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).
