Cerebellar hypermetabolism in alcohol use disorder: compensatory mechanism or maladaptive plasticity?

IF 3.2 3区 医学 Q1 Medicine
L. Ritz, S. Segobin, C. Lannuzel, A. Laniepce, C. Boudehent, N. Cabé, F. Eustache, F. Vabret, H. Beaunieux, A. Pitel
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引用次数: 10

Abstract

BACKGROUND Despite severe structural brain abnormalities within the fronto-cerebellar circuit (FCC), cerebellar metabolism studied with FDG-PET is relatively preserved in patients with alcohol use disorder (AUD). The compensatory role of the cerebellum has been explored mainly through fMRI examination of AUD patients with preserved level of performance. The present study aims at examining cerebellar metabolism and its relationship with regional brain metabolism and neuropsychological functioning in AUD patients. METHODS Thirty-two recently detoxified AUD patients and 23 controls underwent an FDG-PET examination at rest. Participants also performed a neuropsychological battery assessing executive functions, verbal memory and ataxia. RESULTS Compared to controls, AUD patients had higher glucose-uptake in the cerebellar lobules VIII, in association with hypometabolism notably in several nodes of the FCC. Cerebellar hypermetabolism correlated negatively with regional hypometabolism in the premotor and frontal cortices. This pattern of regional hypermetabolism and hypometabolism related to ataxia and working memory deficits. CONCLUSIONS These specific brain-behaviour relationships do not fulfil the criteria for brain compensatory processes. Cerebellar hypermetabolism may rather reflect the involvement of different pathological mechanisms, leading to a maladaptive plasticity phenomenon within the FCC in AUD patients who are early in abstinence. Further studies are required to examine the contributions of structural and functional connectivity alterations in the cerebellar hypermetabolism and the changes of these pathological mechanisms with abstinence or relapse. This article is protected by copyright. All rights reserved.
酒精使用障碍的小脑高代谢:代偿机制还是适应性不良?
尽管在额小脑回路(FCC)中存在严重的脑结构异常,但FDG-PET研究的小脑代谢在酒精使用障碍(AUD)患者中相对保留。小脑的代偿作用主要是通过fMRI检查保留表现水平的AUD患者来探索的。本研究旨在探讨AUD患者小脑代谢及其与局部脑代谢和神经心理功能的关系。方法32例新近解毒的AUD患者和23例对照者静息时行FDG-PET检查。参与者还进行了神经心理学测试,评估执行功能、言语记忆和共济失调。结果与对照组相比,AUD患者在小脑小叶VIII中有更高的葡萄糖摄取,与FCC几个节点的低代谢有关。小脑高代谢与运动前皮层和额叶皮层的区域低代谢呈负相关。这种区域高代谢和低代谢模式与共济失调和工作记忆缺陷有关。结论这些特定的脑行为关系不符合脑代偿过程的标准。小脑高代谢更可能反映了不同病理机制的参与,导致早期戒酒的AUD患者FCC内出现适应性可塑性不良现象。需要进一步的研究来检验小脑高代谢的结构和功能连接改变的贡献,以及这些病理机制在戒断或复发时的变化。这篇文章受版权保护。版权所有。
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来源期刊
CiteScore
5.90
自引率
9.40%
发文量
219
审稿时长
1 months
期刊介绍: Alcoholism: Clinical and Experimental Research''s scope spans animal and human clinical research, epidemiological, experimental, policy, and historical research relating to any aspect of alcohol abuse, dependence, or alcoholism. This journal uses a multi-disciplinary approach in its scope of alcoholism, its causes, clinical and animal effect, consequences, patterns, treatments and recovery, predictors and prevention.
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