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)

The antiparkinsonian activity of bromocriptine and of lergotrile was investigated in monkeys with surgically induced tremor and in parkinsonian patients. Both drugs effectively relieve tremor in experimental monkeys and induce less pronounced abnormal involuntary movements than L-dopa or piribedil. Both drugs were shown to be of therapeutic value in a group of patients with advanced Parkinson's disease who were no longer responsive to levodopa combined with carbidopa. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance ("on-off" effect) were decreased, while mental changes were increased. The interactions of bromocriptine and of lergotrile with dopamine and alpha-adrenergic receptors were investigated. Both drugs have mixed agonist-antagonist activities with respect to the dopamine receptors; lergotrile has a higher affinity for the agonist site while bromocriptine has a higher affinity for the antagonist site of the receptors. Both drugs effectively displace the binding of the alpha-adrenergic antagonist WB-4101 to cerebral cortex membranes. The mechanisms underlying the antiparkinsonian efficacies of these two drugs were discussed.
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PMID:Bromocriptine, lergotrile: the antiparkinsonian efficacy and the interaction with monoaminergic receptors. 2 45

Lergotrile mesylate, an ergot alkaloid derivative and putative dopamine agonist, was effective in the majority of patients with Parkinson's disease who were showing signs of disease progression despite treatment with levodopa combined with a peripheral decarboxylase inhibitor (carbidopa). Among 20 patients completing a six-month trial, there was a significant (P less than .01) reduction in rigidity, tremor, bradykinesia, gait disturbance, and total score when lergotrile was added to levodopa plus carbidopa. Mean daily dose of lergotrile mesylate was 52 mg, and the mean daily dose of levodopa was reduced by 15%. Abnormal involuntary movements were decreased on addition of lergotrile and reduction in levodopa while mental changes and orthostatic hypotension were increased. Elevations in serum transaminase levels were noted in three patients. The ergot alkaloids promise to be an important new class of antiparkinsonian drugs.
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PMID:Treatment of Parkinson's disease with lergotrile mesylate. 33 94

The antiparkinsonian activity of bromocriptine, a presumed dopaminergic receptor agonist, was investigated in monkeys with surgically induced tremor and in a group of parkinsonian patients. A single administration of bromocriptine resulted in a dose-dependent relief of tremor in monkeys. Repeated administration enhanced this effect. Only mild abnormal involuntary movements were observed and only after repeated administration. Eleven patients with Parkinson's disease were treated with bromocriptine (mean dose, 26.4 mg a day). Clinically obvious improvement was noted in one or more of the cardinal signs of the disease in six patients (responders). No obvious improvement in any of the cardinal signs was noted in the remaining five patients (nonresponders). Clinically, the responders were older and more severely affected and had been on a higher dose of levodopa. However, they had had the disease for a shorter period. It is suggested that failure to respond to bromocriptine may be related to a decrease in the sensitivity of postsynaptic dopaminergic receptors.
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PMID:The antiparkinsonian efficacy of bromocriptine. 81 21

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P less than 0.01) improvement in rigidity, tremor, bradykinesia, gait disturbance and total score. In seven patients levodopa with carbidopa was completely replaced by bromocriptine (mean dose, 70 mg), with improvement in four. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance (on-off effect) were decreased whereas orthostatic hypotension and mental changes were increased. Bromocriptine appears to be a major new agent in Parkinson's disease that is especially promising in patients no longer responding to levodopa.
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PMID:Treatment of parkinson's disease with bromocriptine. 98 85

A double-blind study comparing the effects of carbidopa and levodopa combined in a single tablet with levodopa alone was undertaken in 50 patients with Parkinson's disease. After 6 months, there was a statistically significant improvement over baseline in total score, rigidity, and tremor only in the patients randomized to carbidopa/levodopa. In addition, 40 percent of the patients treated with carbidopa/levodopa showed obvious clinical improvement (a greater than 50 percent reduction in their total score) over treatment with levodopa alone. However, after 2 years, only 20 percent continued to show this improvement. Nausea, vomiting, and anorexia developed in 56 percent of patients on levodopa but in only 27 percent of patients on carbidopa/levodopa. However, abnormal involuntary movements, observed in 48 percent of patients on levodopa, were present in 77 percent of patients on carbidopa/levodopa. Despite the increase in abnormal involuntary movements, carbidopa/levodopa is more effective than levodopa.
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PMID:Comparison of dopa decarboxylase inhibitor (carbidopa) combined with levodopa and levodopa alone in Parkinson's disease. 110 Oct 99

Twelve parkinsonian patients with an unsatisfactory therapeutic result on L-Dopa alone due to nausea, vomiting and involuntary movements were treated WITH L-Dopa and decarboxylase inhibitor. The daily dose reached 800mg L-Dopa and 200 mg decarboxylase inhibitor. Single doses of each of the components were also given. Electrophysiological examination of hypokinesia, tremor and rigidity, and clinical observation revealed clear evidence of rapid improvement on small doses of L-Dopa combined with decarboxylase inhibitor. Most of the improvement occurred during the 1st week before the maximal dose was reached. A single oral dose of decarboxylase inhibitor resulted in an improvement, suggesting the presence in the organism of a small AMOUNT OF L-Dopa. This work also shows the absence of liver toxicity of the drug used. Elimination of the extracerebral side effects nausea and vomiting in our opinion is a principle advantage of the compound compared to L-Dopa alone, wheras abnormal involuntary movements, which were found in all patients, remain the limiting adverse side effect.
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PMID:Treatment of parkinsonism with l-dopa and a decarboxylase inhibitor. An electrophysiological and clinical study. 114 54

