Hertfordshire Partnership University NHS Foundation Trust, Welwyn Garden City, Hertfordshire, United Kingdom.
University of Hertfordshire, Department of Postgraduate Medicine, College Lane Hatfield, United Kingdom.
Int J Neuropsychopharmacol. 2018 Jan 1;21(1):42-58. doi: 10.1093/ijnp/pyx088.
Compulsions are repetitive, stereotyped thoughts and behaviors designed to reduce harm. Growing evidence suggests that the neurocognitive mechanisms mediating behavioral inhibition (motor inhibition, cognitive inflexibility) reversal learning and habit formation (shift from goal-directed to habitual responding) contribute toward compulsive activity in a broad range of disorders. In obsessive compulsive disorder, distributed network perturbation appears focused around the prefrontal cortex, caudate, putamen, and associated neuro-circuitry. Obsessive compulsive disorder-related attentional set-shifting deficits correlated with reduced resting state functional connectivity between the dorsal caudate and the ventrolateral prefrontal cortex on neuroimaging. In contrast, experimental provocation of obsessive compulsive disorder symptoms reduced neural activation in brain regions implicated in goal-directed behavioral control (ventromedial prefrontal cortex, caudate) with concordant increased activation in regions implicated in habit learning (presupplementary motor area, putamen). The ventromedial prefrontal cortex plays a multifaceted role, integrating affective evaluative processes, flexible behavior, and fear learning. Findings from a neuroimaging study of Pavlovian fear reversal, in which obsessive compulsive disorder patients failed to flexibly update fear responses despite normal initial fear conditioning, suggest there is an absence of ventromedial prefrontal cortex safety signaling in obsessive compulsive disorder, which potentially undermines explicit contingency knowledge and may help to explain the link between cognitive inflexibility, fear, and anxiety processing in compulsive disorders such as obsessive compulsive disorder.
强迫是一种重复的、刻板的思维和行为,旨在减少伤害。越来越多的证据表明,介导行为抑制(运动抑制、认知灵活性)、反向学习和习惯形成(从目标导向到习惯反应的转变)的神经认知机制有助于广泛的障碍中强迫活动。在强迫症中,分布式网络干扰似乎集中在前额叶皮层、尾状核、壳核及其相关神经回路周围。强迫症相关的注意力定势转移缺陷与神经影像学上背侧尾状核与腹外侧前额叶皮层之间静息状态功能连接减少相关。相比之下,强迫症症状的实验诱发减少了与目标导向行为控制相关的大脑区域(腹内侧前额叶皮层、尾状核)的神经激活,而与习惯学习相关的区域(辅助运动区、壳核)的激活增加。腹内侧前额叶皮层起着多方面的作用,整合情感评估过程、灵活的行为和恐惧学习。在对条件反射恐惧反转的神经影像学研究中发现,尽管强迫症患者的初始恐惧条件反射正常,但他们无法灵活地更新恐惧反应,这表明强迫症患者的腹内侧前额叶皮层缺乏安全信号,这可能破坏了明确的关联知识,并有助于解释认知灵活性、恐惧和焦虑处理之间的联系,如强迫症等强迫性障碍。