Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that the autosomal recessive mutation, gray tremor (gt) was associated in the homozygous state (gt/gt) with a rapidly fatal spongiform encephalopathy. Heterozygotes (+/gt) developed mild asymptomatic spongiform brain lesions as did recipient inbred mice inoculated with gt/gt brain homogenates, some of whom also showed behavioral abnormalities [Sidman, R. L., Kinney, H. C. & Sweet, H. O. (1985) Proc. Natl. Acad. Sci. USA 82, 253-257]. In these studies, inbred NFS/N mice inoculated intracerebrally at birth or as adults with gt/gt or first passage gt brain homogenates developed a progressive disease characterized by tremor, ataxia, and spasticity. The symptoms were milder and more slowly progressive than in the gt/gt homozygote, in the paralytic syndrome that followed neonatal inoculation of NFS/N mice with a wild murine leukemia virus (Cas-Br-M MuLV), or in the rapidly progressive ataxia and terminal bradykinesia that followed scrapie inoculation of NFS/N mice. The noninflammatory spongiform encephalopathy in affected NFS/N mice resembled that observed in gt/gt homozygotes, +/gt heterozygotes, and asymptomatic recipient inbred mice inoculated with gt/gt brain homogenates. Neither infectious MuLV nor MuLV proteins were detected in gt/gt brain homogenates or in affected recipient mouse brains. Scrapie-associated fibrils, readily identifiable in subcellular fractions of brains from scrapie-inoculated NFS/N mice, were not detected in similar brain fractions from NFS/N mice inoculated with gt brain homogenates. These results confirm and extend the suggestion that gt spongiform encephalopathy has both heritable and transmissible properties. Moreover, the transmissible agent of gt disease differs from both Cas-Br-M MuLV and scrapie in its disease-inducing properties in NFS/N mice. The capacity of NFS/N mice to express transmitted gt encephalopathy as clinical disease, to rapidly express Cas-Br-M MuLV spongiform encephalomyelopathy, and to develop mouse-adapted scrapie after a very short incubation time suggest a distinct sensitivity of NFS/N mice to transmissible spongiform encephalopathy.
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PMID:Transmission in NFS/N mice of the heritable spongiform encephalopathy associated with the gray tremor mutation. 347 86

A child was seen because of encephalopathy and metabolic ketoacidosis at 19 months. She was found to have a cobalamin-responsive form of methylmalonic acidemia of the cbl A complementation group. However, after treatment with cyanocobalamin and a protein-restricted diet, with recovery from the encephalopathy, she was found to have a tremor and bilateral dystonic posturing in association with lucencies in the globus pallidi shown by computed tomographic scan.
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PMID:Bilateral lucency of the globus pallidus complicating methylmalonic acidemia. 376 21

In 9 patients undergoing chronic hemodialysis for 2-10 years and suffering from encephalopathy (dialysis dementia) and peripheral neuropathy, 10 mg of biotin was given daily in three doses for 1-4 years. Within 3 months there was a marked improvement in all patients in respect to disorientation, speech disorders, memory failure, myoclonic jerks, flapping tremor, restless legs, paresthesia and difficulties in walking. It is recommended to start giving biotin regularly in any patient with advanced renal failure before severe neural or muscular lesions become manifest. The correlation of biotin with uremic neurologic disorders and the possible mechanism of its therapeutic action are discussed.
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PMID:Biotin in the management of uremic neurologic disorders. 632 32

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Vidarabine (adenine arabinoside, ara-a) has been found to be useful in the treatment of various viral infections. Its adverse neurological effects include tremor and encephalopathy. Two cases of vidarabine encephalopathy are reported and the five other cases in the literature are reviewed. The clinical features of the tremor and encephalopathy are discussed.
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PMID:Vidarabine encephalopathy. 651 57

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
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PMID:Frequent neurologic toxicity associated with amiodarone therapy. 653 58

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

The coma-inducing effect of phenol was studied in normal 300 +/- 50 gm Sprague-Dawley rats. Dose-response curves were developed which showed that one-half the animals became deeply comatose with 540 mumol of intraperitoneal phenol and 100% with 600 mumol. Five stages of encephalopathy were readily distinguished. In stage I, spontaneous activity was noticeably decreased, posture was upright, back-leg control normal, muscle tonus slightly increased, and response to stimuli normal. In Stage V, activity was gone, the rats were deeply unconscious, righting reflex and back-leg control were gone, muscles were completely relaxed, and there was no response to stimuli. With a coma-inducing dose of phenol, spontaneous activity decreased. After 1 min a body tremor developed interspersed with unpredictable jumping, and all four limbs began to shake. Leg control and then the righting reflex were lost by 2 min. Within 5 min rats were deeply unconscious and muscles completely relaxed while shaking of limbs continued until recovery 20 to 60 min later or death. With 480 mumol or less, none of the rats became comatose, but the shaking of limbs was present. The coma-inducing dose of phenol was reduced by 10% to 20% with simultaneous injection of subcoma doses of NH4+ or OA and by 20% to 30% with simultaneous DMDS leads to 2 methanethiol. Conversely, a subcoma dose of phenol reduced the coma-inducing doses of NH4+, OA, and DMDS by approximately 20% to 25%. Thus phenol, which accumulates in human hepatic failure, induces coma by itself in rats and acts synergistically with other hepatic failure toxins.
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PMID:Encephalopathic effect of phenol in rats. 683 29

During a 6-year period, 23 Navajo adolescents were hospitalized 47 times for presumed lead intoxication secondary to gasoline sniffing. Most patients were male (87%) and sniffed gasoline as a social activity, more frequently in spring and summer. Sixty-five percent of the patients first presented with toxic encephalopathy. Of total episodes, 31% involved asymptomatic lead overload; 31% involved tremor, ataxia, and other neurologic signs; and 38% involved encephalopathy with disorientation and hallucinations. Free erythrocyte protoporphyrin levels were not consistently high, although blood lead levels were all elevated. One death occurred. Approximately 11% of 537 Navajo adolescents said they inhaled gasoline for enjoyment at least occasionally. Among 147 junior high school students, blood lead levels averaged 18 +/- 6 micrograms/dL with no values greater than 40 micrograms/dL. Three of these students had elevated zinc protoporphyrin levels and all three were anemic. No correlation was found between levels of blood lead or zinc protoporphyrin and whether or not the youth reported sniffing gasoline. However, sniffing gasoline was associated with poor school performance and delinquent behavior. Although apparently many Navajo adolescents experiment with gasoline inhalation, only a few engage in this activity frequently enough to develop either asymptomatic or symptomatic lead overload.
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PMID:Gasoline sniffing and lead toxicity in Navajo adolescents. 684 58

Chronic, excessive ingestion of alcohol, with its accompanying subnutrition and intermittent drug withdrawal (partial or complete), has produced many neurologic disorders. These problems include involuntary movement disorders which may be reviewed under three major headings: withdrawal tremulous states, cerebellar system dysfunction, and hepatic related disorders.The tremor of alcohol withdrawal resembles that of physiologic tremor when exacerbated by anxiety. It is the most common neurologic manifestation of alcohol withdrawal, and the tremor amplitude is usually greatest some 10 to 20 hours after cessation of drinking. A tremulous state, which may be transient or persistent, also occurs in infants born to alcoholic mothers.The common hepatic encephalopathy may be accompanied by a flapping tremor and multiple other tremors and jerking movements. Chronic porto-systemic encephalopathy is accompanied by choreoathetoid movements and persistent coarse tremors.
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PMID:Extrapyramidal dysfunction in alcoholism. 705 44


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