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以跨诊断方法映射快感缺乏特异性功能障碍:一项激活可能性估计元分析。

Mapping anhedonia-specific dysfunction in a transdiagnostic approach: an ALE meta-analysis.

作者信息

Zhang Bei, Lin Pan, Shi Huqing, Öngür Dost, Auerbach Randy P, Wang Xiaosheng, Yao Shuqiao, Wang Xiang

机构信息

Medical Psychological Institute, The Second Xiangya Hospital of Central South University, 139 Renmin (M) Road, Changsha, Hunan, 410011, People's Republic of China.

Key Laboratory of Biomedical Information Engineering of Education Ministry, Institute of Biomedical Engineering, Xi'an Jiaotong University, Xi'an, Shanxi, 710049, People's Republic of China.

出版信息

Brain Imaging Behav. 2016 Sep;10(3):920-39. doi: 10.1007/s11682-015-9457-6.

Abstract

Anhedonia is a prominent symptom in neuropsychiatric disorders, most markedly in major depressive disorder (MDD) and schizophrenia (SZ). Emerging evidence indicates an overlap in the neural substrates of anhedonia between MDD and SZ, which supported a transdiagnostic approach. Therefore, we used activation likelihood estimation (ALE) meta-analysis of functional magnetic resonance imaging studies in MDD and SZ to examine the neural bases of three subdomains of anhedonia: consummatory anhedonia, anticipatory anhedonia and emotional processing. ALE analysis focused specifically on MDD or SZ was used later to dissociate specific anhedonia-related neurobiological impairments from potential disease general impairments. ALE results revealed that consummatory anhedonia was associated with decreased activation in ventral basal ganglia areas, while anticipatory anhedonia was associated with more substrates in frontal-striatal networks except the ventral striatum, which included the dorsal anterior cingulate, middle frontal gyrus and medial frontal gyrus. MDD and SZ patients showed similar neurobiological impairments in anticipatory and consummatory anhedonia, but differences in the emotional experience task, which may also involve affective/mood general processing. These results support that anhedonia is characterized by alterations in reward processing and relies on frontal-striatal brain circuitry. The transdiagnostic approach is a promising way to reveal the overall neurobiological framework that contributes to anhedonia and could help to improve targeted treatment strategies.

摘要

快感缺失是神经精神疾病中的一个突出症状,在重度抑郁症(MDD)和精神分裂症(SZ)中最为明显。新出现的证据表明,MDD和SZ在快感缺失的神经基质上存在重叠,这支持了一种跨诊断方法。因此,我们对MDD和SZ的功能磁共振成像研究进行激活可能性估计(ALE)元分析,以研究快感缺失三个子领域的神经基础:消费性快感缺失、预期性快感缺失和情绪加工。后来使用专门针对MDD或SZ的ALE分析,将特定的快感缺失相关神经生物学损伤与潜在的疾病一般性损伤区分开来。ALE结果显示,消费性快感缺失与腹侧基底神经节区域的激活减少有关,而预期性快感缺失与除腹侧纹状体之外的额叶-纹状体网络中的更多基质有关,其中包括背侧前扣带回、额中回和额内侧回。MDD和SZ患者在预期性和消费性快感缺失方面表现出相似的神经生物学损伤,但在情绪体验任务上存在差异,这也可能涉及情感/情绪的一般性加工。这些结果支持快感缺失的特征是奖励加工的改变,并依赖于额叶-纹状体脑回路。跨诊断方法是揭示导致快感缺失的整体神经生物学框架的一种有前景的方式,并且有助于改进靶向治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2d6/5002053/9fc9f995993f/11682_2015_9457_Fig1_HTML.jpg

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