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Dilip V. Jeste, MD; Richard Jed Wyatt, MD
Adult Psychiatry Branch Division of Special Mental Health Research National Institute of Mental Health St Elizabeths Hospital Washington, DC 20032

Arch Gen Psychiatry. 1983;40(4):470.

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In Reply—

The letter by Lieberman et al presents a new and interesting perspective on the studies of bromocriptine in the treatment of TD. Bromocriptine is believed to be a partial DA agonist. The main rationale for using low-dose bromocriptine in patients with TD has been a putative dopamine autoreceptor stimulation produced by the drug.¹ Such an action would be expected to inhibit the synthesis and release of dopamine.² Lieberman et al suggest that the relative inefficacy of bromocriptine in two reports^1,3 may be attributable to the study design, while the beneficial effects of the drug in the third study⁴ might be explained on the basis of the attractive hypothesis of receptor sensitivity modification as postulated by Alpert and Friedhoff.⁵

The explanation offered by Lieberman et al is quite plausible. It is likely that the doses of bromocriptine used in the earlier trials (10 mg or higher) were . . . [Full Text PDF of this Article]

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