Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tardive dyskinesia is a potentially irreversible syndrome of involuntary hyperkinetic movements that occur in predisposed persons receiving extended neuroleptic (antipsychotic) drug therapy. It is usually characterized by choreoathetoid dyskinesias in the orofacial, limb, and truncal regions, but subtypes of this syndrome may include tardive dystonia and tardive akathisia. Although the mechanisms underlying the pathogenesis and pathophysiology of this disorder are unproven, altered dopaminergic functions will likely play a role in any explanation of it. Tardive dyskinesia develops in 20% of neuroleptic-treated patients, but high-risk groups such as the elderly have substantially higher rates. Risk factors include age, female sex, affective disorders, and probably those without psychotic diagnoses, including patients receiving drugs with antidopaminergic activity for nausea or gastrointestinal dysfunction for extended periods. Total drug exposure is positively correlated with tardive dyskinesia risk. Management strategies include a careful evaluation of both the psychiatric and neurologic states, a broad differential diagnosis, and adjustment of neuroleptic agents to the lowest effective dose that controls psychosis and minimizes motor side effects. No drug therapy is uniformly safe and effective for treating this disorder. A favorable long-term outcome of improvement or resolution correlates with younger age, early detection, lower drug exposure, and duration of follow-up.
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PMID:Tardive dyskinesia. 197 5

Twenty-nine inpatients with major psychotic disorders were treated for 14 days with a clinician-determined dose of haloperidol and with either benztropine or placebo given by double-blind random assignment on days 1 through 7. No differences were noted in haloperidol mean dose, haloperidol blood levels, or BPRS scores during the first seven days between benztropine (N = 14) and placebo (N = 15) groups. Benztropine-treated patients demonstrated increased dry mouth and diminished sweat and a non-significantly lower rate of dystonia compared to placebo (14% vs. 33%). Dystonic patients were significantly younger than nondystonic patients, but did not differ in haloperidol mean dose or plasma concentration. The effect of benztropine on the incidence of dystonia was consistent with other studies, which, when analyzed together, demonstrate the efficacy of anticholinergic prophylaxis. The relatively low incidence of anticholinergic side effects, coupled with the lack of effect on haloperidol blood levels or antipsychotic efficacy, suggest that moderate doses of benztropine in conjunction with haloperidol are a rational approach for the treatment of acute psychosis in young patients.
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PMID:The effect of benztropine on haloperidol-induced dystonia, clinical efficacy and pharmacokinetics: a prospective, double-blind trial. 205 36

Eighty-six patients with acute psychotic exacerbations were treated with fixed dosage regimens of oral fluphenazine up to 10-30 mg/day in randomized, double-blind studies. Dystonic reactions occurred in 33.8% of the subjects at risk. Of these, 58% occurred by the third day, 88% by the fourth day, and 100% by the ninth day of treatment; most occurred later in the interdose interval. Significant predictors of dystonic reactions were higher fluphenazine mg/kg dosage and younger age. There was a trend toward a lower risk of dystonia in patients who received amobarbital sodium for agitation. Results are discussed in relation to possible mechanisms of neuroleptic-induced dystonia.
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PMID:Acute dystonia during fixed-dose neuroleptic treatment. 228 8

Three schizophrenic patients who had transient recurrence of auditory hallucinations during acute dystonia precipitated by neuroleptic medication are reported. If it is accepted that psychotic symptoms result from dopaminergic overactivity, such phenomena suggest that acute dystonia might also have been caused by increased dopaminergic neurotransmission in these cases.
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PMID:Transient recurrence of auditory hallucinations during acute dystonia. 253 46

The long term effects of a de novo treatment with levodopa versus bromocriptine were compared in respectively 13 and 15 previously untreated patients with Parkinson's disease in a prospective randomised trial. Thirteen patients were treated with levodopa alone (mean dose 444, SEM 63 mg daily) whereas 15 others received bromocriptine alone (mean dose 50, SEM 6 mg daily) during 37, SEM 4 and 32, SEM 4 months respectively. For a similar decrease in the Columbia rating scale, the nature of long term side effects was different in the two groups: three patients on levodopa developed peak-dose dyskinesias and one other dystonia. With bromocriptine, one patient developed a severe psychosis whereas 3 others suffered from primary lack of efficacy (1 case) or late decrease in efficacy (2 cases). These results demonstrate the potential of D2 dopamine agonists (like bromocriptine) in the de novo treatment of Parkinson's disease; however, their use is limited by their lack of efficacy and/or the occurrence of neuropsychiatric side effects.
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PMID:A randomised controlled study of bromocriptine versus levodopa in previously untreated Parkinsonian patients: a 3 year follow-up. 266 89

