Psychosomatic Medicine 9:242-245 (1947)
© 1947 American Psychosomatic Society

Studies Concerning the Etiology and Pathogenesis of Neurocirculatory Asthenia

VI. Episodic Neurogenic Discharge as a Manifestation of the Syndrome

¹ Harold Brunn Institute for Cardiovascular Research, Mount Zion Hospital San Francisco, California

In the preceding paragraphs, evidence was obtained to indicate that a considerable number of N.C.A. patients were subject to episodic attacks of cardiovascular, respiratory, peripheral neurogenic dysfunction, and syncope, a phenomenon not stressed in the present literature. The recognition of the occurrence of such attacks in N.C.A. patients while at rest appeared to us to be of prime importance in an approach to an understanding of the pathogenesis of this syndrome. For these abrupt unpredictable exacerbations of the usual manifestations of this illness furnished irrefutable contradiction to those theories which explained the disorder as one of functional breakdown during the expenditure of effort alone. Furthermore, the occurrence of these attacks implicated the involvement of some portion of the central nervous system containing many closely situated and integrated centers concerned with adrenergic and cholinergic functions.

In view of the fact that the hypothalamus has been found (1, 15) to contain not only the governing centers of the autonomic nervous system but also centers concerned with respiration, it seemed quite likely that this area of the diencephalon was the focus from which the various types of discharge arose. It should be pointed out that experimental stimulation of the hypothalamus has been found (14, 15, 16) to be followed by the appearance of practically all of the phenomena which were observed in this study except for syncope. Even the appearance of this last phenomenon might have been due to augmentation of the normal sinus discharge (3) rather than sensitivity of the carotid sinus itself, an augmentation primarily due to some dysfunction of the supposed area of consciousness in the hypothalamus (14). The emotional discharge seen in several of the patients following sinus massage also might have been of hypothalamic origin, for the somatic display of emotion without cortical recognition of such has been described (13) in hypothalamic excitation.

In this and previous studies, much evidence has been obtained which suggested that the hypothalamus was of prime concern in the pathogenesis of many if not all of the somatic manifestations of neurocirculatory asthenia. It must be stressed, however, that the evidence suggested that the hypothalamus was the mediating, not necessarily the initiating, source for the production of the N.C.A. syndrome. Whether this hypothalamic involvement was due to a) factors directly affecting the hypothalamus initially or b) factors direcdy acting upon other presumably higher centers of the central nervous system (which in turn effected changes in the hypothalamus) could not be determined.

The similarity of the types of discharge described in this present communication to those seen in patients suffering from an overt anxiety neurosis was striking. The only true difference was that in our study the discharge occurred in patients who did not present in an overt fashion the typical personality seen in patients with an anxiety neurosis.