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Tardive dyskinesia. A discontinuation study.

W M Glazer, D C Moore, N R Schooler

    Archives of General Psychiatry
    |June 1, 1984
    PubMed
    Summary

    Discontinuing neuroleptic therapy for tardive dyskinesia (TD) rarely leads to complete reversal. However, sustained neuroleptic abstinence for 18 months offers an 87.2% chance of significant movement improvement in TD patients.

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    Area of Science:

    • Neuroscience
    • Psychiatry
    • Movement Disorders

    Background:

    • Tardive dyskinesia (TD) is a persistent side effect of neuroleptic medications.
    • Understanding the long-term outcomes of neuroleptic discontinuation is crucial for patient management.

    Purpose of the Study:

    • To evaluate the long-term effects of neuroleptic discontinuation on tardive dyskinesia.
    • To determine the time course and probability of improvement in TD symptoms after stopping neuroleptics.

    Main Methods:

    • A longitudinal follow-up study of 33 outpatients (21 nonschizophrenic, 12 schizophrenic) diagnosed with tardive dyskinesia.
    • Neuroleptic therapy was discontinued for all participants.
    • Movement ratings were assessed to track symptom severity and improvement over time.

    Main Results:

    • Only one patient experienced complete reversal of TD symptoms.
    • The median time to achieve a 50% reduction in movement severity was seven months.
    • No significant difference in time to improvement was observed between schizophrenic and nonschizophrenic groups.
    • An 18-month duration of neuroleptic abstinence predicted an 87.2% probability of at least 50% movement reduction.
    • In nonschizophrenic patients, depressed mood correlated negatively with abnormal movement severity.

    Conclusions:

    • Complete remission of tardive dyskinesia after neuroleptic discontinuation is uncommon.
    • Extended periods of neuroleptic abstinence significantly increase the likelihood of substantial improvement in TD symptoms.
    • Depressed mood may influence the experience of movement abnormalities in nonschizophrenic individuals with TD.

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