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Abraham Dorevitch, PharmD
Talbia Psychiatric Hospital PO Box 39 Jerusalem, Israel

Arch Neurol. 1984;41(1):15-16.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—Clough et al,¹ in describing a case of oculogyric crisis and parkinsonism, stated that oculogyric crises can occur as an idiosyncratic response to drugs, mainly phenothiazines.

While oculogyric crises, as well as other acute dystonic and extrapyramidal reactions, result from administration of all antipsychotic drugs, the incidence of these adverse effects is more often associated with high-potency neuroleptic agents. More specifically, the butyrophenone haloperidol (Haldol) is the most potent dopamine blocker on a milligram-for-milligram basis and is most likely to precipitate extrapyramidal reactions, including oculogyric crises. The piperazine phenothiazine fluphenazine hydrochloride (Prolixin) and the thioxanthene thiothixene (Navane) follow haloperidol in potency.

The low-potency neuroleptic agents, including the aliphatic phenothiazine chlorpromazine (Thorazine) and the piperidine phenothiazine thioridazine (Mellaril), while associated with oculogyric crises, are much less likely to cause an oculogyric crisis. This can most likely be attributed to the inherent anticholinergic effect of these agents.^2,3 . . . [Full Text PDF of this Article]

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