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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Movement abnormalities in neuroleptic-treated, psychiatric patients are classified as (a) initial syndromes, including dystonia, parkinsonism, and hyperkinetic abnormalities such as initial dyskinesia (ID) and akathisia, all of which are related to the neuroleptic dose and can be considered as overdose phenomena; (b) tardive syndromes, mainly the classic tardive dyskinesia (TD) syndrome, more seldom tardive akathisia and tardive dystonia, which may all develop or aggravate after withdrawal of neuroleptic treatment; and (c) age-related, spontaneous dyskinesia, akathisia, and dystonia, and schizophrenia-related, hyperkinetic, often stereotyped, movements and restlessness. ID and TD can occur simultaneously, and may depend, at least partially, on identical mechanisms. The pathophysiology of TD is still not clear, and the traditional dopamine (DA) hypersensitivity model seems inadequate. Animal experiments suggest that blockade of some DA receptors in the brain (e.g., in ventromedian striatum) may counteract hyperkinesia and produce parkinsonism, while a concomitant blockade of other similar receptors in other brain regions (e.g., in anterodorsal striatum) may aggravate movements. This offers an explanation for the concomitant occurrence of parkinsonism and hyperkinetic movement abnormalities (ID and akathisia) relatively early in a neuroleptic treatment, and may also contribute to the understanding of the pathophysiology of TD. It is concluded that pathophysiologically TD is a heterogeneous syndrome depending on a subtle balance between several neurotransmitters in the brain, including DA receptor blockade and hypersensitivity of DA and GABA receptors.
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PMID:Pathophysiological mechanisms underlying tardive dyskinesia. 286 Jun 66

Nine tardive dystonia cases were compared with 13 tardive dyskinesia cases selected for the severity and persistence of their involuntary movements. Both groups were neurological referrals from an identical source. While advanced age and female preponderance were prominent features in tardive dyskinesia, onset in most tardive dystonia cases occurred in young adulthood, and the sex distribution showed a slight majority of males. Other differences in the dystonia group included gait abnormalities in four cases, lower tolerance of neuroleptic discontinuance, with the reappearance of psychoses, and a poorer prognosis for reversibility after follow-up. In fact, none of the dystonia patients reversed as opposed to seven of the tardive dyskinesia patients. In order to identify the full spectrum of tardive dystonia and exclude any referral bias, systematic epidemiological studies on psychiatric populations should include young adults of both sexes.
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PMID:Tardive dystonia and severe tardive dyskinesia. A comparison of risk factors and prognosis. 286 17

Tardive dyskinesia seems to occur as a result of diminished cholinergic and enhanced dopaminergic activity in the striatum. Meclofenoxate has been shown to increase cerebral cholinergic activity. To ameliorate the tardive dyskinesia, meclofenoxate was given orally, 600-1200 mg/day, for 6-12 weeks. The effects of the drug were evaluated by scoring the degree of involuntary movement. Among 11 subjects with tardive dyskinesia or dystonia, 4 improved markedly, 1 moderately, 2 slightly, and there was no improvement in 4. One patient with subacute oral dyskinesia, induced by administration of neuroleptics for 1 month, improved markedly. The possibility that meclofenoxate may be effective in dealing with dyskinesias that are induced by neuroleptics warrants further attention.
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PMID:Meclofenoxate therapy in tardive dyskinesia: a preliminary report. 286 61

We have briefly reviewed the literature on late-onset akathisia, dystonia, and Tourette-like syndrome in patients on long-term neuroleptic treatment. To date, there is no satisfactory epidemiologic or other evidence directly implicating neuroleptics in the etiology of these so-called tardive syndromes. Similarities between these disorders and tardive dyskinesia, however, make them worthy of some consideration.
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PMID:Neuroleptic-associated tardive syndromes. 287 Apr 79

The authors describe 19 patients with severe tardive dyskinesia, 11 of whom had a diagnosis of affective or schizoaffective disorder rather than schizophrenia. Most patients had been receiving long-term neuroleptic treatment with few interruptions and had received only one or two different neuroleptics. Frequent eye blinking was the most prevalent prodromal sign of tardive dyskinesia (in seven patients). Four subtypes of tardive dyskinesia could be distinguished: choreoathetosis, tardive dystonia, blepharospasm, and tardive akathisia. Optimal pharmacotherapy most often consisted of combinations of neuroleptics, lithium carbonate, benzodiazepines, and antiparkinsonian drugs. However, after an average of 62 months, only five patients had markedly improved.
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PMID:Clinical forms of severe tardive dyskinesia. 288 62

