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

John Nutt, Adrian Williams, Charles Plotkin, Nancy Eng, Michael Ziegler, Donald B. Calne

Research output: Contribution to journalArticle

27 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)337-343
Number of pages7
JournalCanadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
Issue number3
StatePublished - Aug 1979


ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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