Increased white matter signal hyperintensities in long-term abstinent alcoholics compared with nonalcoholic controls.
Increased white matter signal hyperintensities in long-term abstinent alcoholics compared with nonalcoholic controls.
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DOI：
10.1111/j.1530-0277.2008.00812.x
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发表时间：
2009-01
期刊：
影响因子：
--
通讯作者：
Harper C
中科院分区：
文献类型：
--
作者：
Fein G;Shimotsu R;Di Sclafani V;Barakos J;Harper C
酒精依赖（AD）对大脑结构和功能的有害影响已被充分证明，其中许多人通过充分的戒酒来解决。白色信号高强度（WMSH）被认为最有可能是继发于血管的后果（即，高血压和动脉粥样硬化）的影响。我们假设这种影响将持续到长期戒酒，并评估他们在中年长期戒酒者（LTAA）与年龄和性别相当的非酒精对照（NAC）。97名参与者（51名LTAA和46名NAC）接受了认知、精神和结构脑MRI评估。通过内部开发的自动算法识别WMSH并标记为深部或脑室周围。比较各组WMSH体积，并在组内检查WMSH测量与人口统计学、酒精使用、精神和认知测量的相关性。LTAA比NAC有更多的WMSH。有一个显着的年龄组的相互作用，随着年龄的增长，WMSH在LTAA，但不是在NAC。在LTAA内，WMSH负荷与酒精负荷和年龄独立呈正相关。WMSH量与戒酒时间、家庭饮酒史、教育年限或精神病学或认知变量之间没有明显关联。酒精滥用的程度与WMSH体积的增加有关。在LTAA中存在年龄效应，但在对照组中不存在，这表明存在协同效应，其中酒精促进了衰老相关WMSH形成的发生。增加的WMSH负荷似乎没有任何显著的临床相关性，表明我们样本中的白色病变可能没有严重到足以表现为认知缺陷。该研究的局限性在于，我们没有关于血管风险因素（如高血压、吸烟或糖尿病）的存在或严重程度的数据或当前指数。
The harmful effects of alcohol dependence (AD) on brain structure and function have been well documented, with many resolving with sufficient abstinence. White matter signal hyperintensities (WMSH) are thought to most likely be consequences secondary to the vascular (i.e., hypertension and atherosclerosis) effects of AD. We hypothesized such effects would persist into long-term abstinence, and evaluated them in middle-aged long-term abstinent alcoholics (LTAA) compared with age and gender comparable non-alcoholic controls (NAC). 97 participants (51 LTAA and 46 NAC) underwent cognitive, psychiatric, and structural brain MRI evaluations. WMSH were identified and labeled as deep or periventricular by an automated algorithm developed in-house. WMSH volumes were compared between groups, and the associations of WMSH measures with demographic, alcohol use, psychiatric and cognitive measures were examined within group. LTAA had more WMSH than NAC. There was a significant group by age interaction, with WMSH increasing with age in LTAA, but not in NAC. Within LTAA, WMSH load was independently positively associated with alcohol burden and with age. No associations were evident between WMSH volumes and abstinence duration, family drinking history, years of education, or psychiatric or cognitive variables. The magnitude of alcohol abuse was related to increased WMSH volume. The presence of an age effect in the LTAA but not the controls indicates a synergistic effect wherein alcohol advances the onset of aging-related WMSH formation. The increased WMSH load did not appear to have any significant clinical correlates, indicating that the white matter lesions in our sample may not have been severe enough to manifest as cognitive deficits. A limitation of the study is that we did not have data on the presence or severity of lifetime or current indices of vascular risk factors such as, hypertension or smoking, or diabetes.
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