"Extrapyramidal" reactions to antipsychotic drugs include acute dystonias, akathisia, Parkinson's syndrome, and tardive dyskinesia. Recent research suggests efficacy of prophylactic antiparkinson drugs in diminishing the incidence of acute dystonia in high-risk patients, although the use of lower neuroleptic doses also might lower the risk and cause fewer unwanted effects. New in the treatment of akathisia is the use of beta-blockers, specifically propranolol (Inderal and others). Many patients require maintenance antiparkinson drug therapy during prolonged antipsychotic drug treatment. There is no effective treatment for tardive dyskinesia, the prevalence of which may be growing, with an estimated annual incidence of new cases of 3%-4%; the elderly and patients with affective illness may be at greatest risk. Clinicians are also attending to the related syndrome of tardive dystonia.
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PMID:Treating extrapyramidal reactions: some current issues. 288 54

Antipsychotic drugs have an important place in pharmacologic treatment of depression. Major depression with psychotic features responds poorly to treatment if an antipsychotic is not used in addition to an antidepressant; however, an antipsychotic confers no additional benefit in nonpsychotic depression. Antipsychotic drugs do have significant short- and long-term side effects, including pseudoparkinsonism, dystonia, akathisia, and tardive dyskinesia. The possibility of a good therapeutic response with minimal side effects can be increased if psychotic depression is diagnosed accurately and the antipsychotic is prescribed according to established clinical guidelines.
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PMID:Use of antipsychotic drugs in depression. Problems and opportunities. 289 Nov 24

Tardive dyskinesia (TD) is a syndrome of involuntary movements that develops in predisposed individuals during neuroleptic drug treatment, with an average prevalence of 15%. Neuroleptic (antidopaminergic) drugs are the predominant etiological factor. Although no simple correlation can be established, both dosage and treatment duration seem to be of importance for the development of dyskinesia. It is still uncertain whether some neuroleptics carry a higher risk than others, but it appears that the atypical neuroleptic clozapine, which causes no or minimal dystonia, parkinsonism, or akathisia, also carries no or minimal risk of TD. The pathophysiological mechanisms underlying TD are unclear. The traditional dopamine hypersensitivity theory is no longer viable, whereby new hypotheses have been advanced: TD can be due to the blockade of a subset of striatal dopamine receptors, while parkinsonism is due to the blockade of another such subset, and/or can be due to a reduced GABA turnover in a subgroup of neurons connecting striatum with globus pallidus and substantia nigra. TD is best prevented by a course of neuroleptic medication involving as little antidopamine effect as possible, including minimal doses and shortest possible length of treatment. The main TD treatment principle consists of a gradual dose reduction, possibly over years. It should be added, however, that more recent investigations indicate that traditional antidopaminergic treatment in moderate doses may be safely continued over a long period without an increased risk of TD progression.
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PMID:Tardive dyskinesia. 289 70

The authors present a study in which 33 chronic schizophrenic patients who, when withdrawn from antipsychotic drug treatment for more than 2 weeks, presented with concurrent signs of akathisia and tardive dyskinesia; however, signs of akinesia, facial masking, rigidity, or dystonia were not concurrent with the patients' akathetic presentation. In a subsequent study phase, these patients were treated with antipsychotics for up to 6 weeks. The dyskinetic signs that had been dramatically more severe in those patients exhibiting akathisia following withdrawal from antipsychotic medication continued for up to 6 weeks following the renewal of antipsychotic drug therapy. These findings help to confirm a relationship between tardive dyskinesia and a persistent akathisia of later onset known as tardive akathisia.
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PMID:Antipsychotic-withdrawal akathisia versus antipsychotic-induced akathisia: further evidence for the existence of tardive akathisia. 290 41

Initially, the reality of the existence of tardive dyskinesia raised some controversy, but rapidly this syndrome was recognized as a complication arising from usually long-term administration of neuroleptics. These extrapyramidal abnormal movements represent an important problem due to their prevalence, their potential irreversibility, their complex and still disputed physiopathologic mechanism, the absence of specific and generally effective treatment, and more recently the medico-legal problems entailed. At first, it was believed that these dyskinetic movements, of various intensity, were localized only at the oro-facial area (face, tongue, maxillary), or consisted of limited or generalized choreo-athetosic movements, or were a mixture of both types of movements. However, digestive and respiratory tardive dyskinesia also occur. Tardive dyskinesia can develop insidiously during neuroleptic treatment, or appear when this medication is decreased or ceased. It can coexist with parkinsonian signs. Age (over 50) and gender (female) appear to be risk factors. Other types of tardive syndromes associated with neuroleptic administration have been reported, such as tardive akathisia, tardive dystonia and a tardive Tourette-like syndrome. Involuntary movements resembling tardive dyskinesia can be observed in elderly individuals who never received neuroleptic medication. With respect to the rabbit syndrome, a rapid tremor of the perioral area, with a rhythmicity similar to the parkinsonian tremor, it is clearly different from tardive dyskinesia. It is essential to detect as precociously as possible tardive dyskinesia. The diagnosis is sometimes difficult and even if the clinical features seem pathognomonic of tardive dyskinesia, it is nevertheless important to establish a differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical aspects of tardive dyskinesias induced by neuroleptics]. 290 48


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