Sleep electroencephalogram in seasonal affective disorder and in control women: Effects of midday light treatment and sleep deprivation

• Published in: Biological psychiatry (1969) Vol. 40; no. 6; pp. 485 - 496
• Main Authors: Brunner, Daniel P., Kräuchi, Kurt, Dijk, Derk-Jan, Leonhardt, Georg, Haug, Hans-Joachim, Wirz-Justice, Anna
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.09.1996; Elsevier Science
• Subjects: Adult; Aged; Biological and medical sciences; depression; Electroencephalography; Female; Humans; light treatment; Medical sciences; Middle Aged; Miscellaneous; Phototherapy; Polysomnography; Psychiatric Status Rating Scales; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Seasonal affective disorder; Seasonal Affective Disorder - physiopathology; Seasonal Affective Disorder - therapy; Sleep - physiology; sleep deprivation; Sleep Deprivation - physiology; sleep EEG; sleep homeostasis; spectral analysis; Treatments; Seasonal affective disorder; sleep deprivation; spectral analysis; sleep homeostasis; sleep EEG; depression; light treatment; Human; Mood disorder; Deprivation; Depression; Electroencephalography; Biological rhythm; Circadian rhythm; Phototherapy; Sleep; Treatment; Seasonal variation; Adult; Female; Season
• ISSN: 0006-3223; 1873-2402
• DOI: 10.1016/0006-3223(95)00656-7

The role of sleep regulation in Seasonal Affective Disorder (SAD) was studied in 11 female SAD patients and eight controls in winter before and after light treatment (LT, 6000 lux, 10–14h, 5 days). The sleep electroencephalogram (EEG) was recorded at baseline and after the total sleep deprivation (TSD) of a 40-h constant routine. The well-known effects of TSD on sleep parameters and on EEG power spectra were replicated, indicating normal homeostatic sleep regulation in SAD. Sleep improved after LT in both groups. Since the condition following LT was the second session, these improvements may be an order effect and/or an effect of LT itself. After LT, sleep EEG spectra of SAD patients, but not of controls, showed modifications resembling those of recovery sleep. Since only SAD patients curtailed their sleep while remitting during the LT period, these EEG modifications can be explained by normal sleep regulation alone. We conclude that the robust antidepressant effect of LT in SAD is unlikely to be mediated by changes in sleep, and that sleep regulatory mechanisms are not a crucial factor in the pathogenesis of winter depression.