Reinecke A, Filippini N, Berna C, Western D G, Hanson B, Cooper M J, Taggart P, Harmer C J
Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK.
Centre for Functional Magnetic Resonance Imaging of the Brain, University of Oxford, Oxford, UK.
Transl Psychiatry. 2015 Nov 3;5(11):e673. doi: 10.1038/tp.2015.160.
Impairments in emotion regulation are thought to have a key role in the pathogenesis of anxiety disorders, but the neurobiological underpinnings contributing to vulnerability remain poorly understood. It has been a long-held view that exaggerated fear is linked to hyperresponsivity of limbic brain areas and impaired recruitment of prefrontal control. However, increasing evidence suggests that prefrontal-cortical networks are hyperactive during threat processing in anxiety disorders. This study directly explored limbic-prefrontal neural response, connectivity and heart-rate variability (HRV) in patients with a severe anxiety disorder during incidental versus intentional emotion regulation. During 3 Tesla functional magnetic resonance imaging, 18 participants with panic disorder and 18 healthy controls performed an emotion regulation task. They either viewed negative images naturally (Maintain), or they were instructed to intentionally downregulate negative affect using previously taught strategies of cognitive reappraisal (Reappraisal). Electrocardiograms were recorded throughout to provide a functional measure of regulation and emotional processing. Compared with controls, patients showed increased neural activation in limbic-prefrontal areas and reduced HRV during incidental emotion regulation (Maintain). During intentional regulation (Reappraisal), group differences were significantly attenuated. These findings emphasize patients' ability to regulate negative affect if provided with adaptive strategies. They also bring prefrontal hyperactivation forward as a potential mechanism of psychopathology in anxiety disorders. Although these results challenge models proposing impaired allocation of prefrontal resources as a key characteristic of anxiety disorders, they are in line with more recent neurobiological frameworks suggesting that prefrontal hyperactivation might reflect increased utilisation of maladaptive regulation strategies quintessential for anxiety disorders.
情绪调节障碍被认为在焦虑症的发病机制中起关键作用,但导致易感性的神经生物学基础仍知之甚少。长期以来,人们一直认为过度恐惧与边缘脑区的反应过度以及前额叶控制功能的受损有关。然而,越来越多的证据表明,在焦虑症患者的威胁处理过程中,前额叶 - 皮质网络是过度活跃的。本研究直接探究了重度焦虑症患者在偶然与有意情绪调节过程中的边缘 - 前额叶神经反应、连接性和心率变异性(HRV)。在3特斯拉功能磁共振成像期间,18名恐慌症患者和18名健康对照者执行了一项情绪调节任务。他们要么自然地观看负面图像(维持),要么被指示使用先前教授的认知重新评估策略有意下调负面影响(重新评估)。在整个过程中记录心电图,以提供调节和情绪处理的功能指标。与对照组相比,患者在偶然情绪调节(维持)期间,边缘 - 前额叶区域的神经激活增加,HRV降低。在有意调节(重新评估)期间,组间差异显著减弱。这些发现强调了如果为患者提供适应性策略,他们调节负面影响的能力。它们还将前额叶过度激活作为焦虑症精神病理学的一种潜在机制提了出来。尽管这些结果挑战了提出前额叶资源分配受损是焦虑症关键特征的模型,但它们与最近的神经生物学框架一致,该框架表明前额叶过度激活可能反映了焦虑症典型的适应不良调节策略的更多使用。