Crisalid Unit (FJ5), CHI Clermont de l'Oise, Clermont, France.
Inserm Unit U669, Maison de Solenn, Universities Paris, Paris, France.
Alcohol Clin Exp Res. 2022 Jun;46(6):994-1010. doi: 10.1111/acer.14845. Epub 2022 May 10.
Diminished uptake of fluorodeoxyglucose (FDG) has been observed in patients with alcohol use disorder (AUD) but little statistical contrast of the regional brain deficits has been undertaken. This study examined prefrontal cortex inter-regional Brodmann area differences to delineate patterns associated with behavioral, neurotransmitter, and general toxicity hypotheses of cerebral involvement in AUD.
We obtained data from FDG positron emission tomography (PET) and anatomical magnetic resonance imaging (MRI) for 87 patients with AUD and 41 age- and sex-matched healthy volunteers. Patients were alcohol dependent and had negative breathalyzer tests at the time of imaging. They were assessed with the Beck Depression Inventory, Alcohol Urge Questionnaire, Obsessive Compulsive Drinking Scale, Spielberger State/Trait Anxiety Scale, Buss-Durkee Hostility Inventory, and the Drinker Inventory of Consequences (DrInC). PET images were co-registered to MRI and both voxel × voxel statistical mapping and stereotaxic regions of interest were obtained.
Compared with healthy volunteers, patients with AUD had lower relative metabolic rates in the frontal, temporal, and parietal lobes, localizable most prominently to the dorsolateral and nearly all orbital prefrontal cortex, superior temporal gyrus, and inferior parietal lobule. In contrast, metabolic rates in the medial orbitofrontal and anterior cingulate cortex, and the subcortical structures (thalamus, cerebellum, ventral striatum, and the dorsal raphe nucleus) in patients were significantly greater. The severity of alcohol-related consequences as assessed by the DrInC scale was most highly associated with lower metabolism in the caudate, dorsolateral prefrontal, frontopolar, and anteroposterior cingulate cortex.
Despite widespread metabolic abnormalities, decreases in AUD were most marked in frontal executive areas, consistent with diminished impulse control, and increases were most prominent in the striatum and cingulate areas, consistent with a suppressed reward system.
在患有酒精使用障碍（AUD）的患者中，已经观察到氟脱氧葡萄糖（FDG）摄取减少，但很少进行区域性脑缺陷的统计学对比。本研究检查了前额叶皮层的 Brodmann 区差异，以描绘与行为、神经递质和一般毒性假设相关的大脑参与 AUD 的模式。
我们从 87 名 AUD 患者和 41 名年龄和性别匹配的健康志愿者那里获得了 FDG 正电子发射断层扫描（PET）和解剖磁共振成像（MRI）的数据。患者依赖酒精，在成像时进行了阴性呼气酒精测试。他们接受了贝克抑郁量表、酒精冲动问卷、强迫性饮酒量表、斯皮尔伯格状态/特质焦虑量表、布斯-德克敌意量表和饮酒后果问卷（DrInC）的评估。PET 图像与 MRI 配准，获得了体素×体素统计映射和立体定向感兴趣区。
与健康志愿者相比，AUD 患者的额叶、颞叶和顶叶的相对代谢率较低，主要定位于背外侧和几乎所有眶额前皮质、颞上回和下顶叶。相比之下，患者的内侧眶额和前扣带回皮质以及皮质下结构（丘脑、小脑、腹侧纹状体和中缝核）的代谢率显著增加。DrInC 量表评估的与酒精相关的后果的严重程度与尾状核、背外侧前额叶、额极和前后扣带回皮质的代谢降低最相关。
尽管存在广泛的代谢异常，但 AUD 的减少在额叶执行区域最为明显，与冲动控制减弱一致，而在纹状体和扣带回区域最为明显，与抑制的奖励系统一致。
