Positron emission tomographic studies of cerebral benzodiazepine‐receptor binding in chronic alcoholics

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Abstract
Positron emission tomography was used with [11C] flumazenil (FMZ) and [18F] fluorodeoxyglucose to study GABA type A/benzodiazepine (GABA‐A/BDZ) receptors and cerebral metabolic rates for glucose (1CMRglc) in 17 male patients with severe chronic alcoholism (ALC), 8 with (ACD) and 9 without alcoholic cerebellar degeneration (non‐ACD). In comparison with male normal controls of similar ages, the ALC group had significantly reduced FMZ ligand influx (K1), FMZ distribution volume (DV), and 1CMRglc bilaterally in the medial frontal lobes, including superior frontal gyrus and rostral cingulate gyrus; the ACD group had significant reductions of K1, DV, and ICMRglc bilaterally in the same distribution, and also in the superior cerebellar vermis; and the non‐ACD group had significant reductions of K1, DV, and ICMRglc bilaterally in the same regions of the frontal lobes but not in the superior cerebellar vermis. When compared with the non‐ACD group, the ACD group had significant reductions of K1 and DV bilaterally in the superior cerebellar vermis. The results suggest that severe chronic alcoholism damages neurons containing GABA‐A/BDZ receptors in the superior medial apsects of the frontal lobes, and in patients with clinical signs of ACD, neurons containing GABA‐A/BDZ receptors in the superior cerebellar vermis.