HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Eisler, T. Articles by Calne, D. B. Search for Related Content PubMed PubMed Citation Articles by Eisler, T. Articles by Calne, D. B.

Deprenyl in Parkinson disease

From the Experimental Therapeutics Branch (Dr. Eisler and Mr. Nelson, Ms. Krebs, Drs. Teravainen and Calne), National Institute of Neurological and Communicative Disorders and Stroke, the Laboratory of Clinical Science (Ms. Weise, Drs. Lake, Ebert, and Kopin), National Institute of Mental Health, Bethesda, the Division on Neurophannacological Drug Products (Mr. Nelson), Food and Drug Administration, Rockville, and the Clinical Neuropharmacology Branch (Ms. Whetzel and Dr. Murphy), National Institute of Mental Health, Bethesda, MD.

(–)Deprenyl, a specific monoamine oxidase subtype B inhibitor (MAOI-B), has been reported to be a safe and valuable adjunct to conventional treatment of parkinsonism. A double-blind, clinical comparison of (–)deprenyl with placebo was undertaken in 11 parkinsonian patients; the efficacy of 10 mg daily was studied over 4 weeks. In four cases the clinical score for parkinsonian deficits improved during deprenyl therapy, and in five it deteriorated; there was no change in one patient. Two subjects failed to complete the study. (–)Deprenyl induced euphoria and insomnia. It was concluded that any advantages deriving from the use of (–)deprenyl in parkinsonism are limited, and probably dominated by its elevation of mood. Biochemical analysis failed to reveal any significant increase in platelet or plasma catecholamine concentrations during deprenyl therapy. There was, however, a significant decrease in plasma epinephrine (p <0.05) and platelet MA0 activity (p <0.005).

Address correspondence and reprint requests to Dr. Calne, Building 10, Room 6D20, NIH, Bethesda, MD 20205.

Accepted for publication March 20, 1980

This article has been cited by other articles:

				R. A. Hauser and T. A. Zesiewicz Clinical trials aimed at detecting neuroprotection in Parkinson's disease Neurology, May 23, 2006; 66(10_suppl_4): S58 - S68. [Abstract] [Full Text]

				The Parkinson Study Group Effects of Tocopherol and Deprenyl on the Progression of Disability in Early Parkinson's Disease N. Engl. J. Med., January 21, 1993; 328(3): 176 - 183. [Abstract] [Full Text]

				N. C. Reynolds Jr and G. K. Montgomery Factor Analysis of Parkinson's Impairment: An Evaluation of the Final Common Pathway Arch Neurol, October 1, 1987; 44(10): 1013 - 1016. [Abstract] [PDF]