Abstract
Chronic cigarette smoking is associated with numerous abnormalities in brain neurobiology, but few studies specifically investigated the chronic effects of smoking (compared to the acute effects of smoking, nicotine administration, or nicotine withdrawal) on cerebral perfusion (i.e., blood flow). Predominately middle-aged male (47 ± 11 years of age) smokers (n = 34) and non-smokers (n = 27) were compared on regional cortical perfusion measured by continuous arterial spin labeling magnetic resonance studies at 4 Tesla. Smokers showed significantly lower perfusion than non-smokers in the bilateral medial and lateral orbitofrontal cortices, bilateral inferior parietal lobules, bilateral superior temporal gyri, left posterior cingulate, right isthmus of cingulate, and right supramarginal gyrus. Greater lifetime duration of smoking (adjusted for age) was related to lower perfusion in multiple brain regions. The results indicated smokers showed significant perfusion deficits in anterior cortical regions implicated in the development, progression, and maintenance of all addictive disorders. Smokers concurrently demonstrated reduced blood flow in posterior brain regions that show morphological and metabolic aberrations as well as elevated beta amyloid deposition demonstrated by those with early stage Alzheimer disease. The findings provide additional novel evidence of the adverse effects of cigarette smoking on the human brain.
Highlights
That include abnormalities in regional brain morphology [4,5,6,7,8,9,10,11], metabolite concentrations [12,13,14,15], white matter microstructural integrity [16], and functional connectivity [17,18]. These neurobiological abnormalities appear to be most prominent in the anterior cingulate cortex (ACC), dorsal prefrontal cortex (DPFC), orbitofrontal cortex (OFC), and insula, which are cortical components of the brain reward-executive oversight system (BREOS; [19,20]); the cortical and subcortical components of the BREOS are implicated in the development, progression, and maintenance of all addictive disorders [21,22]
This study investigated the effects of chronic smoking on regional cerebral perfusion in young to middle-aged adults (e.g., 25–60), who represent the greatest proportion of active smokers in the United States [31]
The primary findings from this cohort of predominately middle-aged males were: (1) smokers demonstrated significantly lower perfusion than non-smokers in the bilateral medial and lateral OFC of the BREOS; (2) smokers showed significantly lower perfusion than non-smokers in the left posterior cingulate, right isthmus of the cingulate, right supramarginal gyrus, and bilateral inferior parietal lobule of the Alzheimer’s disease (AD) regions; (3) significantly lower perfusion in smokers in Non-BREOS/AD cortical regions was observed in the bilateral superior temporal gyrus, right pars orbitalis, and right frontal pole; (4) in smokers, greater lifetime years of smoking was significantly associated with lower perfusion in multiple BREOS and Non-BREOS/AD regions
Summary
That include abnormalities in regional brain morphology [4,5,6,7,8,9,10,11], metabolite concentrations [12,13,14,15], white matter microstructural integrity [16], and functional connectivity [17,18]. A limitation of these previous studies is that blood flow or glucose metabolism measurements were obtained over the entire cortical gray matter or involved an average of multiple bilateral cortical regions. It is unclear if there are specific regional differences between chronic smokers and non-smokers in cortical perfusion. Regional cortical brain perfusion levels in predominately male, middle-aged smokers and non-smokers were compared via 4 Tesla magnetic resonance continuous arterial spin labeling
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