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)

One hundred and eighty-one patients with treated Parkinson's disease completed a self-administered questionnaire on symptoms, and their responses were compared with those of 263 control subjects randomly selected from a general practice population. Nine symptoms were reported by the patients with more than a fivefold excess when compared with the controls. These included jerking of the limbs, shaking of the hands, excessive salivation, poor mental concentration, grimacing, being frozen or rooted to the spot, and hallucinations. Compared with the general control population, the patients did not have an excess of stomach or limb pain, indigestion, headache, or any decrease of interest in sex. This observational survey, unlike a randomised controlled trial, could not ensure that the different treatment groups were comparable in important respects. However, certain associations were apparent; for example, patients receiving both a decarboxylase inhibitor and levodopa tended to report fewer attacks of being frozen to the spot, fewer problems with salivation, and a reduced frequency of defaecation. Patients receiving anticholinergic drugs reported an excess of dry mouth, faintness, and dyskinesia, and fewer hot flushes.
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PMID:The symptoms of patients treated for Parkinson's disease. 400 65

Thirty patients with various extrapyramidal movement disorders were treated for prolonged periods with 75 to 225 mg. daily of tetrabenazine. In patients with choreiform and hemiballistic motor activity the involuntary movements were diminished or abolished. In patients with cerebellar or Parkinsonian tremor the tremor was aggravated in moderately severe cases, but was uninfluenced in severe cases. In all cases the dyskinesia returned when- the drug was stopped.Side-effects were inconsiderable and disappeared on reducing the dose slightly. Hence the drug may be an important alternative to neurosurgical treatment of hyperkinesias and especially suitable for severely disabled patients.
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PMID:Effect of tetrabenazine on extrapyramidal movement disorders. 423 53

In squirrel monkeys that had undergone repeated treatment with haloperidol at intervals of 7--14 days, subsequent acute administration of haloperidol induced dystonia and dyskinesias. This acute effect of haloperidol was dose-related and occurred at the same doses that impaired Sidman avoidance performance. Chlorpromazine, fluphenazine, metoclopramide, tetrabenazine, and Su-23397, all of which have been associated with extrapyramidal side effects, reliably elicited dyskinesias in these monkeys. Dyskinesias were less mared after thioridazine and absent after clozapine, corresponding to the reported lower incidence of extrapyramidal side effects in the clinic. The non-neuroleptics, baclofen, and diazepam, failed to elicit dyskinesias. In contrast to the dyskinetic syndrome, the incidence of catalepsy or tremor did not accurately predict propensity to elicit extrapyramidal symptomatology. The acute dyskinetic syndrome in squirrel monkeys may therefore serve as an animal model for predicting the ability of antipsychotics to cause extrapyramidal dysfunction, and may yield insight into the mechanisms of these drug-induced motor disorders.
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PMID:Neuroleptic-induced acute dyskinesias in squirrel monkeys: correlation with propensity to cause extrapyramidal side effects. 610 37

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

In a previous clinical investigation, jerky foot movements were observed in patients with akathisia. Tremographic techniques were employed in the present study to characterise this motor activity. Six psychiatric patients with signs and symptoms of akathisia, six control patients matched for antipsychotic drug dose, and five drug-free normal subjects, were selected and assessed for evidence of drug-induced movement disorders. The two patient groups proved to be closely matched on clinical and demographic variables. An accelerometer was used to record finger and toe tremor in all subjects according to a standard procedure. Analysis of the amplitude, frequency and wave-form data collected revealed that the akathisia patients were characterised by the presence of large amplitude, low frequency (less than 4 Hz), rhythmic foot movements. Changes in the severity of akathisia at follow-up were reflected in changes in the amplitude and frequency of this dyskinesia. Possible clinical and pathophysiological implications of the findings are presented.
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PMID:Coarse, jerky foot tremor: tremographic investigation of an objective sign of acute akathisia. 614 88

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
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PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

Four cases of dystonia occurring in two families are reported. The first symptoms consisting of dystonia and rigidity appeared early in childhood, in the first months in one family and of ages two and five years respectively in the other. In two cases, transient tremor was noted. These four children have been treated with L-dopa with prompt spectacular results, in cases 1 and 2, with more gradual less complete results in the others. L-dopa treatment was continued twelve, eleven, six, and five years, respectively, without any developmental problems. Motor function remains satisfactory and school work is normal. The only secondary effect observed was the occurrence of dyskinesia. The relation between L-dopa responsive dystonia and Parkinson's disease is discussed.
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PMID:Dystonia--L-dopa responsive or juvenile parkinsonism? 658 12

In previous work, we demonstrated in animals and humans an antidopaminergic effect of estradiol at the level of the striatum. In the present study, we tested the effect of a large dose of estradiol (0.5 mg s.c.) administered either acutely or during several days in four female ovariectomized monkeys, displaying a persistent buccolingual dyskinesia due primarily to a midbrain lesion, but which is markedly enhanced by dopaminergic agonists. One of the monkeys also displayed a lesion-induced parkinsonian-like tremor of the opposite limbs. Chronic administration of estradiol markedly reduced the apomorphine-induced potentiation of the dyskinesia but did not affect the tremor. A single dose of estradiol was followed after 24 h by a 75% reduction of the effect of apomorphine on the dyskinesia but a 50% increase in the response to apomorphine was seen after 2 weeks. The response was at the control level after 30 days. Domperidone, a peripheral dopamine agonist that does not cross the blood-brain barrier and which causes an elevation of prolactin similar to that seen after estradiol, is followed by a similar biphasic modification of the response to apomorphine. Our results suggest that estradiol may have opposite effects on the sensitivity of the striatal dopamine receptors and therefore on dyskinesia, depending on the time of observation. An elevation of prolactin appears to have similar effects. Moreover, some effects of these hormones may be delayed by several days to weeks in primates.
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PMID:Biphasic effect of estradiol and domperidone on lingual dyskinesia in monkeys. 662 6

1. Estrogens have been shown to decrease the effect of apomorphine in a variety of animal behavioral models reflecting the sensitivity of striatal and mesolimbic dopamine receptors. 2. These include circling, and locomotor activity, in rats and suppression of midbrain tremor as well as lingual dyskinesia in monkeys. 3. Estradiol also increases the haloperidol-induced catalepsy in rats. Moreover estradiol increases 3H spiroperidol specific binding in the rat striatum and potentiates the increase caused by haloperidol or denervation with 6-hydroxydopamine. 4. These findings point to an action of estradiol similar to a week neuroleptic. 5. Thyrotropin-releasing hormone when injected into the head of the caudate nucleus in cats induces a head turning response which may be ipsilateral or contralateral depending upon the injection site. The response is similar to the effect of dopamine injected into the same site. 6. The effect of dopamine but not that of TRH is blocked by prior administration of haloperidol indicating that although TRH has a dopamine-like action in the caudate nucleus, it is not mediated via the dopamine terminals or the dopamine receptors.
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PMID:Estradiol, TRH and striatal dopaminergic mechanisms. 681


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