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Jeffrey Lieberman, MD; Michael Lesser, MD; Ronald Brenner, MD
Long Island Jewish-Hillside Medical Center PO Box 38 Glen Oaks, NY 11004

Arch Gen Psychiatry. 1983;40(4):469-470.

	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. —

We would like to elaborate on one point of the excellent article "Therapeutic Strategies Against Tardive Dyskinesia" by Jeste and Wyatt (ARCHIVES 1982;39:803-816). The authors classified bromocriptine mesylate as a treatment of dopamine (DA) antagonism, ie, decreasing DA neurotransmission. This may not be entirely accurate for the three studies cited.^1-3 Although the use of an "autoreceptor strategy" in the treatment of tardive dyskinesia (TD) with DA agonists has been described,¹ in the case of bromocriptine this probably was never effected. This strategy was based on the belief that bromocriptine binds preferentially at different DA receptor sites in different concentrations.^1,4 However, in view of the fact that multiple classes of DA receptors exist in the nigrostriatal system, which is believed to be the critical neuroanatomic area in TD, and that the oral dosage of bromocriptine required to obtain precisely the desired pharmacodynamic effect . . . [Full Text PDF of this Article]

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