Abstract:
Background: Results from recent neuroimaging studies suggest that cigarette smoking is associated with morphological abnormalities in the brain. Grey matter abnormalities have been consistently reported, for example, within the prefrontal cortex, anterior cingulate cortex, and the temporal lobes of a smoker’s brain. Cigarette smoking also leads to abnormal white matter, especially within the corpus callosum (i.e., the brain’s largest white matter fibre tract). However, existing study outcomes are sparse and remain inconsistent. Thus, I aimed to examine the links between cigarette smoking and callosal morphology in a relatively large sample (n=294), including 25 current smokers, 100 people who have smoked in the past but quit smoking (quit smokers) and 169 non-smokers. Method: I analysed T1-weighted data of the brain acquired using magnetic resonance imaging (MRI). More specifically, the area of the corpus callosum was calculated in MATLAB and the thickness was measured at 100 equidistant points using an advanced surface modelling approach. Subsequently, I compared the three groups - current smokers, quit smokers, and non-smokers - against each other. Results: Significant group differences between combined smokers (current smokers and quit smokers) and non-smokers were observed within the callosal genu and anterior midbody, with thinner regions in combined smokers. Follow-up analysis revealed significant group differences between current smokers and non-smokers within the anterior midbody, and also between quit smokers and non-smokers within the rostral body and posterior midbody of the corpus callosum. In addition, I found significant negative correlations between callosal thickness and the number of packs per day in the callosal rostral body, anterior midbody, posterior midbody and splenium, and also between callosal thickness and the number of smoking years in the rostral body, anterior midbody, and splenium of the corpus callosum. In contrast, I found a significant positive correlation between callosal thickness and the number of smoking years and the number of pack-years in the callosal rostrum. Conclusion: In summary, the data suggests that cigarette smoking leads to thinner callosal subregions in smokers. A thinner corpus callosum is likely to indicate a smaller number of callosal fibres which might be linked to poorer signal conduction in smokers than in nonsmokers. Given that the corpus callosum is a crucial structure responsible for interhemispheric communication and integration of information, the effects of cigarette smoking may have far reaching consequences on the brain.