484

  10. Framework Surgery for Treatment of Unilateral Vocal Fold Paralysis

    PubMed Central

    Daniero, James J.; Garrett, C. Gaelyn; Francis, David O.

    2014-01-01

    Laryngeal framework surgery is the current gold standard treatment for unilateral vocal fold paralysis. It provides a permanent solution to glottic insufficiency caused by injury to the recurrent laryngeal nerve. Various modifications to the original Isshiki type I laryngoplasty procedure have been described to improve voice and swallowing outcomes. The success of this procedure is highly dependent on the experience of the surgeon as it epitomizes the intersection of art and science in the field. The following article reviews the evidence, controversies, and complications related to laryngoplasty for unilateral vocal fold paralysis. It also provides a detailed analysis of how and when arytenoid-positioning procedures should be considered, and summarizes the literature on postoperative outcomes. PMID:24883239