ON THE TREATMENT OF NEURODERMATITIS WITH A MONOAMINE OXIDASE INHIBITOR

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Abstract
The abstract of the preceding paper proposed a model for the treatment of psychosomatic diseases. The central clinical aspect of this model was that suppression of the rapid eye movement (REM) phase of the sleep-dream cycle (and its daytime counterpart of the ultradian biorhythm) should lead to improvement of such disorders in a controlled double blind study. Neurodermatitis was the “classical” psychosomatic disease chosen and treatment consisted of REM suppression by the monoamine oxidase (MAO) inhibitor, phenelzine sulfate, 75 mg/day. The control drug used was diazepam because it has general effects similar to those of phenelzine and it also has an effect on the REM-non-REM cycle, blocking stage IV sleep. Fifteen randomly assigned subjects (eight experimental, seven control) had a 5-week introductory period during which time they all received a dose of phenelzine sulfate (30 mg/day), too small to block the REM state. This was followed by a 5-week double blind study. Neurodermatitis is characterized by pruritis, erythema, papules, lichenification, and scaling. Each symptom area was rated during a weekly examination on a scale from 0 (asymptomatic) to 4 (maximum severity). A total combined score was also kept. The essential hypotheses were that there would be no improvement during the preliminary weeks, that control subjects should not improve during the 5 experimental weeks, that experimental subjects should improve significantly during the experimental weeks, and that experimental subjects should improve significantly more than control subjects during the 5-week double blind study. The statistic used was the significance of difference between two means, one-tailed t-test. Of the 24 predictions, 23 were supported by the results. The degree of statistical significance was especially great in the primary symptoms of pruritus, erythema, and papules, where structural change is less and reversibility is more rapid. The significant findings do not comprise a crucial experiment since alternate models can account for the results. Two possibilities are that the antidepressant effects of phenelzine might alleviate psychosomatic symptoms unrelated to ultradian cycle desynchronization. Similarly, MAO inhibitors may effect central nervous system circuits and neurochemical processes, changing the course of a psychosomatic disease independent of its effects on the biorhythm. Future research can test these possibilities but the present report elevates the model of ultradian cycle synchronization to a level of viability deserving further study.

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