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PubMed2004

Absence of ion channels CACN1AS and SCN4A mutations in thyrotoxic hypokalemic periodic paralysis.

Muscle weakness in patients with thyrotoxicosis during hypokalemic episodes (thyrotoxic periodic paralysis [TPP]) occurs sporadically and mostly in males. It is treated by infusion or oral supplementation with potassium and with resolution of the thyrotoxicosis state. The clinical features of TPP resemble familial hypokalemic periodic paralysis (hypoKPP), which has been linked to two mutations in the gene encoding the skeletal muscle calcium channel alpha-1 subunit (CACN1AS; Arg528His and Arg1239His) and to the sodium channel alpha-subunit (SCN4A; Arg672His). We screened for the mutations (CACN1AS by polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP]; SCN4A by single-strand conformation polymorphism analysis) described in hypoKPP in 20 unrelated patients with documented episodes of TPP (mean age, 40.0 +/- 12.3 years 19 males). Forty-eight patients with hyperthyroidism resulting from Graves' disease (48.5 +/- 12.3 years; 13 males), 1 patient with idiopathic hypoKPP (a 32-year-old male) and 32 healthy subjects (41.0 +/- 19.1 years; 16 males) were included. We found none of the TPP patients carry CACN1AS and SCN4A mutations. The hyperthyroid patients and control subjects were also negative for the mutations. The patient with idiopathic hypoKPP was genotyped to have the Arg528His mutation. These results suggest that despite close similarities between TPP and hypoKPP, a likely genetic basis for TPP does not involve the same gene mutations associated with hypoKPP.

Adult↗

PubMed2006

Marek's disease virus-induced transient paralysis is associated with cytokine gene expression in the nervous system.

Marek's disease (MD)-associated transient paralysis (TP) was experimentally induced in chickens by intraperitoneal inoculation of RB1B strain of Marek's disease virus (MDV). Between 7 and 11 days post-infection (d.p.i.), neck and limb paralysis was observed in 18% of infected chickens, which was associated with various degrees of edema, vacuolation, perivascular cuffing of mononuclear cells, and glial cell infiltration mainly in the cerebrum, cerebellum, and brain stem. The chickens that were infected but did not progress to develop TP until 12 d.p.i. also had similar lesions suggestive of encephalitis in the cerebrum, cerebellum, and brain stem. Chickens infected with MDV had more interleukin (IL)-6, IL-12, and interferon (IFN)-gamma in their brain tissues compared to uninfected chickens. Moreover, IL-18 was significantly increased in brain tissues of birds showing clinical signs of TP compared to uninfected birds. Importantly, the expression of IL-6, IL-18, and IFN- gamma in brain tissues of MDV-infected chickens with signs of TP was significantly increased compared to that in asymptomatic MDV-infected birds. MDV genome load in the brain of chickens showing clinical signs of TP was higher than that in asymptomatic MDV-infected chickens but was not statistically significant. The lesions in the cervical, thoracic, and lumbar spinal cord segments in MDVinfected chickens were characterized mainly by perivascular cuffing of mononuclear cells irrespective of the group. The expression of mRNA for IL-18 and IFN-gamma genes was not significantly different in spinal cord tissues of chickens with TP compared to clinically normal, MDV-infected and noninfected chickens. These results suggest possible underlying immunologic mechanisms for MDV-induced TP.

Animals↗

PubMed2003

Combined deficiency of vitamins E and C causes paralysis and death in guinea pigs.

BACKGROUND: On the basis of in vitro studies, the antioxidant nutrients vitamins E and C are postulated to interact in vivo. OBJECTIVE: We developed a guinea pig model to evaluate the combined deficiency of vitamins E and C in vivo. DESIGN: Weanling guinea pigs were fed a control diet or a vitamin E-deficient diet for 14 d, after which one-half of each group had vitamin C removed from their diet, thus creating 4 diet groups. Some animals were observed for clinical signs. Others were killed for evaluation. RESULTS: Of 21 guinea pigs that were observed after being fed the diet deficient in both vitamins, 8 died 9 +/- 2 d (x +/- SD) after starting the diet. Eight additional guinea pigs developed a characteristic syndrome at 11 +/- 3 d. First, they became paralyzed in the hind limbs. Within a few hours, the paralysis progressed to include all 4 limbs and caused difficulty in breathing, which would have caused death had the animals not been euthanized. Histopathologic evaluation did not identify a lesion in the muscles or nervous system that could account for the paralysis. Biochemical measurements confirmed the deficiencies and indicated that the double deficiency caused lipid peroxidation in the central nervous system. CONCLUSIONS: A distinct clinical syndrome of combined vitamin E and vitamin C deficiency occurs in guinea pigs. This syndrome indicates that these antioxidant vitamins are related in vivo. We speculate that acute oxidative injury in the central nervous system underlies the clinical syndrome.

