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)

A mutant mouse (wriggle mouse sagami, WMS) with neurological disorders was found in a colony of the BALB/c strain. The clinical signs included tremor, dystonia and involuntary movements. The concentrations of the neurotransmitter substances, noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT) and acetylcholine (ACh), were measured simultaneously with their metabolites in dissected brain regions by high-performance liquid chromatography with electrochemical detection. The turnover of 5-HT was significantly higher in the cerebral cortex, hippocampus, hypothalamus, midbrain and pons-medulla of WMS than of the genetic control, BALB/c. The intrastriatal DA and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid were increased. However, there was no evidence to suggest an increase in turnover rate of this neurotransmitter. An increase in concentration of and decrease in turnover rate of NA were observed in the cerebellum of this mutant. These findings suggest that multiple disturbance of the neurotransmitter system was largely responsible for the manifestation of the clinical signs of WMS.
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PMID:Functional difference in monoamine transmitters in the behaviorally abnormal mouse mutant (wriggle mouse sagami). 281 21

Forty-seven railroad workers who were exposed to polychlorinated phenols, including dioxin (TCDD), during 1979 while cleaning up the chemical spillage following damage to a tank car filled with these chemicals were followed medically for the subsequent 6 years. Two committed suicide. The initial neurological complaints included a sense of fatigue and muscle aching, both of which have been reported in other individuals following dioxin exposure. On detailed neurological examination in December, 1985, 24 of 45 had dystonic writer's cramp and/or other action dystonias of the hands. None of the involved individuals had a family history of dystonia, and all 24 dated the onset of the dystonia to the first 2 to 3 years subsequent to their toxic exposure. The dystonias varied in severity but were usually mild. No other types of dystonic involvement were recognized. Thirty-five of the 45 individuals also manifested postural and terminal intention tremor which resembled benign essential tremor. None of the involved individuals had a family history of tremor, and all 35 of those affected dated the onset of the tremor to some time subsequent to their toxic exposure. Forty-three of 45 patients had histories and findings suggestive of peripheral neuropathy. This is the first report relating any type of dystonia to prior dioxin exposure and the first report relating action dystonia, such as dystonic writer's cramp, and postural/terminal intention tremor, to toxic exposure of any type.
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PMID:Dystonia and tremor following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 284 55

The recognition of specific types of abnormal movements in patients receiving chronic neuroleptic therapy is discussed. Characteristics of the four major categories of such movements--tremor, chorea, tics, and dystonia--are listed. These abnormal movements can be seen in several other syndromes and disease processes, which are briefly reviewed.
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PMID:Recognition and diagnosis of tardive dyskinesia. 285 77

Clinical and electrical evidence of peripheral neuropathy may result from long term treatment with phenytoin or barbiturates, especially in combination, or after repeated exposure to toxic blood concentrations of either drug. Prolonged acute toxicity with phenytoin may rarely lead to permanent residual ataxia. Reversible dystonia may occasionally be precipitated by phenytoin or carbamazepine; asterixis by phenytoin, barbiturates or carbamazepine; and, more commonly, tremor by valproate. All the major anticonvulsant drugs, especially in combination, can produce occasional subacute cognitive or behavioural syndromes. In varying degrees, the drugs also impair attention, concentration, memory, mental speed or processing, or motor speed. Possible mechanisms of impaired mental function include neuronal damage, or disturbance of folic acid, monoamine or hormonal metabolism. The relative influence on neurological or psychological function is an important factor in the choice of anticonvulsant drug for the treatment of epilepsy.
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PMID:Adverse neuropsychiatric effects of anticonvulsant drugs. 286 Oct 75

Four infants suffering from benign non-fluctuating, idiopathic dystonia with onset in the first year are presented. The discussion includes the relationship to childhood-onset dystonia, the significance of the tremor, the neurotransmitters in the CSF, spontaneous recovery, the risk of recurrence and the preference not to intervene orthopaedically.
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PMID:Benign idiopathic dystonia with onset in the first year of life. 287 71

