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Neuroleptic-induced acute dystonic reactions may be due to enhanced dopamine release on to supersensitive postsynaptic receptors

From the University Department of Neurology, Institute of Psychiatry, and King's College Hospital Medical School, Denmark Hill, London, England.

Address correspondence and reprint requests to Dr. Marsden, University Department of Neurology, Institute of Psychiatry and King's College Hospital Medical School, Denmark Hill, London SE5, UK.

Oral administration of butaperazine (40 mg per kilogram) to rats increased dopamine turnover, as measured by elevation of striatal and mesolimbic concentrations of homovanillic acid and 3,4-dihydroxyphen-ylacetic acid, for 24 to 48 hours. Initially, this dose of butaperazine inhibited stereotyped behavior in response to subcutaneous administration of apomorphine, but this effect was reversed at 12 hours. Later, animals had normal or exaggerated responses to apomorphine. The data suggest that at the critical 20- to 28-hour period after butaperazine administration, when most human acute dystonic reactions occur, normal or supersensitive cerebral dopamine receptors are exposed to an excessive synaptic release of dopamine. This may be responsible for the drug-induced dystonia.

Accepted for publication July 22, 1980.