Jennifer R Goldschmied1, Philip Cheng2, Roseanne Armitage3, Patricia J Deldin4. 1. Center for Sleep & Circadian Neurobiology, University of Pennsylvania, 125 S.31st St, Philadelphia, PA 19104, United States. Electronic address: jrgolds2@pennmedicine.upenn.edu. 2. Sleep Disorders and Research Center, Henry Ford Health System, 39450 W 12 Mile Rd, Novi MI 48377, United States. Electronic address: pcheng1@hfhs.org. 3. Department of Psychiatry, University of Michigan, 4250 Plymouth Rd, Ann Arbor, MI 48109, United States. Electronic address: roseanne.armitage@sbcglobal.net. 4. Department of Psychiatry, University of Michigan, 4250 Plymouth Rd, Ann Arbor, MI 48109, United States. Electronic address: pjdeldin@umich.edu.
Abstract
BACKGROUND: Both EEG slow-wave activity (SWA) during sleep and EEG theta activity during waking have been shown to increase with extended waking, and decrease following sleep, suggesting that both are markers of sleep propensity. In individuals with major depressive disorder (MDD), however, altered patterns of SWA have been noted, suggesting that sleep homeostasis is dysregulated. This study aimed to examine if slow-wave disruption would alter sleep propensity differently in healthy controls (HC) and those with MDD. METHODS: 25 individuals (13 diagnosed with MDD and 12 HC) participated. Following one night of adaptation sleep, participants underwent one night of baseline sleep, and one night of selective slow-wave disruption by auditory stimuli. In the evening, before sleep, and in the morning following sleep, waking EEG was recorded from participants in an upright position, with eyes open. RESULTS: Repeated measures ANOVA revealed a significant three-way interaction, such that AM theta activity was significantly lower following slow-wave disruption in those with MDD, but not in HC. Additionally, SWA was not correlated with theta activity in MDD. LIMITATIONS: These data are based on a relatively small sample size of unmedicated individuals with MDD. CONCLUSIONS: These data may suggest that SWA plays a differential role in the homeostatic regulation of sleep in HC, and in MDD, and provide additional evidence that the presence of SWA may be maladaptive in MDD.
BACKGROUND: Both EEG slow-wave activity (SWA) during sleep and EEG theta activity during waking have been shown to increase with extended waking, and decrease following sleep, suggesting that both are markers of sleep propensity. In individuals with major depressive disorder (MDD), however, altered patterns of SWA have been noted, suggesting that sleep homeostasis is dysregulated. This study aimed to examine if slow-wave disruption would alter sleep propensity differently in healthy controls (HC) and those with MDD. METHODS: 25 individuals (13 diagnosed with MDD and 12 HC) participated. Following one night of adaptation sleep, participants underwent one night of baseline sleep, and one night of selective slow-wave disruption by auditory stimuli. In the evening, before sleep, and in the morning following sleep, waking EEG was recorded from participants in an upright position, with eyes open. RESULTS: Repeated measures ANOVA revealed a significant three-way interaction, such that AM theta activity was significantly lower following slow-wave disruption in those with MDD, but not in HC. Additionally, SWA was not correlated with theta activity in MDD. LIMITATIONS: These data are based on a relatively small sample size of unmedicated individuals with MDD. CONCLUSIONS: These data may suggest that SWA plays a differential role in the homeostatic regulation of sleep in HC, and in MDD, and provide additional evidence that the presence of SWA may be maladaptive in MDD.