Animals↗

PubMed2002

Enhanced inactivation and pH sensitivity of Na(+) channel mutations causing hypokalaemic periodic paralysis type II.

Hypokalaemic periodic paralysis (hypoPP) is a dominantly inherited muscle disorder characterized by episodes of flaccid weakness. Previous genetic studies revealed mutations in the voltage-gated calcium channel alpha1-subunit (CACNA1S gene) in families with hypoPP (type I). Electrophysiological studies on these mutants in different expression systems could not explain the pathophysiology of the disease. In addition, several mutations (Arg669His, Arg672His, Arg672Gly and Arg672Ser) in the voltage sensor of the skeletal muscle sodium channel alpha-subunit (SCN4A gene) have been found in families with hypoPP (type II). For Arg672Gly/His a fast inactivation defect was described, and for Arg669His an impairment of slow inactivation was reported. Except for the substitution for serine, we have now expressed all mutants in a human cell-line and studied them electrophysiologically. Patch-clamp recordings show an enhanced fast inactivation for all three mutations, whereas two of them reveal enhanced slow inactivation. This may reduce the number of functional sodium channels at resting membrane potential and contribute to the long-lasting periods of paralysis experienced by hypoPP patients. The gating of both histidine mutants (Arg669His, Arg672His) can be modulated by changes of extra- or intracellular pH. The inactivation defects of Arg669His and Arg672His can be alleviated by low pH to a significant degree, suggesting that the decrease of pH in muscle cells (e.g. during muscle work) might lead to an auto-compensation of functional defects. This may explain a delay or prevention of paralytic attacks in patients by slight physical activity. Moreover, the histidine residues may be the target for a potential therapeutic action by acetazolamide.

Arginine↗

PubMed2005

Envenoming bites by kraits: the biological basis of treatment-resistant neuromuscular paralysis.

Beta-bungarotoxin, a neurotoxic phospholipase A2 is a major fraction of the venom of kraits. The toxin was inoculated into one hind limb of young adult rats. The inoculated hind limb was paralysed within 3 h, and remained paralysed for 2 days. The paralysis was associated with the loss of synaptic vesicles from motor nerve terminal boutons, a decline in immunoreactivity of synaptophysin, SNAP-25 and syntaxin, a loss of muscle mass and the upregulation of NaV(1.5) mRNA and protein. Between 3 and 6 h after the inoculation of toxin, some nerve terminal boutons exhibited clear signs of degeneration. Others appeared to be in the process of withdrawing from the synaptic cleft and some boutons were fully enwrapped in terminal Schwann cell processes. By 12 h all muscle fibres were denervated. Re-innervation began at 3 days with the appearance of regenerating nerve terminals, a return of neuromuscular function in some muscles and a progressive increase in the immunoreactivity of synaptophysin, SNAP-25 and syntaxin. Full recovery occurred at 7 days. The data were compared with recently published clinical data on envenoming bites by kraits and by extrapolation we suggest that the acute, reversible denervation caused by beta-bungarotoxin is a credible explanation for the clinically important, profound treatment-resistant neuromuscular paralysis seen in human subjects bitten by these animals.

Acetylcholine↗

PubMed1983

Polio-like motor paralysis associated with acute hemorrhagic conjunctivitis in an outbreak in 1981 in Bombay, India: clinical and serologic studies.

High and rising neutralizing antibody titers (NATs) to enterovirus type 70 (EV70) were detected in the serum and cerebrospinal fluid (CSF) of patients with polio-like motor paralysis accompanying acute hemorrhagic conjunctivitis (AHC) in an outbreak of AHC in 1981 in Bombay, India. Fifty-four (88.5%) of 61 patients with AHC with or without neurologic disease had serum NATs of greater than or equal to 1:16, and some paired sera from these patients showed significant increases in NAT. Serum from noninfected control subjects had no significant neutralizing antibody to EV70. Thirty-six (94.7%) of 38 CSF specimens from 30 patients with spinal or a combination of spinal and cranial motor paralysis associated with AHC had NATs ranging from 1:2 to 1:256. No neutralizing antibody was found in CSF specimens from patients with AHC alone or in those from non-infected control subjects, and a reduced ratio of serum NAT to CSF NAT was detected in patients with neurologic disease. Therefore, it is highly likely that intrathecal synthesis of antibody occurred in response to direct invasion of the central nervous system by EV70. The results represent strong laboratory evidence of the neurovirulence of EV70.

