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NEUROLOGY 1985;35:755
© 1985 American Academy of Neurology

Brain amino compounds in a Huntington's disease pratient on isoniazid therapy

Thomas L. Perry, MD, Richard A. Wall, PhD and Shirley Hansen, BA

Department of Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, Vancouver, BC, Canada.

We describe biochemical abnormalities in autopsied brain of a patient with early Huntington's disease (HD) who died of pentobarbital overdosage while under treatment with isoniazid (INH). The brain contained hydrazine, a terminal metabolite of INH, which inhibits {gamma}-aminobutyric acid (GABA) aminotransferase. GABA content in the basal ganglia was higher than expected for HD, and GABA content was supranorma1 in some brain regions. Homocarnosine (GABA-histidine) content was greatly elevated in all brain regions, suggesting chronic GABA elevation in life. Therefore, the increase in brain GABA content observed in experimental animals given INH or hydrazine also occurs in human patients.

Address correspondence and reprint requests to Dr. Perry, Department of Pharmacology and Therapeutics, The University of British Columbia, Vancouver, BC, V6T 1W5, Canada.

Supported by the Medical Research Council of Canada and the Huntington Society of Canada.

Accepted for publication September 19, 1984.






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