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NEUROLOGY 1981;31:1356
© 1981 American Academy of Neurology

Prolactin secretion in Parkinson disease

T. Eisler, M.D., M. O. Thorner, MB., M.R.C.P., R. M. MacLeod, Ph.D., D. L. Kaiser, Dr. Ph.H and D. B. Calne, D.M., F.R.C.P.

Experimental Therapeutics Branch (Drs. Eider and Calne), National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD, and the Department of Internal Medicine (Drs. Thorner, MacLeod, and Kaiser), University of Virginia School of Medicine, Charlottesville, VA.

We studied the dopaminergic control of lactotroph cells in the anterior pituitary of parkinsonian patients and age-matched normal subjects. The resting levels of prolactin and the TRH-induced rise in prolactin were normal in Parkinson disease. Levodopa elicited a normal suppression of prolactin concentrations in parkinsonian subjects; the major abnormality to emerge was attenuation of the response to thyrotropin-releasing hormone (TRH) in the parkinsonian patients following administration of Sinemet (levodopa plus carbidopa) or bro-mocriptine. These findings imply pathology of extrastriatal dopamine systems in Parkinson disease. Since the addition of cilrbidopa enhanced the suppression of prolactin induced by levodopa, exogenous levodopa probably acts predominantly through the formation of dopamine in the hypothalamus, but inside the blood-brain barrier, rather than as a direct effect of circulating dopamine on the anterior pituitary or arms of the hypothalamus outside the blood-brain barrier.

Address correspondence and reprint requests to Dr. Calne, Building 10, Room 6D20, National Institutes of Health, Bethesda, MD 20205.

Accepted for publication January 8, 1981.






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