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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.
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PMID:[Electrophysiological and pharmacological analysis of L-dopa-induced dyskinesia and tardive dyskinesia (author's transl)]. 611 68

In a double-blind crossover placebo controlled trial the effectivity of piracetam in neuroleptic-induced extrapyramidal side effects was confirmed. 40 psychotic patients treated with neuroleptics in an average daily dose equal to 600 mg of chlorpromazine were included in this study. Akathisia, tremor, muscle rigidity and dyskinesia were evaluated on a 4-point scale. The patients were randomly divided into two subgroups--40 g of piracetam or placebo from identic ampoules were given i.v. with a crossover readministration after 60 min. The intensity of the extrapyramidal side effects was evaluated at 30-min intervals during 2 h. Piracetam was proved to be significantly effective in both subgroups, the onset of its action being between 30 and 60 min after i.v. administration. Possible interpretations of the observed piracetam effectivity are considered. Further trials with piracetam in neurologic complications during neuroleptic treatment, tardive dyskinesia included, are suggested.
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PMID:Effect of piracetam on extrapyramidal side effects induced by neuroleptic drugs. 612 31

Fourteen patients with neuroleptic-induced akathisia were treated with propranolol in an open trial. All patients demonstrated substantial improvement of their akathisia; nine of the 14 obtained complete remission. Response was quite rapid, occurring within 24 hours in most cases. Doses required for improvement were low (30-80 mg/day), and side effects were few. Lithium-induced tremor improved considerably, but symptoms of parkinsonism and tardive dyskinesia showed little change. Preliminary results with certain other beta blockers suggest that they are less effective than propranolol in the treatment of akathisia.
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PMID:Propranolol in the treatment of neuroleptic-induced akathisia. 614 57

Electromyographic (EMG) activity of abnormal involuntary movements and their modifications after Piribedil, a dopaminergic agonist, were analysed in patients presenting with tremor or tardive dyskinesia induced by treatment with neuroleptics. Quantitative analysis of EMG bursts and of their phase relationships with bursts of antagonist muscles revealed differences between tremor and tardive dyskinesia; three separate EMG types of the latter were found. In tremor, EMG activity was coordinated between agonists and antagonists. Length and frequency of bursts are characteristic. In tardive dyskinesia, phase histograms of antagonist muscle bursts showed an absence of reciprocal organisation of EMG activity. This activity was made up of either rhythmical bursts (type I and II according to the frequency) or irregular discharges (type III). Piribedil decreased tremor but facilitated EMG activity in tardive dyskinesia. These results give an objective measurement or classification of tremor and tardive dyskinesia induced by neuroleptics.
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PMID:EMG patterns in abnormal involuntary movements induced by neuroleptics. 614 81

Six patients with akathisia were treated with clonidine in an open, on-drug/off-drug trial. All six patients demonstrated substantial improvement of their akathisia, with four of the six obtaining complete remission. The dose of clonidine used to treat the remaining two patients was limited by the development of symptomatic hypotension. Daily doses ranged from 0.2 to 0.8 mg, and maximal response to a particular dose occurred within 24 to 48 hours. Although no effects on lithium tremor, parkinsonism, or tardive dyskinesia were observed, two bipolar patients exhibited considerable improvement in their manic and psychotic symptoms during treatment with clonidine.
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PMID:Use of clonidine in treating neuroleptic-induced akathisia. 615 54

Excluding surgical procedures, this article focuses on clinical pharmacotherapeutic approaches to treatment of parkinsonism and tremor, chorea, dystonia, tic, and tardive dyskinesia.
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PMID:Involuntary movement disorders. 623 89

The descriptive aspects of all types of movement disorders and their related syndromes and terminologies used in the literature are reviewed and described. This comprises the features of (a) movement disorders secondary to neurological diseases affecting the extrapyramidal motor system, such as: athetosis, chorea, dystonia, hemiballismus, myoclonus, tremor, tics and spasm, (b) drug induced movement disorders, such as: akathisia, akinesia, hyperkinesia, dyskinesias, extrapyramidal syndrome, and tardive dyskinesia, and (c) abnormal movements in psychiatric disorders, such as: mannerism, stereotyped behaviour and psychomotor retardation. It is intended to bring about a more comprehensive overview of these movement disorders from a phenomenological perspective, so that clinicians can familiarize with these features for diagnosis. Some general statements are made in regard to some of the characteristics of movement disorders.
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PMID:Clinical features of movement disorders. 662 43

