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The British Journal of Psychiatry 173: 116-122 (1998)
© 1998 The Royal College of Psychiatrists
AR Lingford-Hughes, PD Acton, S Gacinovic, J Suckling, GF Busatto, SJ Boddington, E Bullmore, PW Woodruff, DC Costa, LS Pilowsky, PJ Ell, EJ Marshall and RW Kerwin
Department of Psychological Medicine, Institute of Psychiatry, London. sphaarl@iop.bpmf.ac.uk
BACKGROUND: We tested the hypothesis that reduced levels of the GABA- benzodiazepine receptor occur in alcohol dependency using single photon emission tomography (SPET) and the specific GABA-benzodiazepine ligand, 123I-iomazenil. METHOD: Neurologically and cognitively unimpaired abstinent alcohol-dependent (n = 12) and non-alcohol-dependent male subject (n = 14) underwent a 123I-iomazenil SPET scan. SPET and magnetic resonance images were co-registered and voxel-based statistical tests performed. Subjects' clinical and alcohol history were obtained with standard questionnaires. The relationships between clinical and alcohol variables and the regional level of GABA- benzodiazepine receptors were investigated using multiple regression analysis. RESULTS: Abstinent alcohol-dependent subjects had decreased levels of GABA-benzodiazepine receptor compared with non-alcohol- dependent subjects within the frontal, parietal and temporal cortices, including regions in which grey matter atrophy was absent. CONCLUSIONS: Alcohol dependency is associated with reduced GABA-benzodiazepine receptor levels in the absence of grey matter atrophy in some cortical regions, such as within the parietal lobe. Regional variability of reduction in GABA-benzodiazepine receptors demonstrates that alcohol does not have a global, toxic effect on the brain.
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