A number of theories purport to refer the etiology of psychoses to a disturbance in the metabolism of the sympathetic neurohumors1,2 or to an alteration in the functional activity of the sympathoadrenal system.3,4 Similarly, some of the explanations advanced to clarify the role of electroconvulsive therapy (ECT) utilize the same frame of reference.5 Such hypotheses ought to be verifiable directly by the investigation of the metabolism of pyrocatechol amines (catechol amines) in psychiatric patients.
The release of pyrocatechol amines at sympathetic postganglionic nerve endings and from the adrenal medulla is well known,6 of course; but very little is understood about this release as it occurs after electrically induced convulsions. The finding by Weil-Malherbe5 of an elevated plasma epinephrine following ECT has provided more direct evidence of sympathetic involvement than had previously been available in man. Pekkarinen et al.7 have reported that administration of electroshock