Acute Disease↗

PubMed1983

Age dependence of paralysis induced by echovirus type 9 in infant mice.

Newborn mice of different strains (including NMRI) infected with 2-5 x 10(6) pfu of echovirus type 9 strain A. Barty developed progressive flaccid paralysis five days after inoculation, followed by death. Suckling mice injected with the same infective dose two, four, or six days after birth disclosed at most transient paresis and survived. Infectivity titrations revealed in all groups a similar rate of virus multiplication exceeding 10(8) 50% tissue culture infective doses per mouse four days after virus inoculation. Histologically, polymyositis resulting in muscle fiber necrosis was seen. The percentage of damaged muscle tissue declined with increasing age of the experimental groups. It is concluded that in order for paralysis to occur, at least 50% of skeletal muscle tissue must be destroyed by virus-induced lesions before the sixth day of life. Electron microscopy demonstrated additional age-dependent, virus-mediated disturbances of postnatal muscle growth. Reparative events in destroyed muscle fibers seemed to be unaffected in all age groups.

Age Factors↗

PubMed2001

Facial nerve paralysis and paraplegia as presenting symptoms of acute myeloid leukemia.

Granulocytic sarcoma is an extramedullary tumor associated with acute or chronic leukemias or myeloproliferative disorders. Rarely, the tumor may be seen before the diagnosis of leukemia. Symptomatic facial nerve paralysis and spinal cord invasion by granulocytic sarcomas are also relatively uncommon. We present here a 17-year-old-female patient who had facial nerve paralysis and paraplegia due to granulocytic sarcoma as the presenting symptoms of acute myeloid leukemia.

Acute Disease↗

PubMed1976

Type C virus expression in lymphoma-paralysis-prone wild mice.

Wild mice trapped near Lake Casitas (LC) in southern California showed a high prevalence of infectious type C virus in the liver, spleen, and thymus within the first few weeks of life. By young adulthood about 80% of LC mice (including their genital tissues) were infected. Virus isolates from these mice cause lymphoma and lower limb paralysis under both natural and experimental conditions. Mice destined to develop paralysis showed higher levels of serum gs antigen early in life, whereas mice destined to develop lymphoma or remain free of these diseases could not be distinguished by this test. The individual variation in virus expression suggested that differences in virus type or in the immune or other host defense mechanisms greatly influenced susceptibility or resistance to indigenous type C virus-caused disease in LC wild mice.

Age Factors↗

PubMed2001

Identification of mutations including de novo mutations in Korean patients with hypokalaemic periodic paralysis.

BACKGROUND: Hypokalaemic periodic paralysis (hypoPP) is an autosomal dominant disorder involving the abnormal function of ion channels and it is characterized by paralysis attacks of varying severity, accompanied by a fall in blood potassium levels. Linkage analysis showed that the candidate locus responsible for hypoPP was localized to chromosome 1q31-32, and this locus encoded the muscle dihydropyridine-sensitive calcium channel alpha(1)-subunit (CACNA1S). So far, three different mutations in CACNA1S gene have been identified in patients with hypoPP: Arg528His, Arg1239His and Arg1239Gly in Caucasian patients. However, there are few reports about the mutations of CACNA1S gene in other races. METHODS: In this study, four Korean families with five hypoPP patients were screened for mutations of CACNA1S gene with polymerase chain reaction-based restriction analysis and single-strand conformation polymorphism analysis. To determine the mode of inheritance, haplotype analysis was done with three microsatellite markers (D1S1726, CACNL1A3, and D1S1723). RESULTS: Arg528His mutation was detected in three families, and one family had no known mutations. Moreover, for the first time, we detected de novo Arg528His mutations in two out of three families with hypoPP. Haplotype analysis using three microsatellite markers (D1S1726, CACNL1A3, and D1S1723) suggested the occurrence of de novo Arg528His mutations in two of the three families with Arg528His mutation. CONCLUSIONS: Arg528His mutations of CACNA1S, including de novo Arg528His mutations, were found in Korean patients with hypoPP. These results imply that de novo mutation, in addition to non-penetrance, is one of the genetic mechanisms that can explain the previous clinical observation that hypoPP occurs sporadically without family history.

