Tardive dyskinesia is an important adverse effect of antipsychotic drug treatment. It is a complex neurological syndrome, consisting of hyperkinetic, involuntary movements, mainly choreoathetoid (but also dystonic) in nature, The movements involve several body areas, and affected patients are usually unaware of the presence of the movements. Tardive dyskinesia affects about one-fifth of patients treated with antipsychotics. Epidemiological studies show that some factors such as age, institutionalisation. a psychiatric diagnosis of mood disorders and a history of acute estrapyramidal syndromes increase the risk of developing tardive dyskinesia. Treatment variables are less clearly correlated with risk, but lower doses seem to reduce the risk and new atypical antipsychotics, in particular clozapine. seem to have a reduced risk of inducing the syndrome, As the greatest factor for risk is patient vulnerability, the best way to reduce the risk of tardive dyskinesia is to use antipsychotic drugs in a conservative manner. Recognising and treating tardive dyskinesia is of paramount importance and results in a more favourable course of the disorder. Reducing antipsychotic exposure to the minimum clinically effective dose and duration increases the possibility of improvement and remission. Active treatment is required for patients with severe tardive dyskinesia, but to date no treatment has been demonstrated to be significantly effective in the majority of patients, except for the suppressive effects of antipsychotics themselves. Benzodiazepines, in particular clonazepam, and atypical antipsychotics, especially clozapine, provide some benefits. The neuroprotective effects of tocopherol (vitamin E) seem useful in some patients. Other treatments may be limited by seven adverse effects and have little proven efficacy. Nevertheless, subgroups of patients may respond to a particular treatment, suggesting the heterogeneity of this condition.

ANTIPSYCHOTIC-INDUCED TARDIVE-DYSKINESIA - RECOGNITION, PREVENTION AND MANAGEMENT

CAVALLARO , ROBERTO;
1995

Abstract

Tardive dyskinesia is an important adverse effect of antipsychotic drug treatment. It is a complex neurological syndrome, consisting of hyperkinetic, involuntary movements, mainly choreoathetoid (but also dystonic) in nature, The movements involve several body areas, and affected patients are usually unaware of the presence of the movements. Tardive dyskinesia affects about one-fifth of patients treated with antipsychotics. Epidemiological studies show that some factors such as age, institutionalisation. a psychiatric diagnosis of mood disorders and a history of acute estrapyramidal syndromes increase the risk of developing tardive dyskinesia. Treatment variables are less clearly correlated with risk, but lower doses seem to reduce the risk and new atypical antipsychotics, in particular clozapine. seem to have a reduced risk of inducing the syndrome, As the greatest factor for risk is patient vulnerability, the best way to reduce the risk of tardive dyskinesia is to use antipsychotic drugs in a conservative manner. Recognising and treating tardive dyskinesia is of paramount importance and results in a more favourable course of the disorder. Reducing antipsychotic exposure to the minimum clinically effective dose and duration increases the possibility of improvement and remission. Active treatment is required for patients with severe tardive dyskinesia, but to date no treatment has been demonstrated to be significantly effective in the majority of patients, except for the suppressive effects of antipsychotics themselves. Benzodiazepines, in particular clonazepam, and atypical antipsychotics, especially clozapine, provide some benefits. The neuroprotective effects of tocopherol (vitamin E) seem useful in some patients. Other treatments may be limited by seven adverse effects and have little proven efficacy. Nevertheless, subgroups of patients may respond to a particular treatment, suggesting the heterogeneity of this condition.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/2953
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