Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy.
paper
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- Authors
- Lingford-Hughes, A R; Acton, P D; Gacinovic, S; Suckling, J; Busatto, G F; Boddington, S J; Bullmore, E; Woodruff, P W; Costa, D C; Pilowsky, L S; Ell, P J; Marshall, E J; Kerwin, R W
- Year
- 1998
- Journal
- The British journal of psychiatry : the journal of mental science
- PMID
- 9850223
- DOI
- 10.1192/bjp.173.2.116
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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