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April 1984

Tardive Dyskinesia and Thioridazine

Author Affiliations

Maryland Psychiatric Research Center Baltimore, MD 21228
Veterans Administration Medical Center and Oregon Health Sciences University Portland, OR 97207
Psychopharmacology Program McLean Hospital Belmont, MA 02178
Illinois State Psychiatric Institute Chicago, IL 60612
Long Island Jewish-Hillside Medical Center Glen Oaks, NY 11004
Maryland Psychiatric Research Center Baltimore, MD 21228

Arch Gen Psychiatry. 1984;41(4):415-416. doi:10.1001/archpsyc.1984.01790150105016

To the Editor.—  Recent advertisements for thioridazine—"Sandoz Answers Common Questions About: Tardive Dyskinesia: Are Some Neuroleptics Less Likely to Cause It?"—raise provocative questions about how to manage TD and how to translate metapharmacologic theory in psychiatric practice. This advertisement presents scientific hypothesis as fact and relies on controversial findings to draw conclusions.The central theme of this advertising revolves around the issue of neuroleptic site specificity and dopamine receptors. Does thioridazine have a greater effect on dopamine receptors in centers modulating schizophrenic symptoms than in centers modulating extrapyramidal movements?1 This concept can only be considered theoretical; it is intriguing but not proved. The failure to replicate the initial results,2 notwithstanding methodologic differences, means the laboratory foundation for the theory is controversial.More important is the inference from receptor effects to clinical effects. The pathogenetic relationship between TD and striatal dopamine receptor hypersensitivity is not fully proved. While the cause of

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