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December 1980

γ-Acetylenic GABA in Tardive Dyskinesia

Author Affiliations

From Departments H (Drs Casey, Gerlach, and Christensen), and E (Dr Magelund), Set Hans Hospital, Roskilde, Denmark, and the Departments of Medical Research, Psychiatry, and Neurology (Dr Casey), Veterans Administration Medical Center and University of Oregon Health Sciences Center, Portland.

Arch Gen Psychiatry. 1980;37(12):1376-1379. doi:10.1001/archpsyc.1980.01780250062007

• Brain γ-aminobutyric acid (GABA) has been proposed to play a role in the modulation of extrapyramidal motor function. The effects of increasing brain GABA with γ-acetylenic GABA (GAG), a drug that inhibits GABA transaminase, were evaluated in ten patients with stable tardive dyskinesia during a blind placebo-controlled trial. Drug effects during active treatment and two placebo periods were evaluated by scoring randomly sequenced videotapes of tardive dyskinesia and parkinsonian symptoms recorded weekly during a standardized examination. Tardive dyskinesia was significantly reduced, and preexisting parkinsonism increased slightly. The largest decrease in tardive dyskinesia symptoms occurred in patients receiving higher neuroleptic doses, suggesting an interaction between GABA and dopamine. Prolactin values increased but growth hormone values were unchanged. Psychiatric symptoms were also unchanged during GAG treatment.

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