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Treatment of Parkinson's Disease with Sodium Valproate: Clinical, Pharmacological, and Biochemical Observations

Published online by Cambridge University Press:  18 September 2015

John Nutt ,
Adrian Williams ,
Charles Plotkin ,
Nancy Eng ,
Michael Ziegler  and
Donald B. Calne
John Nutt*
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
Adrian Williams
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
Charles Plotkin
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
Nancy Eng
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
Michael Ziegler
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
Donald B. Calne
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland and the University of Texas Medical Branch, Galveston, Texas
*
University of Oregon Health Sciences Center, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201 U.S.A.
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Because there is biochemical evidence of decreased GABAergic function in Parkinson's disease, sodium valproate, an inhibitor of GA BA catabolism, was administered to eight Parkinsonian patients. Valproate treatment did not significantly alter any Parkinsonian feature, but tended to increase the dyskinesia in the “on-off” patients. The increased dyskinesias were not a result of altered peripheral metabolism of L-dopa. Despite obtaining high plasma levels of valproate, no consistent alteration of CSF GABA levels could be demonstrated. Thus, in these patients, an effect of valproate on GABA metabolism is unproven, and in turn, the role of GABA in Parkinsonism and dyskinesia uncertain.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 6 , Issue 3 , August 1979 , pp. 337 - 343
Copyright
Copyright © Canadian Neurological Sciences Federation 1979

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