Computed tomographic (CT) studies have demonstrated structural brain abnormalities including cortical atrophy and enlarged lateral ventricles in a subset of schizophrenic patients including those with abnormal involuntary movements. In the following series of studies, we present our findings pertaining to neuroradiological covariates of drug-induced Parkinsonism and Tardive dyskinesia in schizophrenic patients. In these studies we have explored the relationship of Parkinsonism and Tardive dyskinesia to pineal and choroid plexus calcification. In addition, we also investigated the relationship of pineal calcification to schizophrenia, and specifically to the paranoid and nonparanoid subgroups. In a further series of studies, we investigated the neuroradiological covariates of disorders of gait and posture as well as tremor in schizophrenic patients with drug-induced Parkinsonism. In addition, we explored the relationship of Tardive dyskinesia and its subsyndromes to CT scan measurements of cortical and subcortical atrophy in schizophrenia. Our findings highlight the significance of the pineal gland in the pathophysiology of schizophrenia and drug-induced movement disorders. Furthermore, these studies underscore the heterogeneity of Parkinsonism and Tardive dyskinesia.
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PMID:Neuroradiological covariates of drug-induced parkinsonism and tardive dyskinesia in schizophrenia. 193 76

1. Monkeys with surgical unilateral ventromedial tegmental lesions of the brain stem served as models for investigating abnormalities in Parkinson's disease and Lesch-Nyhan syndrome. 2. The animals exhibited some neurological deficits which are similar to those observed in Parkinson's disease or Lesch-Nyhan syndrome. 3. In monkeys with unilateral ventrolateral tegmental lesions, the levels of dopamine and the activities of catecholamine-synthesizing enzymes were reduced on the lesion side of the striatum, and hypokinesia and tremor developed on the contralateral extremities. 4. Dopa or dopamine agonists relieve tremor and evoke abnormal involuntary movements which are similar to the responses observed in patients with Parkinson's disease. 5. The antitremor effect of Dopa is potentiated by catechol-O-methyltransferase inhibition, suggesting a therapeutic potential for these types of agents. 6. Evidence was obtained that stimulation of D2 dopamine receptors by selective dopamine agonists exerts antitremor activity and evokes abnormal involuntary movements. 7. Combined administration of D1 and D2 dopamine agonists seems to enhance the antitremor activity. 8. Partial dopamine agonists exert antitremor activity and produce less severe abnormal involuntary movements than full dopamine agonists. 9. In a group of monkeys with unilateral ventromedial tegmental lesions of the brain stem the administration of mixed D1/D2 dopamine agonists results in the occurrence of self-biting behavior of the forelimb digits and spasticity of the hindlimbs and these symptoms are similar to those observed in patients with Lesch-Nyhan syndrome. 10. The self-biting behavior seems to be associated with the stimulation of central D1 dopamine receptors and therefore the possible involvement of dopamine neuronal abnormalities in Lesch-Nyhan syndrome deserves further investigation.
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PMID:Monkeys with unilateral ventromedial tegmental lesions of the brain stem: models for Parkinson's disease and Lesch-Nyhan syndrome. 250 25

Tardive dyskinesia (TD); abnormal involuntary movements appearing late in neuroleptic treatment) was described shortly after introduction of chlorpromazine and other antipsychotic agents in the 1950s. Consideration of this disorder as a common, progressive, and relentless problem of major public-health and medicolegal concern in the 1970s now appears to have been somewhat exaggerated. Several symptom patterns associated with neuroleptic treatment may or may not appropriately be lumped with the concept of TD (acute and withdrawal-emergent dyskinesias, dystonias, and akathisia, in particular); parkinsonism (with bradykinesia, rigidity, and tremor, including perioral tremor of the "rabbit syndrome") should be differentiated from TD, even though elements of both may occur together. Dyskinesias, more or less similar to TD, can occur in chronically ill neuropsychiatric patients not exposed to neuroleptics. Some may represent stereotyped behaviors of schizophrenia or undiagnosed neurological disorders, but a risk of spontaneous dyskinesias indistinguishable from TD averages about 5% (probably less in young patients). Mean prevalence rates for TD, corrected for spontaneous dyskinesias, average about 15-20% with higher risks at advancing ages. Incidence rates are less certain, but estimates average about 5% a year for at least several years in young patients, with higher rates within the first two years of treatment of elderly patients. Risk factors most clearly defined are advancing age, use of neuroleptic agents at relatively high daily doses for more than six months, and perhaps the diagnosis of a major affective disorder. Female gender and relatively high plasma levels of neuroleptic agents are less significant risk factors and other metabolic or neuroradiological indicators of risk remain unproved. The etiology of TD remains obscure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A summary of current knowledge of tardive dyskinesia. 290 54

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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