Although physiological corroboration of the target is essential in functional stereotactic surgery, the collected data can also be used for the offline study of normal and abnormal brain function. Such studies have the advantage of being made in actual clinical states with the unique opportunity of communicating with the patient. Correlations were made between microelectrode recordings and microstimulation at the same thalamic site with the same microelectrode in 'normal' patients, in those with tremor and in those with central and deafferentation pain. Human somatosensory organization is similar to that of subhuman primates. Five types of tremor cells have been identified-unresponsive nonsynchronous, unresponsive synchronous, kinaesthetic, voluntary, and voluntary with receptive field. While the last two qualify in latency and connectivity as tremor pacemakers, system analysis suggests an important element of long loop feedback as well. In the pain patients, five features were identified-somatotopic reorganization, altered firing in reorganized cells, bursting cells induction of burning widespread in thalamus and reproduction of the patient's pain by microstimulation-possibly a 'central allodynia' found in deafferented somatosensory thalamus particularly in patients with allodynia or hyperpathia. All but the latter effects may be merely the consequence of deafferentation and were seen in a 'control' stroke patient with dystonia, sensory loss but no pain.
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PMID:Microelectrode techniques in localization of stereotactic targets. 288 38

Initially, the reality of the existence of tardive dyskinesia raised some controversy, but rapidly this syndrome was recognized as a complication arising from usually long-term administration of neuroleptics. These extrapyramidal abnormal movements represent an important problem due to their prevalence, their potential irreversibility, their complex and still disputed physiopathologic mechanism, the absence of specific and generally effective treatment, and more recently the medico-legal problems entailed. At first, it was believed that these dyskinetic movements, of various intensity, were localized only at the oro-facial area (face, tongue, maxillary), or consisted of limited or generalized choreo-athetosic movements, or were a mixture of both types of movements. However, digestive and respiratory tardive dyskinesia also occur. Tardive dyskinesia can develop insidiously during neuroleptic treatment, or appear when this medication is decreased or ceased. It can coexist with parkinsonian signs. Age (over 50) and gender (female) appear to be risk factors. Other types of tardive syndromes associated with neuroleptic administration have been reported, such as tardive akathisia, tardive dystonia and a tardive Tourette-like syndrome. Involuntary movements resembling tardive dyskinesia can be observed in elderly individuals who never received neuroleptic medication. With respect to the rabbit syndrome, a rapid tremor of the perioral area, with a rhythmicity similar to the parkinsonian tremor, it is clearly different from tardive dyskinesia. It is essential to detect as precociously as possible tardive dyskinesia. The diagnosis is sometimes difficult and even if the clinical features seem pathognomonic of tardive dyskinesia, it is nevertheless important to establish a differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical aspects of tardive dyskinesias induced by neuroleptics]. 290 48

A 24-year-old man presented with dystonia, dementia, amyotrophy, choreoathetosis, and ataxia. Partial hexosaminidase A deficiency was documented in serum and leukocytes and confirmed by rectal biopsy with ganglion cells containing membranous cytoplasmic bodies. A brief review of the literature reveals that tremor, dystonia and choreoathetosis are common but neglected symptoms associated with chronic GM2 gangliosidosis.
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PMID:Movement disorders associated with chronic GM2 gangliosidosis. Case report and review of the literature. 308 50

The experience that the supplementation of depleted dopamine in the nigro-striatal system of parkinsonian patients with L-dopa improves the clinical triad, akinesia, rigidity and tremor, mainly applies to long-term treatment in the early phase of Parkinson's disease. Complications in motor performance, like on-off response, wearing-off phenomena, peak-dose dyskinesia, biphasic dyskinesia, off-period dystonia and others, after more than 3 to 5 years following the onset of treatment indicate fluctuations in the dopaminergic feedback control system. It is suggested that these complications are due to progressive presynaptic degeneration and late changes in postsynaptic receptor amplification. However, as fluctuations are not imperative in all patients, an important additional aspect seems to be the topography of denervation, which involves different portions of the striatum to varying degrees. Location and extent of denervation are criteria which appear to have predictive value for the malignancy of the disease, the therapeutic response of drugs and complications in long-term treatment.
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PMID:Factors contributing to fluctuations of the dopaminergic nigro-striatal feedback system in Parkinson's disease. 316 34

Movement disorders are usually of central origin, but sometimes involuntary movements occur after peripheral trauma. Twenty eight patients, 13 women and 15 men, mean age 37 years (range 15-78), were studied with dystonia or tremor in whom the onset of abnormal movements was related, in time and in distribution, to injury of a body part. Among 23 patients with latency of less than one year after injury, focal dystonia of the involved body part was found in 18, nine of whom had associated reflex sympathetic dystrophy (RSD). One of five patients with peripherally induced tremor had RSD. Abnormal electromyography or nerve conduction velocities were found in the affected limb in four patients, but other electrophysiologic techniques provided evidence for disturbed central function. In 15 patients (65%) possible predisposing factors may have contributed to the pathogenesis of the trauma induced abnormal involuntary movements.
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PMID:Dystonia and tremor induced by peripheral trauma: predisposing factors. 322 Dec 19


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