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)

In 45 of 73 patients (organic brain syndromes of complex genesis, schizophrenia, manic phase of manic-depressive psychosis, alcoholism), intake of placebo one week before discharge induced anxiety accompanied by dryness of the mouth, enhanced perspiration and increase of tremor. Anxiety/disappeared after verbal information that the action of this drug is exhausted 1 hour after its intake. Peculiarity of this observation consists in the fact that all placebo responders (61.6% of patients) appeared to be negative, i.e. they had no positive placebo responses. According to the reported data, the negative placebo responses are observed in 10-20% of patients. Anxiety is considered as a symptom provoked by placebo in patients who are in the "neurotic" phase following the cessation of psychotic symptomatology.
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PMID:[Appearance of anxiety after intake of a placebo]. 263 70

For this open study, we selected 21 chronic psychotic female in-patients (16 of them schizophrenics) who were being maintained on oral neuroleptics. After a wash-out period, they were treated by intramuscular depot injections of haloperidol decanoate, once a month for four months. The dose was calculated from the previous oral dosage, and the amount of the first injection was double that of the three following injections. Relatively stable plasma levels of haloperidol were achieved with the first injection, and corresponded to those observed with oral medication. A very significant correlation was found between plasma level and the dose administered, but not between plasma level and therapeutic effect. The clinical condition of about two-thirds of the patients remained unchanged or improved, compared with the period of oral treatment. During the first two months of treatment, there was more rigidity and tremor, but from the third month, the extrapyramidal symptoms were less pronounced than during the period of oral neuroleptics.
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PMID:Pharmacokinetics and therapeutic efficacy of haloperidol decanoate after loading dose administration. 287 1

There are a number of different relationships among aging, psychosis and movement disorders, most of which have been proposed to involve the neurotransmitter dopamine. Dopamine content and dopamine receptors have been shown to decrease with age, which may relate to the time of onset of different motor and psychotic disorders, as well as to the appearance of these disorders. For example, some so-called senile movement disorders, such as senile tremor and senile chorea, may relate to alterations in dopaminergic transmission with age, as might the general findings of increased slowing of movements and mildly increased rigidity with age, although it is not clear how common some of these changes are in the medically healthy elderly. Decrease in dopamine with age may also be associated with the findings that choreiform and psychotic disorders (which have been proposed to be related to excess dopaminergic activity) tend to predominate at younger ages, whereas parkinsonism is more common at later ages. Certain findings support this notion, such as the appearance of both dyskinesia and psychosis in patients treated with L-dopa, the finding that psychosis may be less common in patients with later-onset Huntington's disease, and the fact that neuroleptic-induced parkinsonism is often more severe in the elderly. However, the situation is more complicated than this, because there are a number of phenomena that do not fit the pattern, including the observation of an increased incidence of tardive dyskinesia in the elderly. Age-related changes in other transmitters are undoubtedly important in both movements disorders and psychosis, and even dopamine has been proposed to have both trophic and toxic properties over the aging process. In general, care is warranted in the use of any psychotropic medications in the elderly, because there can be widespread and often unpredictable effects of these drugs on both motor and mental function.
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PMID:Association of psychosis and movement disorders in the elderly. 289 37

Three patients from two families had an unusual phenotypical variant of late-onset hexosaminidase-A deficiency. The clinical picture was dominated by spinal motor neuron involvement mimicking juvenile-onset spinal muscular atrophy. Atypical features included prominent muscle cramps, postural and action tremor, recurrent psychosis, incoordination, corticospinal and corticobulbar involvement, and dysarthria. The presence of these atypical features in patients whose lower motor neuron involvement would otherwise be consistent with juvenile-onset spinal muscular atrophy should raise the suspicion of the presence of hexosaminidase-A deficiency and GM2 gangliosidosis that can be proved by appropriate enzyme assays.
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PMID:Hexosaminidase-A deficiency presenting as atypical juvenile-onset spinal muscular atrophy. 293 15

The mycotoxins cyclopiazonic acid (CPA) and ergotamine, and the neurotransmitter serotonin all have the beta-aminoethylindole moiety in common. These compounds enhanced the peristaltic movements of the jejunum, ileum and estrous uterus and produced broncho-constriction in vitro. Atropine and cyproheptadine were able to counter the CPA-induced peristaltic movements of the ileum and jejunum. L-epinephrine was able to stop the contractions induced by CPA on both estrous and pregnant rat uteri. Unlike chlorpromazine, CPA did not block the inotropic effects of dopamine, epinephrine and serotonin in vas deferens. This indicated that the previously reported toxic effects of CPA (hypothermia, catalepsy, hypokinesia, tremor) which resembled the effects of anti-psychotic drugs (chlorpromazine, reserpine) probably were not due to the blocking of the neurotransmitter-receptors. In contrast to ergotamine, which decreased the inotropic effects of serotonin on the uterus, CPA had no anti-serotonin effects. The uterotonic effect of CPA (similar to that of ergotamine) suggested that CPA also might have an adverse effect on the reproductive function of humans and animals consuming CPA-contaminated foods.
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PMID:Effects of cyclopiazonic acid on the contractility of organs with smooth muscles, and on frog ventricles. 348 54

Forty-four Parkinson patients (19 patients of the rigid-akinetic type, 13, of the rigid-akinetic-tremor type, and 12, of the tremor type) were included in a study in order to analyse correlations of the expression of the motor symptoms tremor, rigidity, akinesia, with other clinical parameters, computertomographic aspect of brain atrophy and psychometrically assessed cognitive parameters. Rigidity and akinesia are significantly positively correlated with the severity of motor dysability, stage of the disease, and brain atrophy, as is akinesia with a history of pharmacotoxic psychosis. Tremor is significantly negatively correlated with motor dysability, stage of the disease, and history of pharmacotoxic psychosis. Akinesia is correlated with visuomotor dysfunction (tested with Bender Gestalt Test) and rigidity with the depression score (Zung scale). The tremor type is favorable, the rigid-akinetic type unfavorable with respect to motor disability and psychosis.
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PMID:Prognostic implications of the motor symptoms of Parkinson's disease with respect to clinical, computertomographic and psychometric parameters. 378 47

The symptoms include, by ascending order of severity: nightmares and insomnia, nausea and vomiting, muscular weakness or tremor, postural hypotension, hyperthermia, muscle twitching, convulsions, confusional state or psychosis. Prominent features are the late onset of these symptoms, several days after treatment has been discontinued, and the sometimes difficult diagnosis, since patients are usually unaware of their dependence on these drugs. Reinstituting benzodiazepine treatment, then withdrawing it progressively are the best curative measures. Prevention is easy if treatment is gradually rather than abruptly withdrawn in all patients who receive the compound in high dosage for more than one month.
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PMID:[Benzodiazepine physical dependence. 6 cases (author's transl)]. 610 22

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

Bromazepam (6 to 18 mg/day in 3 divided doses) was administered during 28 days to 30 patients, (most of them admitted to hospital) presenting with neurotic, psychotic or depressive anxiety. The effects of the drug, as assessed with the Hamilton scale, were satisfactory in 29 out of 30 cases, irrespective of the nature of the anxiety. Bromazepam was well tolerated; the only side-effects recorded were daytime drowsiness in 2 cases, tremor in 2 cases and excitement in 1 case.
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PMID:[Clinical trial of bromazepam in hospital psychiatry (author's transl)]. 612 46

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


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