Smoking and structural brain deficits: a volumetric MR investigation
Smoking and structural brain deficits: a volumetric MR investigation
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DOI：
10.1111/j.1460-9568.2006.05050.x
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发表时间：
2006-09-01
影响因子：
3.4
通讯作者：
Staedtgen, Mario
中科院分区：
文献类型：
--
作者：
Gallinat, Juergen;Meisenzahl, Eva;Staedtgen, Mario
越来越多的动物研究证据表明，接触尼古丁会损害大脑。对人类的研究发现尼古丁和吸烟对大脑功能有广泛的影响，但针对大脑损伤的研究很少。使用磁共振成像和基于体素的形态测定法研究了 22 名吸烟者和 23 名从不吸烟者的大脑结构可能存在的差异。与不吸烟者相比，吸烟者的额叶区（前扣带皮层、前额叶和眶额皮质）、枕叶和颞叶（包括海马旁回）的灰质体积和灰质密度显着较小（P = 0.05，已校正）。在丘脑、小脑和黑质等其他区域也发现了灰质体积或灰质密度的群体差异。吸烟者的大脑任何区域的体积并不比不吸烟者大。终生接触烟草烟雾的程度（包年）与额叶、颞叶和小脑的体积呈负相关（P = 0.001，未校正）。数据表明，与从不吸烟者相比，吸烟者的几个皮质和皮质下区域存在结构性缺陷。群体差异的地形特征显示出与已知介导药物强化、注意力和工作记忆处理的大脑网络有一些相似之处。目前的研究结果可能部分解释了经常报告的长期吸烟者认知功能障碍的原因。
Growing evidence from animal studies indicates brain-damaging properties of nicotine exposure. Investigations in humans found a wide range of functional cerebral effects of nicotine and cigarette smoking, but studies focusing on brain damage are sparse. In 22 smokers and 23 never-smokers possible differences of the cerebral structures were investigated using magnetic resonance imaging and voxel-based morphometry. Significantly smaller grey matter volume and lower grey matter density (P = 0.05, corrected) were observed in the frontal regions (anterior cingulate, prefrontal and orbitofrontal cortex), the occipital lobe and the temporal lobe including parahippocampal gyrus, in smokers than in never-smokers. Group differences of either grey matter volume or grey matter density were also found in the thalamus, cerebellum and substantia nigra, among other regions. Smokers did not show greater volumes than never-smokers in any cerebral region. Magnitude of lifetime exposure to tobacco smoke (pack-years) was inversely correlated with volume of frontal and temporal lobes and cerebellum (P = 0.001, uncorrected). The data indicate structural deficits of several cortical and subcortical regions in smokers relative to never-smokers. The topographic profile of the group differences show some similarities to brain networks known to mediate drug reinforcement, attention and working memory processing. The present findings may explain in part the frequently reported cognitive dysfunctions in chronic cigarette consumers.