Neuroscience Program, SRI International, Menlo Park, CA, United States; Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, United States.
Neuroscience Program, SRI International, Menlo Park, CA, United States; Clinical Psychology, Palo Alto University, Palo Alto, CA, United States.
Drug Alcohol Depend. 2022 Jun 1;235:109435. doi: 10.1016/j.drugalcdep.2022.109435. Epub 2022 Apr 1.
A neural substrate of alcohol-related instability of gait and balance is the cerebellum. Whether disruption of neural communication between cerebellar and cortical brain regions exerts an influence on ataxia in alcohol use disorder (AUD) was the focus of this study.
Study groups comprised 32 abstinent AUD participants and 22 age- and sex-matched healthy controls (CTL). All participants underwent clinical screening, motor testing, and resting-state functional MR imaging analyzed for functional connectivity (FC) among 90 regions across the whole cerebrum and cerebellum. Ataxia testing quantified gait and balance with the Fregly-Graybiel Ataxia Battery conducted with and without vision.
The AUD group achieved lower scores than the CTL group on balance performance, which was disproportionately worse for eyes open than eyes closed in the AUD relative to the CTL group. Differences in ataxia were accompanied by differences in FC marked by cerebellar-frontal and cerebellar-parietal hyperconnectivity and cortico-cortical hypoconnectivity in the AUD relative to the control group. Lifetime alcohol consumption correlated significantly with AUD-related FC aberrations, which explained upwards of 69% of the AUD ataxia score variance.
Heavy, chronic alcohol consumption is associated with disorganized neural communication among cerebellar-cortical regions and contributes to ataxia in AUD. Ataxia, which is known to accelerate with age and be exacerbated with AUD, can threaten functional independence. Longitudinal studies are warranted to address whether extended sobriety quells ataxia and normalizes aberrant FC contributing to instability.
小脑是与酒精相关步态和平衡不稳定有关的神经基础。小脑与皮质脑区之间神经通讯的中断是否会对酒精使用障碍（AUD）患者的共济失调产生影响，是本研究的重点。
研究组包括 32 名戒断的 AUD 参与者和 22 名年龄和性别匹配的健康对照者（CTL）。所有参与者均接受临床筛查、运动测试和静息态功能磁共振成像分析，以评估整个大脑和小脑的 90 个区域之间的功能连接（FC）。采用 Fregly-Graybiel 共济失调量表（Fregly-Graybiel Ataxia Battery）进行睁眼和闭眼测试，以评估步态和平衡。
AUD 组的平衡表现得分低于 CTL 组，且 AUD 组睁眼时的平衡表现明显比 CTL 组差。与 CTL 组相比，AUD 组的共济失调差异伴随着 FC 的差异，表现为小脑-额叶和小脑-顶叶的过度连接，以及皮质内连接的不足。终生饮酒量与 AUD 相关的 FC 异常显著相关，可解释 AUD 共济失调评分差异的 69%以上。
大量、慢性的酒精摄入与小脑-皮质区域之间的神经通讯紊乱有关，并导致 AUD 患者的共济失调。众所周知，共济失调会随年龄增长而加速，并因 AUD 而加剧，可能会威胁到功能独立性。需要进行纵向研究来确定是否延长戒酒时间可以减轻共济失调并使导致不稳定的异常 FC 正常化。
