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)

This study concerns 3 cases of malignant syndrome due to neuroleptics. Our aim is to clarify the nature of this syndrome and to attempt to delimit it from malignant hyperthermia. The etiology suggests that its occurence should increase with the growing use of very active neuroleptics. It consists clinically of an extrapyramidal syndrome with hypertonicity, akinesia, tremor and with a neuro-vegetative syndrome of which the main sign is hyperthermia. On the basis of physiopathology it is attempted to explain, in the light of fresh data, the extrapyramidal signs, the hyperthermia and the rise in the OPK Etiological treatment has, however, proved disappointing.
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PMID:[Malignant syndrome caused by neuroleptics (3 observations)]. 3 12

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

A clinical evaluation was carried out in 20 elderly patients with parkinsonism to assess the effectiveness and acceptability of treatment with a combination preparation of levodopa and benserazide over a period of 9 months. Mean daily maintenance dosage was 612.5 mg levodopa and 140 mg benserazide. The effects of treatment on clinical features and activities of daily living were monitored at monthly intervals. Significant improvement occurred in the first month and optimal improvement was usually reached by the end of 3-months' treatment. Akinesia and rigidity were abolished or improved in the majority of patients but the effect on tremor was less satisfactory. The preparation was well tolerated and side-effects were not troublesome.
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PMID:Levodopa/benserazide ('Madopar') combination therapy in elderly patients with parkinsonism. 37 53

N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON 954) causes a reproducible rest tremor in mice, of rapid onset and short duration with no associated rigidity or akinesia and in the absence of any marked changes in body temperature or accompanying peripheral parasympathomimetic effects. This tremor can be antagonised by the dopamine receptor agonists L-Dopa, bromocriptine, nomifensine and piribedil, as well as by anticholinergic anti-Parkinson drugs having an inhibitory effect on dopamine uptake such as benapryzine and benztropine. In contrast, benzhexol, orphenadrine and amantadine had no effect. LON 954 appears to be more specific than oxotremorine for the detection of drugs having therapeutic potential in the treatment of Parkinson's disease, particularly those exerting their effect through dopaminergic systems. An antagonist (BS 100-141), which is a structural isomer of LON 954, is also described.
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PMID:The production of an alternative laboratory model of the Parkinson syndrome using a new benzylimidoylurea derivative LON 954. 40

Haloperidol (0.25 mg/kg i.m.) was injected daily for 6 months in six normal monkeys. Over a 24 hour period, the following symptoms could be observed: akathisia, circling, akinesia, choreoathetoid and dystonic movements, oro-facial dyskinesias and postural tremor with or without harmaline. Six months after cessation of haloperidol, harmaline-induced postural tremor could still be observed in all animals and oro-facial abnormal movements, in one monkey. The neuropathologic study of the experimental material did not disclose any alteration of the central nervous system.
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PMID:Haloperidol-induced dyskinesias in the monkey. 40 96

In an open study, 60 Parkinson patients with varying aetiology were submitted to a treatment with the long-acting antiparkinsonian drug dexetimide and L-Dopa. Rigor, tremor and akinesia were favourably influenced. An advantage over other antiparkinsonian agents is its long duration of action and the possibility of a simple dosage. Further investigations concerning its long-term effect and elucidation of its interactions with different drugs commonly administered in parkinsonian disorders seem desirable.
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PMID:Treatment of Parkinsonian syndrome with dexetimide. 55 48

