Sleep and sleep electroencephalogram in depressed patients treated with phenelzine

Background: The beneficial effect of antidepressant interventions has been proposed to depend on suppression of rapid eye movement (REM) sleep or inhi bition of electroencephalographic (EEG) slow-wave activity (SWA) in non-REM sleep. Use of the monoamine oxidase inhibitor phenelzine sulfate can elimi nate REM sleep. We studied the relation between REM sleep suppression and a ntidepressant response and the effect of phenelzine therapy on sleep EEG po wer spectra. Methods: Open-labeled prescriptions of 30 to 90 mg of phenelzine were given to 11 patients with major depressive disorder (6 men and 5 women: mean age , 41.4 years); all were physically healthy. Mood, dream recall, sleep, slee p EEG, and ocular and muscular activity during sleep were studied before tr eatment and during the third and fifth weeks of pharmacotherapy. Results: Six patients remitted from depression, 2 responded partially, and 3 showed no antidepressant response. Independent from clinical response, RE M sleep was dramatically suppressed. On average, only 4.9 minutes of REM sl eep was observed in treatment week 5, and it was completely absent in 6 pat ients. This effect was compensated for by increased stage 2 sleep. In non-R EM sleep, EEG power was higher than at baseline between 16.25 and 25 Hz. Sl ow-wave activity (power within 0.75-4.5 Hz) and the exponential decline of SWA during sleep were not affected. Conclusions: Antidepressant response to phenelzine treatment does not depen d on elimination of REM sleep or inhibition of SWA in non-REM sleep. In dep ressed patients, REM sleep is regulated independently from non-REM sleep an d can be manipulated without altering the dynamics of SWA.