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September 1985

Akathisia and Tardive Dyskinesia: Changing Concepts

Author Affiliations

From the Laboratory of Neuropsychopharmacology, Schizophrenia Biologic Research Center, Palo Alto (Calif) Veterans Administration Medical Center; and the Mental Health Clinical Research Center, Department of Psychiatry and Behavioral Sciences, Stanford (Calif) University. Dr Stahl is now with Merck, Sharp and Dohme Research Laboratories, Essex, England.

Arch Gen Psychiatry. 1985;42(9):915-917. doi:10.1001/archpsyc.1985.01790320087012

It is now 30 years since the introduction of neuroleptics into clinical practice, and we are still learning more about the effects of these drugs in our patients. On the positive side, research on second-generation antipsychotics such as BW234U,1 piquindone (R022-1319),2 the substituted benzamides,3 and others has given rise to the hope that control of psychotic symptoms may someday be accomplished with much less risk of akathisia, parkinsonism, and tardive dyskinesia than exists for currently marketed neuroleptics. Until that day, however, we will more and more be forced to deal with the increasingly troublesome short- and long-term side effects of the first-generation compounds.

The article by Barnes and Braude4 in this issue of the Archives deals with one of the relatively neglected side effects of the first-generation neuroleptics, namely akathisia. These authors boldly attempt to make an operational definition of neuroleptic-induced akathisia, to subtype it, to

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