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Initial Observations on Effect of Vigabatrin on In Vivo 1 H Spectroscopic Measurements of γ‐Aminobutyric Acid, Glutamate, and Glutamine in Human Brain
Author(s) -
Petroff Ognen A. C.,
Rothman Douglas L.,
Behar Kevin L.,
Mattson Richard H.
Publication year - 1995
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1995.tb00486.x
Subject(s) - vigabatrin , glutamate receptor , glutamine , anticonvulsant , aminobutyric acid , gaba transaminase , human brain , in vivo , gamma aminobutyric acid , medicine , endocrinology , epilepsy , chemistry , nuclear magnetic resonance , pharmacology , biochemistry , glutamate decarboxylase , biology , amino acid , psychiatry , physics , enzyme , receptor , microbiology and biotechnology
Summary: Recent developments involving 1 H nuclear magnetic resonance (NMR) spectroscopic editing techniques have allowed noninvasive measurements of γ‐aminobutyric acid (GABA) in human cerebrum. The additional information gained from GABA and macromolecule measurements permitted more precise glutamate (Glu) and glutamine (Gln) measurements. Occipital lobe GABA in 10 nonepileptic, healthy subjects was 1.0 μmol/g brain [95% confidence interval (CI) 0.9–1.1]. Vigabatrin (VGB) is a safe and effective antiepileptic drug (AED)that irreversibly inhibits neuronal and glial GABA transaminase. GABA levels were increased in all patients treated with VGB. With a standard dose of 3–6 g/day, GABA levels were 2.6 μmol/g (95% CI 2.3–2.8).Mean occipital GABA level measured in epileptic patients not receiving VGB was 0.9 μmol/g (95% CI 0.7–1.1). Gln was increased by 1.9 μmol/g and Glu was decreased by 0.8 μmol/g in patients receiving VGB as compared with patients receiving standard medications alone.