Carr D B, Sheehan D V
J Clin Psychiatry. 1984 Aug;45(8):323-30.
Previously unrecognized similarities among metabolic responses to various maneuvers used to evoke anxiety in patients with panic disorder are described. On the basis of these observations, a new biological model is proposed for panic disorder, in which the primary defect--which is neuroendocrine rather than psychiatric--is operationally placed within the redox-regulating apparatus of the brain stem. This model is consistent with many clinical features of panic disorder and also provides a theoretical framework for further studies of the pathophysiology of this and related conditions (e.g., hyperventilation syndrome).
本文描述了在惊恐障碍患者中，用于诱发焦虑的各种操作所引发的代谢反应之间先前未被认识到的相似性。基于这些观察结果，提出了一种针对惊恐障碍的新生物学模型，其中主要缺陷（是神经内分泌而非精神方面的）在操作上被定位在脑干的氧化还原调节装置内。该模型与惊恐障碍的许多临床特征相符，也为进一步研究这种疾病及相关病症（如换气过度综合征）的病理生理学提供了理论框架。
