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Brain γ-Aminobutyric Acid Abnormality in Tardive Dyskinesia Reduction in Cerebrospinal Fluid GABA Levels and Therapeutic Response to GABA Agonist Treatment

Gunvant K. Thaker, MD; Carol A. Tamminga, MD; Larry D. Alphs, MD, PhD; Jeffrey Lafferman, MD; Thomas N. Ferraro, PhD; Theodore A. Hare, PhD
Arch Gen Psychiatry. 1987;44(6):522-529. doi:10.1001/archpsyc.1987.01800180032006.
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• A double-blind, placebo-controlled trial of γ-vinyl γ-aminobutyric acid (GVG) and 4,5,6,7-tetrahydroisoxazolo-(5,4-c) pyridine-3-ol (THIP) was carried out in drug-free schizophrenic patients with tardive dyskinesia. A significant decrease in dyskinetic symptoms occurred with the administration of GVG, associated with a twofold increase in cerebrospinal fluid levels of GABA; THIP produced a more moderate, yet consistent decrease in the involuntary movements. A pathophysiologic role for γ-aminobutyric acid (GABA)-mediated neuronal transmission in tardive dyskinesia was explored by analyzing cerebrospinal fluid GABA concentrations in drugfree schizophrenic patients with and without tardive dyskinesia. A significant reduction in cerebrospinal fluid levels of GABA was observed in the dyskinetic schizophrenics compared with the nondyskinetic controls. These data compliment a growing body of experimental evidence suggesting a critical role for GABA-ergic neurons in the pathophysiology of tardive dyskinesia.


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