In this work, we have attempted to reproduce dyskinesia similar to tardive dyskinesia by two methods. In the first experiment, we have administered to 6 macaca mulatta, haloperidol 0.25 mg/kg daily for six months. During that period we observed in all monkeys, after each dose: restlessness, akinesia and tremor. One monkey developed choreoathetoid movements, which were seen each day after the first month. They disappeared however upon cessation of the drug administration. Only one animal developed a bucco lingual dyskinesia after two months which was still present when they were sacrificed six month after the drug administration was discontinued. At that time, harmaline 3 mg/kg induced a postural tremor in all monkeys suggesting a lesion of the rubro-olivo-cerebello rubral loop. Histological analysis of the brains revealed no gross abnormality. In a second experiment, a left midbrain electrolytic lesion was performed in twelve monkeys. One monkey, developed a contralateral tremor but five including the trembling one developed a buccolingual dyskinesia which has now lasted more than a year. This dyskinesia is present at rest but increased by dopaminergic agents and blocked by haloperidol. Histological analysis of the brain of one of the monkeys revealed a dorsal lesion involving the region of the nucleus parafascicularis thalami. The substantia nigra was spared.
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PMID:Experimental tardive dyskinesia. 689 21

A unique case reported of a patient with right-sided Parkinson's disease and left-sided tardive dyskinesia. This situation occurred because the patient's parkinsonian tremor was treated with antipsychotic drugs. After several months she developed tardive dyskinesia on the left side of the body. Successful treatment was achieved nine years later, using dopamine-depleting drugs (combination reserpine and alpha-methylparatyrosine) to suppress the tardive dyskinesia and trihexyphenidyl to reduce the parkinsonism. Control of the symptoms was complicated with parkinsonism symptoms later increased on the right and developed on the left, due to the dopamine-depleting drugs. A small amount of carbidopa/levodopa restored the proper balance of symptoms, effectively reducing the parkinsonism while not aggravating the tardive dyskinesia. This unique case provides insight into the pathogeneis of Parkinson's disease, the pathogenesis of tardive dyskinesia, their successful therapeutic approaches, and possibly the effect of drugs in blocking the progression of Parkinson's disease.
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PMID:Unilateral Parkinson's disease and contralateral tardive dyskinesia: a unique case with successful therapy that may explain the pathophysiology of these two disorders. 693 20

Recent research on the role of clozapine in the treatment of Parkinson's disease and other movement disorders is discussed. Most clinical trials have shown resolution of or improvement in psychotic symptoms accompanying Parkinson's disease without worsening of parkinsonian symptoms. Adverse effects appear to be mild at dosages of < 100 mg/day; sedation is the most frequent problem. Most of these studies have serious limitations, however; until better studies have been completed, the decision to use clozapine for Parkinson's disease-related psychosis should be made on a case-by-case basis, with thorough evaluation of risks, benefits, and other therapeutic options. Some patients with Parkinson's disease have shown improvement in tremor and other abnormal movements when given clozapine. Clozapine cannot be recommended for treating tardive dyskinesia on the basis of the research done so far; some trials show dramatic resolution of symptoms, others no benefit. Anticholinergics or dopamine-reuptake inhibitors should be considered before clozapine is given to patients with tardive dyskinesia because of clozapine's potential for serious adverse effects. A few patients with Huntington's disease have responded to clozapine, but again no conclusions can be drawn. Clozapine appears to offer no real advantage over haloperidol for treating choreiform movements in Huntington's disease. The frequency of tics in Tourette's syndrome does not seem to be reduced by clozapine. Clozapine has shown some efficacy as a treatment for psychosis and abnormal movements in Parkinson's disease. Results have been less promising for other movement disorders. Further study in larger populations is needed before any definitive conclusions about clozapine's place in movement disorder therapy can be made.
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PMID:Clozapine therapy for Parkinson's disease and other movement disorders. 853 51


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