BACKGROUND: Although approximately 80% of individuals with alcohol use disorders are chronic smokers and despite reported associations between chronic cigarette smoking and lower cerebral perfusion in nonalcoholics, previous brain perfusion studies with alcoholics did not account for the potential effects of concurrent chronic cigarette smoking. METHODS: One-week-abstinent alcohol-dependent individuals in treatment (ALC) [19 smokers (sALC) and 10 nonsmokers (nsALC)] and 19 healthy light drinking, nonsmoking control participants (nsLD) were scanned with a pulsed arterial spin labeling method to measure cerebral perfusion without an exogenous contrast agent. Studies were performed with 2 different postlabeling delay times (time from labeling pulse to the excitation pulse; PLD=1,500 ms and PLD=1,200 ms) to assess the potential effect of arterial blood transit time on the perfusion. Average gray matter (GM) and white matter (WM) perfusion for the frontal and parietal lobes were calculated for each hemisphere from voxels containing at least 90% GM and 100% WM. RESULTS: At PLD=1,500 ms, multivariate analyses compared ALC (combined sALC and nsALC) with nsLD (p=0.04) and contrasted sALC, nsALC, and nsLD (p=0.006). ALC, as a group, showed 13% lower frontal GM perfusion (p=0.005) and 8% lower parietal GM perfusion than nsLD (p=0.03). With ALC separated into smokers and nonsmokers, sALC showed 19% lower frontal GM perfusion (p=0.001) and 12% lower parietal GM perfusion than nsLD (p=0.004). In sALC, a higher number of cigarettes smoked per day was associated with lower perfusion. Overall, regional perfusion did not differ significantly between nsALC and nsLD. Results obtained with PLD=1,200 ms generally confirmed the 1,500 ms findings. CONCLUSIONS: This study provides preliminary evidence that chronic cigarette smoking adversely affects cerebral perfusion in frontal and parietal GM of 1-week-abstinent alcohol-dependent individuals. These results are in line with our spectroscopic and structural magnetic resonance studies that suggest chronic cigarette smoking compounds the detrimental effects of alcohol dependence on brain neurobiology.
BACKGROUND: Although approximately 80% of individuals with alcohol use disorders are chronic smokers and despite reported associations between chronic cigarette smoking and lower cerebral perfusion in nonalcoholics, previous brain perfusion studies with alcoholics did not account for the potential effects of concurrent chronic cigarette smoking. METHODS: One-week-abstinent alcohol-dependent individuals in treatment (ALC) [19 smokers (sALC) and 10 nonsmokers (nsALC)] and 19 healthy light drinking, nonsmoking control participants (nsLD) were scanned with a pulsed arterial spin labeling method to measure cerebral perfusion without an exogenous contrast agent. Studies were performed with 2 different postlabeling delay times (time from labeling pulse to the excitation pulse; PLD=1,500 ms and PLD=1,200 ms) to assess the potential effect of arterial blood transit time on the perfusion. Average gray matter (GM) and white matter (WM) perfusion for the frontal and parietal lobes were calculated for each hemisphere from voxels containing at least 90% GM and 100% WM. RESULTS: At PLD=1,500 ms, multivariate analyses compared ALC (combined sALC and nsALC) with nsLD (p=0.04) and contrasted sALC, nsALC, and nsLD (p=0.006). ALC, as a group, showed 13% lower frontal GM perfusion (p=0.005) and 8% lower parietal GM perfusion than nsLD (p=0.03). With ALC separated into smokers and nonsmokers, sALC showed 19% lower frontal GM perfusion (p=0.001) and 12% lower parietal GM perfusion than nsLD (p=0.004). In sALC, a higher number of cigarettes smoked per day was associated with lower perfusion. Overall, regional perfusion did not differ significantly between nsALC and nsLD. Results obtained with PLD=1,200 ms generally confirmed the 1,500 ms findings. CONCLUSIONS: This study provides preliminary evidence that chronic cigarette smoking adversely affects cerebral perfusion in frontal and parietal GM of 1-week-abstinent alcohol-dependent individuals. These results are in line with our spectroscopic and structural magnetic resonance studies that suggest chronic cigarette smoking compounds the detrimental effects of alcohol dependence on brain neurobiology.
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