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From the Laboratory of Neuropharmacology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health (Drs. Kartzinel and Calne), and the Department of Neurology, University of Rochester School of Medicine, Rochester, NY (Dr. Shoulson).
Caffeine was administered to six patients with idiopathic parkinsonism in an attempt to potentiate the therapeutic response of bromocriptine, a dopamine (DA) receptor agonist, by inhibition of phosphodiesterase. In a double-blind study at doses of 1,000 mg daily, caffeine failed to enhance the antiparkinsonian action of bromocriptine (40 mg daily) given concomitantly. Although effective in potentiating the action of levodopa and other agonists in animal models of parkinsonism, caffeine is inactive in parkinsonism in man.
Requests for reprints should be addressed to Bldg. 10, Room 6D20, NIH, 9000 Rockville Pike, Bethesda, MD 20014.
Received for publication November 17, 1975.
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