Clozapine has had a uniquely favorable motor system side effect profile since its initial evaluations. This has been convincingly corroborated by many double blind, single blind, and open studies treating acute and chronic psychosis. The acute extrapyramidal syndromes of dystonia, akathisia and parkinsonism infrequently occur, whereas these syndromes develop in up to 75% of patients receiving traditional neuroleptics. Tardive dyskinesia can be suppressed with higher doses of clozapine given over extended periods. However, an antipsychotic effect can be achieved in many patients at doses below the dyskinesia suppressing level. There is no established causative relationship between clozapine and tardive dyskinesia, but there is a theoretical basis that this may occur. Preliminary data suggest clozapine has mild antiparkinsonian effects as well as efficacy in controlling dopamine agonist-induced psychosis without aggravating parkinsonism. A much wider use of clozapine will further characterize the magnitude of differences compared to other neuroleptics, and identify additional indications for this special compound.
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PMID:Clozapine: neuroleptic-induced EPS and tardive dyskinesia. 268 32

In an open clinical multi-centre trial carried out in five Danish psychiatric departments, patients suffering from acute psychosis including mania or exacerbation of chronic psychosis were given injections of 5% zuclopenthixol acetate in 'Viscoleo'. The object of the trial was to evaluate the treatment by means of a global assessment of the severity of the psychosis, the therapeutic effect and the side-effects. The results showed that the treatment was rapidly effective in reducing the severity of psychotic symptoms combined with an advantageous unspecific sedation. The side-effect profile was similar to that after other neuroleptics. Special attention should be paid, however, to a possible occurrence of acute dystonia which was observed particularly in young men with acute psychosis.
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PMID:Acute psychotic disorders treated with 5% zuclopenthixol acetate in 'Viscoleo' ('Cisordinol-Acutard'), a global assessment of the clinical effect: an open multi-centre study. 268 95

The administration of neuroleptics in the treatment of psychosis and nonspecific behavioral disorders associated with psychotic symptoms in elderly patients is not without consequences. The potential side effects (e.g., dystonia, parkinsonian syndrome, and akathisia) of medications used in treating delirium, dementia, or confusional states are discussed. General guidelines are presented regarding choice of sedatives and antipsychotics and dosage, with attention to management of the individual elderly patient with psychosis.
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PMID:Antipsychotic medication and the elderly. 285 80

The role of neuroleptics in causing the tardive dyskinesia syndrome is controversial. To properly assess the contribution of drugs as the etiology of dyskinesias, the effects of aging, the natural history of psychosis, and characteristics of spontaneous dyskinesias must be considered. Though the buccolinguo-masticatory triad is seen more often in tardive than in spontaneous dyskinesias, these two disorders have many symptoms in common. Other dyskinesias, such as idiopathic and tardive dystonia or tardive Tourette's syndrome and dyskinesias in untreated schizophrenia, are poorly understood. Chronic neuroleptic treatment may only precipitate TD in those already predisposed to develop such movement disorders. Tardive dyskinesia is not a unique movement disorder, but rather spans several clinical and epidemiological phenomena which must be considered in a balanced evaluation of how much of the permanent dyskinesias should be attributed to neuroleptic drugs.
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PMID:Is tardive dyskinesia a unique disorder? 286 Jun 61

The relationship between acute dystonic reactions and serum calcium levels in 17 acutely psychotic patients was studied. Previous studies have implicated an association between a lowered serum calcium value and acute dystonia. This study failed to note a significant incidence of hypocalcemia in a group of psychotic patients. It is not known whether other factors related to calcium-magnesium balance may be related to dystonia.
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PMID:Relationship between dystonia and serum calcium levels. 287 30


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