Geiger Maximilian J, Neufang Susanne, Stein Dan J, Domschke Katharina
Department of Psychiatry, University of Würzburg, Würzburg, Germany.
Hum Psychopharmacol. 2014 Nov;29(6):599-603. doi: 10.1002/hup.2436. Epub 2014 Oct 14.
Although a great deal of information about the neurobiology of panic disorder is now available, there is a need for an updated etiological model integrating recent findings on the neurobiology of the arousal system and its relationship with higher cortical functions in panic disorder. The current mini-review presents psychophysiological, molecular biological/genetic and functional neuroimaging evidence for dysfunction in major arousal systems of the brain. Such dysfunction may influence the development of panic disorder by precipitating autonomic bodily symptoms and at the same time increasing vigilance to these sensations by modulating cortical attentional networks. A multilevel model of arousal, attention and anxiety-including the norepinephrine, orexin, neuropeptide S and caffeine-related adenosine systems-may be useful in integrating a range of data available on the pathogenesis of panic disorder.
尽管目前已有大量关于惊恐障碍神经生物学的信息,但仍需要一个更新的病因模型,该模型要整合近期关于惊恐障碍中唤醒系统神经生物学及其与高级皮层功能关系的研究结果。本综述简要介绍了大脑主要唤醒系统功能障碍的心理生理学、分子生物学/遗传学及功能性神经影像学证据。这种功能障碍可能通过引发自主身体症状来影响惊恐障碍的发展,同时通过调节皮层注意力网络来提高对这些感觉的警觉性。一个包括去甲肾上腺素、食欲素、神经肽S和与咖啡因相关的腺苷系统在内的唤醒、注意力和焦虑的多层次模型,可能有助于整合一系列关于惊恐障碍发病机制的现有数据。