Firk Christine, Mainz Verena, Schulte-Ruether Martin, Fink Gereon, Herpertz-Dahlmann Beate, Konrad Kerstin
Department of Child and Adolescent Psychiatry, University Hospital RWTH Aachen, Aachen, Germany.
Institute of Neuroscience and Medicine (INM-3), Research Centre Juelich, Juelich, Germany.
J Child Psychol Psychiatry. 2015 Nov;56(11):1168-76. doi: 10.1111/jcpp.12384. Epub 2015 Jan 26.
Previous studies have reported that cognitive deficits occur in patients with anorexia nervosa (AN) and that these deficits may represent a predisposition towards developing AN or perpetuate the disorder. Specifically, dysfunctional implicit learning may contribute to the development of highly resistant dieting behaviours that are fundamental to the persistence of the disorder. Thus, the aims of this study were (a) to investigate implicit sequence learning in adolescent patients with AN before and after weight recovery and (b) to elucidate the associated neural mechanisms in acute AN relative to healthy controls.
In a behavioural study, implicit sequence learning was assessed using a serial reaction time task in 27 adolescents with AN before (T1) and after weight recovery (T2) compared with age-matched healthy controls (HC) who were assessed at similar time intervals. The neural correlates of implicit sequence learning were subsequently investigated in 19 AN patients shortly after they were admitted to the hospital and 20 HC using functional magnetic resonance imaging (fMRI).
At T1, AN patients showed reduced sequence learning compared with HC. However, no behavioural differences between HC and AN patients were found at T2. At the neural level, acute AN patients showed reduced thalamic activation during sequence learning compared with HC subjects.
Our data suggest that the impaired implicit learning observed in adolescent AN patients before weight gain is a state-related dysfunction that normalises with weight gain. Thus, implicit learning deficits do not appear to represent a predisposition towards developing AN; rather, these deficits should be considered when planning psychotherapeutic interventions for acute AN. Reduced thalamic activation during the acute stage of AN may indicate a starvation-induced dysfunction of the neural circuitry that is involved in behavioural flexibility.
先前的研究报告称,神经性厌食症(AN)患者存在认知缺陷,这些缺陷可能是患AN的易感性因素,或使该疾病持续存在。具体而言,功能失调的内隐学习可能导致高度顽固的节食行为的发展,而这种行为是该疾病持续存在的根本原因。因此,本研究的目的是:(a)调查青少年AN患者体重恢复前后的内隐序列学习情况;(b)阐明急性AN患者相对于健康对照者的相关神经机制。
在一项行为研究中,使用序列反应时任务评估了27名青少年AN患者体重恢复前(T1)和恢复后(T2)的内隐序列学习情况,并与在相似时间间隔接受评估的年龄匹配的健康对照者(HC)进行比较。随后,使用功能磁共振成像(fMRI)对19名刚入院的AN患者和20名HC进行了内隐序列学习的神经相关性研究。
在T1时,与HC相比,AN患者的序列学习能力降低。然而,在T2时,未发现HC与AN患者之间存在行为差异。在神经层面,与HC受试者相比,急性AN患者在序列学习过程中丘脑激活减少。
我们的数据表明,青少年AN患者体重增加前观察到的内隐学习受损是一种与状态相关的功能障碍,体重增加后可恢复正常。因此,内隐学习缺陷似乎并非患AN的易感性因素;相反,在为急性AN患者制定心理治疗干预计划时应考虑这些缺陷。AN急性期丘脑激活减少可能表明饥饿导致参与行为灵活性的神经回路功能障碍。