The tremorogenic properties of a series of benzylimidoylurea derivatives are described. The most potent member, N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON-954), produces a reproducible, dose-dependent rest tremor in the mouse with oral doses of 5-100 mg/kg which is also seen in other species (rat, cat, dog, rabbit). The tremor is of constant frequency, rapid onset and short duration. It is not accompanied by akinesia, muscle ridigity, antinociceptive activity, parasympathomimetic effects or marked hypothermia and in these respects differs from tremor produced by oxotremorine. Pretreatment with a microsomal enzyme inhibitor had no effect on the tremor. An LD50 of 165 mg/kg p.o. was calculated in the mouse. After repeated administration both acute and chronic tolerance developed to the tremorogenic effects of LON-954. Evidence for a central site of action is presented, since the tremor could be reproduced following injection of small quantities (50-100 microgram) into the cerebral ventricles of the mouse. Furthermore, the use of spinal, decorticate and and decerebrate rats indicated that although tremor is not of cortical origin, it arises in an area rostral to the inferior colliculi. The mechanism underlying the tremor appears to involve dopaminergic pathways, since the action of LON-954 was antagonised by L-dopa and apomorphine and potentiated by pimozide. Atropine and carbachol were without effect. It is suggested that LON-954 could be used as an alternative to oxotremorine for the detection of anti-Parkinson drugs, particularly those exerting their effects through dopaminergic mechanisms.
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PMID:The pharmacology of N-carbamoyl-2-(2,6-dichlorophenyl)acetamidine hydrochloride (LON-954) a new tremorogenic agent. 58 44

Patients with Parkinson's disease performed several different stereotyped elbow flexion tasks, and the electromyographic (EMG) patterns from biceps and triceps were compared with previously established normal standards. The EMG pattern during a smooth flexion task was almost always abnormal and was characterized by alternating activity in biceps and triceps. The EMG patterns during a fast flexion task were also usually abnormal although they were always composed of bursts of EMG activity of normal duration appearing alternately in the agonist and antagonist muscles. These bursts, associated with movements of the limb, have a superficially similar appearance to the EMG bursts seen with tremor-at-rest, but certain physiological differences are demonstrated. This study demonstrates that both slow (ramp) and fast (ballistic) movements are clearly abnormal in these patients with disease of the basal ganglia. In a task designed to investigate antagonist inhibition before agonist activity, a majority of the patients performed normally. This suggests that, contrary to previous claims, slowness of movement (akinesia/bradykinesia) is not due either to failure to relax or to rigidity of antagonist muscle.
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PMID:Analysis of stereotyped voluntary movements at the elbow in patients with Parkinson's disease. 59 80

Twenty-six patients affected by Parkinson's disease were treated with a 2-Br-alpha-ergocriptine (CB 154): 14 cases were given CB 154 alone, and 12 were given CB 154 along with L-dopa plus benserazide (Madopar). Both CB 154 and combined therapy (CB 154+Madopar) induced a significant improvement in total disability score, tremor, rigidity, akinesia, self-sufficiency, and some motor performance tests (dynamic tests). No significant difference was found between results obtained with CB 154 therapy and with Madopar treatment, while the improvement induced by combined therapy (CB 154+Madopar) was significantly higher than that obtained by Madopar alone. The averse reactions caused by CB 154 alone or associated with Madopar are similar to those observed during other dopaminergic treatment. CB 154 alone or combined with Madopar appears to be a useful advance in the management of Parkinson's disease.
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PMID:Bromocriptine alone or associated with L-dopa plus benserazide in Parkinson's disease. 59 82

Before and during a standardized course of trifluoperazine therapy, 18 schizophrenic patients underwent repeated examinations for extrapyramidal motor signs, clinical psychopathology, and urinary excretion of free and conjugated forms of dopamine and its metabolites. Patients excreting more free dopamine and metabolites, or showing less complete conjugation, before drug treatment, were much less likely than others to develop parkinsonian akinesia and rigidity during drug treatment. Neither catatonic rigidity nor akinesia before treatment was predictive of a parkinsonian response to trifluoperazine, but pretreatment tremor may have been. The severity of schizophrenic psychopathology was unrelated to dopamine excretion. This study of schizophrenic patients, and our previous research in Parkinson's disease, suggest that urinary dopamine excretion may reflect dopaminergic function of the extrapyramidal motor system in both conditions.
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PMID:Dopamine excretion and vulnerability to drug-induced Parkinsonism. Schizophrenic patients. 61 44


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