ALTERATIONS OF BENZODIAZEPINE RECEPTORS IN TYPE-II ALCOHOLIC SUBJECTSMEASURED WITH SPECT AND [I-123] IOMAZENIL

Citation
A. Abidargham et al., ALTERATIONS OF BENZODIAZEPINE RECEPTORS IN TYPE-II ALCOHOLIC SUBJECTSMEASURED WITH SPECT AND [I-123] IOMAZENIL, The American journal of psychiatry, 155(11), 1998, pp. 1550-1555
Citations number
31
Categorie Soggetti
Psychiatry,Psychiatry
ISSN journal
0002953X
Volume
155
Issue
11
Year of publication
1998
Pages
1550 - 1555
Database
ISI
SICI code
0002-953X(1998)155:11<1550:AOBRIT>2.0.ZU;2-7
Abstract
Objective: Alterations in cortical benzodiazepine receptor density hav e been described in postmortem and in vivo studies of alcoholic subjec ts. The authors attempted to replicate these findings using single pho ton emission computed tomography and the benzodiazepine receptor radio tracer [I-123]iomazenil. Method: They measured the distribution volume of benzodiazepine receptors in 11 recently detoxified patients with t ype II alcoholism and 11 healthy comparison subjects. The tracer was g iven as a bolus followed by a continuous infusion to achieve sustained binding equilibrium at the benzodiazepine receptors. Data were analyz ed by using a region of interest method (regions of interest were iden tified on coregistered magnetic resonance imaging scans) and by a pixe l-by-pixel method (distribution volume maps were analyzed with statist ical parametric mapping for between-group differences). Results: The r egion of interest analysis revealed that alcoholic patients had signif icantly lower benzodiazepine distribution volume than comparison subje cts in the frontal, anterior cingulate, and cerebellar cortices. Stati stical parametric mapping revealed two large excursions in which the d istribution volume in alcoholic patients was significantly lower than in comparison subjects: the anterior cingulate, extending into the rig ht middle frontal gyrus, and the left occipital cortex. Conclusions: B enzodiazepine receptor distribution volume is significantly lower in s everal cortical regions and the cerebellum in alcoholic subjects than in healthy comparison subjects. These results are consistent with prev ious reports and might indicate either a toxic effect of alcoholism on benzodiazepine receptors or a vulnerability factor for developing alc oholism.