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)

Sixty cases of Parkinson's disease were treated with piribedil alone (dose : 274 mg/day, duration : 20,4 months). The overall clinical improvement, confirmed by recordings of tremor and EMG, was 34%, tremor being improved of 59%. Before treatment, an intravenous test does of piribedil with recording made it possible to predict the effectiveness of oral treatment. Side-effects (vasomotor, digestive, psychiatric) were moderate. Orthostatic hypotension, dyskinesia and fluctuations were exceptional. The basic indication for piribedil lies in forms of recent onset in which tremor predominates, patients in whom L-dopa is contraindicated and a certain number in whom the latter has failed (tremor, fluctuating action).
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PMID:[Piribedil, dopaminergic agonist. Prolonged clinical and electrophysiological study in 60 parkinsonian patients (author's transl)]. 2 44

In 13 of 27 cases of persistent dyskinesia, treatment with amantadine, in an average dose of 300 mg, brought good to moderate improvement. In 14 patients who showed no response whatever, further treatment, with bromocriptine in doses raised gradually to a final daily dosage of 15 mg, was effective in four cases, though the improvement was generally only moderate. In more than 50 percent of the cases of initial tremor induced by lithium therapy, oxprenolol in daily doses of 160--240 mg produced good effects and moderate improvement was noted in a few further cases. In a series of 20 patients with initial tremor due to neuroleptic therapy, on the other hand, the same treatment proved unsuccessful in the majority of cases. This is the converse of the experience gained with the classical antiparkinson agents, which have proved more effective against tremor induced by neuroleptics than against lithium-induced tremor.
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PMID:Therapy of extrapyramidal side effects, with particular reference to persistent dyskinesia and lithium tremor. 3 49

The authors have experimented tiapride in 37 cases of abnormal movements and 20 cases of shaking anxio depresive origin. The best indication of tiapride corresponds to lingual buccal an facial dyskinesia caused by neuroleptics and senile trembling increased by alcoholism. On the other hand its anxiolytic and anti shaking properties are more limited. Finally in the case of degenerative senile trembling its action is less effective. Tolerance to tiapride seemed to be excellent even at high dose.
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PMID:[Abnormal movements and shaking in geriatrics (author's transl)]. 3 13

The therapeutic action of Tiapridal appeared to the authors particularly precious and constant in delirium tremens, senile agitation and turbulence, whatever the origin, and bucco-linguo-facial dyskinesia, whether the latter were linked to age or whether they formed part of a neuroleptic syndrome. Their experience does not permit them to have any opinion concerning the use of this drug in tremor and chorea, the patients seem to respond favourably to treatment but in an erratic manner. On the other hand the drug was totally inefficacious in patients suffering from spasmodic torticollis and writer's cramp. Finally, it seemed to them useful to emphasise the improvement in comfort in patients suffering from various pains when given Tiapridal. This justifies the place given to Tiapridal among drugs necessary for the daily practice of neurology.
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PMID:[A new therapeutical approach in neurology (author's transl)]. 21 5

The effect of fusaric acid 150-450 mg daily on tardive dyskinesia and mental state was studied in 15 chronic psychogeriatric patients. The patient's previous drug treatment was maintained unchanged during the experiment. Fusaric acid significantly relieved oro-facial dyskinesia, tremor, and rigidity, and it improved the mental state of the patients (BPRS). Akathisia was exacerbated, but this change was not significant. Akinesia and anxiety were not altered.
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PMID:Effect of fusaric acid on tardive dyskinesia and mental state in psychogeriatric patients. A pilot study. 33 75

We present a study of 7 cases of Charcot-Marie-Tooth disease, associated with a dyskinesia clinically identical with essential tremor, in which motor conduction velocity in the upper limbs was normal or slightly diminished. An analysis of age of onset, sex distribution and clinical signs from cases in the literature is compared with the present series. A family with Charcot-Marie-Tooth disease in which affected members have widely different motor conduction velocity values is reported. Stress is laid upon the fact that categorization of this disease on electrophysiological studies in the upper limbs may present considerable difficulties.
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PMID:Charcot-Marie-Tooth disease associated with 'essential tremor' and normal and/or slightly diminished motor conduction velocity. Report of 7 cases. 43 63

The abnormal movements produced by the psychotropic drugs are related to various physiopathological mechanisms: -- dopaminergic receptors blockage provokes neuroleptic parkinsoniam tremor; -- neuroleptic-induced tardive dyskinesia is similar to 1. Dopa abnormal movements; tardive dyskinesia is due to denervation induced hypersensitivity of the dopamine receptor; the 1. Dopa dyskinesia is probably related to altered responsiveness of these receptors due to an increase in dopaminergic receptor sensitivity; -- antidepressant drugs, particularly lithium, provoke tremor, alleviated by beta blockage; it is probably caused by an abnormal sensitivity of the beta noradrenergic receptors.
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PMID:[Abnormal movements induced by psychotropic drugs]. 47 89

Studies on rats with unilateral nigral lesions suggest that a new ergoline, CF 25-397, is a dopaminergic agonist that might improve parkinsonism. CF 25-397 induces less stereotyped behavior than other dopaminergic agents in rats, and might therefore cause less dyskinesia than levodopa in man. We investigated the clinical actions of CF 25-397 in nine patients. During treatment, severe deterioration resulted in hypokinesia and rigidity; five patients showed marked dysphagia and dysphonia. There was statistically significant deterioration in four timed tests. Mild improvement, not statistically significant, was noted in tremor. These results indicate that clinical implication of the response to potential therapeutic agents in rodent models of parkinsonism must be interpreted with caution.
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PMID:Experiences with a new ergoline (CF 25-397) in parkinsonism. 56 12

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

A study of 7 cases of Charcot-Marie-Tooth disease associated with a dyskinesia resembling benign essential tremor is presented. In 4 patients, the family history strongly suggested an autosomal mode of transmission, 2 cases were sporadic without an established genetic pattern and 1 was probably recessive. The distal parts of the upper and lower limbs showed imparied muscle strength with slight or no atrophy in 4 patients and conspicuous weakness and wasting in another 2. One patient was a chairbound. Although essential tremor and the tremor seen in these patients are clinically (phenotypically) similar it seems possible that they result from two different genotypes. Further, it seems that cases with Charcot-Marie-Tooth disease and "essential tremor" are not the result of the association of two separate dominant characteristics which are generally inherited as mendelian dominant traits. In spite of the diversity of the clinical manifestations of the peripheral neuropathy, the semiologically different types of essential tremor and the electrophysiological data, it is concluded that patients who develop a peripheral neuropathy on a familial basis and who exhibit clinical features of similar character, suffer from a common type of pathological disorder. Stress is laid upon the fact that Friedreich's ataxia and Charcot-Marie-Tooth disease share many clinical features. It is suggested that when Friedreich's ataxia and Charcot-Marie-Tooth disease seem to be present in the same individual and/or alternate in different members of the same family, the process is likely to be one of Charcot-Marie-Tooth disease. The value of the type of inheritance, natural history, clinical examination and electrophysiological data in differentiating Charcot-Marie-Tooth disease (with or without essential tremor) from other degenerative disorders is analyzed.
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PMID:Charcot-Marie-Tooth disease associated with "essential tremor": Report of 7 cases and a review of the literature. 93 72


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