Regional brain metabolism during alcohol intoxication

Background: Ethanol has a broad range of actions on many neurotransmitter s ystems. The depressant actions of ethanol in the brain are related in part to facilitation of gamma-aminobutyric acid (GABB) neuro-transmission via it s interaction with the benzodiazepine/GABA receptor complex The purpose of this study was to evaluate the effects of ethanol on regional brain metabol ism in 10 healthy right-handed men. The results were compared with those we previously published in a different group of 16 normal male subjects who r eceived intravenous lorazepam, a benzodiazepine drug that also enhances GAB A neutrotranmission. Methods: The subjects were scanned with positron emission tomography and [F -18] fluorodeoxyglucose twice: 40 min after the end of placebo (diet soda) or ethanol (0.75 g/kg) oral administration, image data sets were analyzed b y using both the region of interest and the statistical parametric mapping (SPM) approach. SPM was used to generate a difference image between baselin e and ethanol, which we compared to the difference image between baseline a nd lorazepam (30 mu g/kg). Results: Ethanol significantly increased self-reports of "high" (p less tha n or equal to 0.0001), dizziness (p less than or equal to 0.003), and intox ication (p less than or equal to 0.0001). Ethanol significantly decreased w hole brain (-25 +/- 6%,p less than or equal to 0.0001) and regional metabol ism. Normalization of the regional measures by whole brain metabolism (rela tive measures) showed that ethanol decreased relative metabolic activity in occipital cortex (-4.9 +/- 4.1%,p less than or equal to 0.006), whereas it increased relative metabolic act in left temporal cortex (+3.5 +/- 2.9%,p less than or equal to 0.006) and left basal ganglia (+9 +/- 6.3%,p less tha n or equal to 0.0009). SPM analyses revealed the same pattern of responses as the relative measures, showing decreases in occipital cortex and increas es in left temporal cortex Comparison of the relative measures and the SPM analyses obtained with lorazepam data revealed a similar pattern of effects , with relative decreases in occipital cortex (-7.8 +/- 4.8%) and relative increases in left temporal cortex (+3.8 +/- 5.7%). Lorazepam, but not ethan ol, also decreased thalamic metabolism (-11.2 +/- 7.2%). Conclusions: These results support similar though not identical mechanisms for the effects of alcohol and benzodiazepines on brain glucose metabolism. The fact that lorazepam, but not alcohol, reduced thalamic metabolism, an effect associated with sleepiness could explain the higher sedative effects of lorazepam than of alcohol.