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Sleep and Sleep Electroencephalogram in Depressed Patients Treated With Phenelzine
Hans-Peter Landolt, PhD;
Eric B. Raimo, MD;
Bradley J. Schnierow, MD;
John R. Kelsoe, MD;
Mark H. Rapaport, MD;
J. Christian Gillin, MD
Arch Gen Psychiatry. 2001;58:268-276.
Background The beneficial effect of antidepressant interventions has been proposed
to depend on suppression of rapid eye movement (REM) sleep or inhibition of
electroencephalographic (EEG) slow-wave activity (SWA) in non-REM sleep. Use
of the monoamine oxidase inhibitor phenelzine sulfate can eliminate REM sleep.
We studied the relation between REM sleep suppression and antidepressant response
and the effect of phenelzine therapy on sleep EEG power 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, sleep EEG,
and ocular and muscular activity during sleep were studied before treatment
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, REM
sleep was dramatically suppressed. On average, only 4.9 minutes of REM sleep
was observed in treatment week 5, and it was completely absent in 6 patients.
This effect was compensated for by increased stage 2 sleep. In non-REM sleep,
EEG power was higher than at baseline between 16.25 and 25 Hz. Slow-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 depend on elimination
of REM sleep or inhibition of SWA in non-REM sleep. In depressed patients,
REM sleep is regulated independently from non-REM sleep and can be manipulated
without altering the dynamics of SWA.
From the Department of Psychiatry, University of California at San
Diego, Veterans Affairs San Diego Healthcare System, San Diego.
Corresponding author and reprints: Hans-Peter Landolt, PhD, c/o J.
Christian Gillin, MD, University of California at San Diego, Mental Health
Clinical Research Center, Psychiatry Service (116-A), Veterans Affairs Medical
Center, 3350 La Jolla Village Dr, San Diego, CA 92161 (e-mail: landolt{at}pharma.unizh.ch).
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