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Sodium Valproate in the Treatment of Cerebellar Disorders

Published online by Cambridge University Press:  18 September 2015

Andreas N. Neophytides ,
Paul F. Teychenne ,
Ronald F. Pfeiffer  and
Donald B. Calne
Andreas N. Neophytides*
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20014
Paul F. Teychenne
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20014
Ronald F. Pfeiffer
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20014
Donald B. Calne
Affiliation:
Experimental Therapeutics Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20014
*
Building 10, Room 6D20, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20014, U.S.A.
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Summary:

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Because of the high concentrations of ɣ-aminobutyric acid (GABA) in the cerebellar cortex and nuclei, an attempt was made to enhance GABAergic transmission in patients with cerebellar disease. Maximum tolerated doses of sodium valproate, a drug which inhibits the degradation of GABA, failed to influence cerebellar deficits in a double blind crossover study on six patients.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 6 , Issue 4 , November 1979 , pp. 455 - 457
Copyright
Copyright © Canadian Neurological Sciences Federation 1979

References

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