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神经性厌食症在不同需求负荷水平下的反应抑制缺陷:一项事件相关电位研究。

Deficits in response inhibition on varied levels of demand load in anorexia nervosa: an event-related potentials study.

机构信息

Department of Clinical Psychology, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, 600 Wan Ping Nan Road, Shanghai, 200030, People's Republic of China.

Department of EEG and Imaging, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, 600 Wan Ping Nan Road, Shanghai, 200030, People's Republic of China.

出版信息

Eat Weight Disord. 2020 Feb;25(1):231-240. doi: 10.1007/s40519-018-0558-2. Epub 2018 Aug 28.

DOI:10.1007/s40519-018-0558-2
PMID:30168032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6997249/
Abstract

PURPOSE

The aim of the present study was to investigate the executive function of inhibitory control in anorexia nervosa (AN), which is considered as an underlying pathophysiology of restricting eating.

METHODS

In this work, we examined the function of response inhibition in 27 unmedicated AN patients and 30 healthy controls (HC) using stop-signal tasks with different demand loads. Two event-related potentials (ERP) during the stop-signal tasks, N2 and P300, were compared between the AN and HC groups.

RESULTS

We found attenuated P300 amplitudes and delayed N2 latencies in AN patients across all three demand loads compared to HCs. We also found significant interaction between group and level of demand load. N2 latencies were prolonged when the inhibitory demand was lower in the AN group, whereas no differences in N2 latencies were found across different demand loads in HCs.

CONCLUSIONS

Taken together, altered P300 amplitudes and N2 latencies may be associated with impaired response inhibition in AN patients. In particular, alterations of fronto-central N2 activations were demand-related, which might contribute to an aberrant inhibitory control process in AN.

LEVEL OF EVIDENCE

Level II, controlled trial without randomization.

摘要

目的

本研究旨在探讨神经性厌食症(AN)的抑制控制执行功能,这被认为是限制进食的潜在病理生理学基础。

方法

在这项工作中,我们使用不同需求负荷的停止信号任务,检查了 27 名未经药物治疗的 AN 患者和 30 名健康对照(HC)的反应抑制功能。比较了 AN 组和 HC 组在停止信号任务期间的两种事件相关电位(ERP),即 N2 和 P300。

结果

与 HC 相比,我们发现 AN 患者在所有三种需求负荷下的 P300 振幅减弱,N2 潜伏期延迟。我们还发现组和需求负荷水平之间存在显著的交互作用。在 AN 组中,当抑制需求较低时,N2 潜伏期延长,而 HC 中在不同需求负荷下,N2 潜伏期没有差异。

结论

综上所述,P300 振幅和 N2 潜伏期的改变可能与 AN 患者的反应抑制受损有关。特别是,额中央 N2 激活的改变与需求有关,这可能导致 AN 中抑制控制过程异常。

证据水平

II 级,无随机对照的对照试验。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/6e9418ba4972/40519_2018_558_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/dbe071de2e9a/40519_2018_558_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/11327095f573/40519_2018_558_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/6e9418ba4972/40519_2018_558_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/dbe071de2e9a/40519_2018_558_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/11327095f573/40519_2018_558_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd3b/6997249/6e9418ba4972/40519_2018_558_Fig3_HTML.jpg

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