Adolescent↗

PubMed1995

Physical therapy management of isolated serratus anterior muscle paralysis.

This case report presents a patient who developed right shoulder pain following strenuous upper-extremity exercise. Approximately 6 weeks later his pain resolved, he noticed persistent right upper-extremity weakness. He was referred to physical therapy for evaluation and treatment. Physical therapy evaluation revealed isolated serratus anterior muscle paralysis. A long thoracic neuropathy was subsequently confirmed by electromyographic testing. The etiology, pathophysiology, and pathokinesiology of serratus anterior muscle paralysis are reviewed. A case is presented, illustrating how the clinical decision making is based on the pathokinesiology and pathophysiology. The patient was followed over the course of 17 months and has recovered full right shoulder active range of motion. His serratus anterior muscle strength has increased to Good minus, and he reports significantly improved functional use of the upper extremity.

Adult↗

PubMed2003

Hypokalaemia and paralysis.

A patient with a severe degree of hypokalaemia (1.8 mmol/l) and paralysis was brought to the emergency department. Hypokalaemic periodic paralysis was an unlikely diagnosis, because an acid-base disorder (metabolic alkalosis) and a high rate of potassium (K(+)) excretion were present. During an imaginary consultation with Professor McCance, the combination of emphasis on principles of integrative physiology, a deductive analysis, common sense, and clinical skills led to an obvious diagnosis. Nevertheless, a surprise was in store, because renal K(+) wasting persisted for almost 2 weeks after removal of the causative agent. Possible explanations for the continued kaliuresis, as well as therapeutic strategies to avoid potential complications, were considered. This case illustrates the value of applying principles of physiology in a quantitative fashion at the bedside.

Aged↗

PubMed1996

Thyrotoxicosis and renal tubular acidosis presenting as hypokalaemic paralysis.

A 34-yr-old Chinese woman presented with hypokalaemic periodic paralysis. She had a goitre and was biochemically thyrotoxic. However, she also had urinary potassium loss with a metabolic acidosis and reduced ability to acidify her urine. The co-existence of distal renal tubular acidosis (RTA) was confirmed. There was no evidence of xerostomia or xerophthalmia, although anti-Ro antibody and rheumatoid factor were positive. Paralytic attacks did not recur after the thyrotoxicosis was controlled with radioactive iodine. Possible pathogenic mechanisms for the association of these disorders are discussed. Female patients presenting with thyrotoxic periodic paralysis (TPP) should be thoroughly investigated for possible additional precipitating factors in view of the strong male predominance of TPP, particularly when there are atypical metabolic features.

Acidosis, Renal Tubular↗

PubMed1987

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

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.

Adolescent↗

PubMed1992

Isolated sleep paralysis elicited by sleep interruption.

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.

Adolescent↗

PubMed1994

Sleep paralysis in Chinese: ghost oppression phenomenon in Hong Kong.

Despite reports of wide variation in the prevalence of sleep paralysis among different ethnic groups, there has never been any study in Chinese. In Hong Kong, a condition known as ghost oppression is descriptively identical to sleep paralysis. To examine this phenomenon, the response of 603 undergraduate students to a questionnaire were analyzed. Thirty-seven percent had experienced at least one attack of ghost oppression. There was no sex difference in the prevalence, and the peak age of onset was at the range of 17-19 for both sexes. A strong familial association was found and 20% of subjects reported a positive family history. Over one sixth of the subjects identified sleep disruption and stress as precipitating events.

Adolescent↗

PubMed1997

An instance of sleep paralysis in Moby-Dick.

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.

Humans↗

PubMed1992

Fatal hypokalemic thyrotoxic periodic paralysis presenting as the sudden, unexplained death of a Cambodian refugee.

For the last decade, death investigators have been aware of an unexplained syndrome of sudden death occurring among young adult Southeast Asian refugees. Presented here is a rare instance of fatal hypokalemic periodic paralysis associated with thyrotoxicosis masquerading as the sudden, unexplained death of a Cambodian refugee. The usual features of this syndrome were present, including relatively occult thyrotoxicosis, paralysis upon awakening following a high-carbohydrate meal, and hypokalemia. This case illustrates the value of thorough background death investigation and also illustrates the potential of misinterpreting traditional folk medicine coin rubbing (Cao Gio) as signs of physical abuse.

Adult↗