SLEEP 2011 Abstract Supplement

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B. Clinical Sleep Science IX. Psychiatric and Behavioral Disorders and Sleep Introduction: Abnormalities in slow wave activity (SWA) have been described in major depressive disorder (MDD), suggesting altered sleepwake homeostasis. Little is known, however, about how waking EEG tracings in MDD are affected by sleep. We examined spontaneous waking high-density electroencephalogram (hd-EEG) recordings and their relationship to slow wave activity during sleep. Methods: 12 right-handed MDD subjects (9 female) and 12 age and sex matched controls were analyzed, taken from a larger study on sleep homeostasis in depression. Two minutes of spontaneous waking hd-EEG (256 channel) was collected in the evening prior to sleep and the mornlowship Program. The authors’ views or opinions do not necessarily represent those of the Department of Veterans Affairs (VA). 0738 ALTERED SLOW WAVE AND SPINDLE RANGE ACTIVITY IN MAJOR DEPRESSION: PRELIMINARY HIGH-DENSITY EEG FINDINGS Wanger TJ, Landsness EC, Plante DT, Goldstein MR, Guokas JJ, Tononi G, Benca R Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA Introduction: Abnormalities in slow wave activity (SWA) and sleep spindle activity have been previously described in major depressive disorder (MDD). We utilized high-density EEG (hd-EEG) to investigate topographic differences in these parameters between MDD and control subjects during sleep. Methods: Unmedicated MDD subjects (n=28; 10 men) and age and sexmatched controls were recruited. Subjects underwent overnight hd-EEG (256 channel) polysomnography. The EEG data were filtered, FFTs performed, and data visually inspected and manually cleaned of artifact. Unpaired t-tests and statistical non-parametric mapping (SnPM) were used to evaluate for topographic differences in SWA and spindle range activity (SRA). Results: All-night SWA normalized to the power in all channels was greater in frontal and lower in posterior channels in MDD subjects relative to controls. SnPM using cluster threshold confirmed the posterior decrease, but not the frontal increase in SWA in MDD. Normalized allnight spindle range activity (12-15 Hz) was greater in frontal regions in MDD subjects relative to controls, but SnPM did not confirm this result. Neither SWA nor SRA findings correlated with age or depression severity. Conclusion: These preliminary findings suggest altered topographic SWA and SRA activity in depression. Further research is indicated to confirm these findings and determine if these findings are specific to subtypes of depression. Support (If Any): This research was funded by the National Institute of Mental Health (5P20MH077967 to GT and RB, and F30MH082601 to EL). 0739 ALTERED SLOW-WAVE ACTIVITY HOMEOSTASIS IN MAJOR DEPRESSIVE DISORDER WITH HYPERSOMNOLENCE: A HIGH DENSITY EEG PILOT STUDY Plante DT, Landsness EC, Peterson MJ, Goldstein MR, Wanger TJ, Guokas JJ, Tononi G, Benca R Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA Introduction: Hypersomnia is a common symptom of major depressive disorder (MDD) that increases the risk of incident depression and may be a residual symptom after resolution of a depressive episode. The pathophysiologic mechanisms underlying hypersomnia in mood disorders are unknown. This post hoc pilot study explored possible high density EEG (hd-EEG) markers that might distinguish MDD with hypersomnolence (MDD-HYS) from healthy controls and MDD with insomnia (MDD-INS). Methods: MDD-HYS subjects (n=8; 5 men) and age- and sex-matched MDD-INS subjects and controls were selected from a larger study on sleep homeostasis in depression. Hypersomnia was defined as a selfreport of sleeping ≥10 hours per day; insomnia as subjective report of difficulty initiating or maintaining sleep. Subjects underwent overnight hd-EEG (256 channel) polysomnography. EEG data were filtered, FFTs performed, and data visually inspected to remove artifact. Statistical analysis included ANOVA and post hoc unpaired t-tests to explore differences between groups in absolute and normalized slow wave activity (SWA; 1-4.5 Hz) during NREM sleep. Results: Left frontal all-night SWA normalized to the power in all channels was significantly higher in MDD-HYS (1.57±0.30) compared to controls (1.15±0.19, p=0.005) and MDD-INS (1.28±0.12, p=0.024). When examining absolute SWA in frontocentral regions for the first 30 minutes of NREM sleep, power was significantly lower in MDD-HYS compared to MDD-INS (29.6μV±13.7 vs. 66.6μV±23.9, p=0.016). No differences in absolute SWA were evident at the end of the night, suggesting a greater homeostatic dissipation of SWA in MDD-INS compared to MDD-HYS. Conclusion: This pilot study suggests there may be alterations in SWA topography and dissipation across the night that segregate depressed subjects with hypersomnia from those with insomnia and healthy controls. Further research is indicated to replicate this finding and determine if hd-EEG findings correlate with hypersomnia severity. Support (If Any): This research was funded by the National Institute of Mental Health (5P20MH077967 to GT and RB, and F30MH082601 to EL) and the National Alliance for Research on Schizophrenia and Depression Young Investigator Award to MP. 0740 CORDANCE AS A BIOMARKER IN SLEEP-EEG FOR DEPRESSION: DIFFERENCES IN RESPONDERS VERSUS NON-RESPONDERS - A NATURALISTIC STUDY AFTER ANTIDEPRESSANT MEDICATION Pawlowski M, Dresler M, Steiger A Max-Planck-Institut for Psychiatry, Munich, Germany Introduction: Cordance is a relatively new quantitative EEG-method, which has shown usability as a biomarker for depression within the resting-state in wake patients. Sleep EEG shows distinctive alterations in a depressive episode and changes after antidepressants. We wanted to test whether differences in Cordance derived from sleep EEG exist between responders and non-responders after antidepressant medication. Methods: 20 in-patients with a depressive episode [ICD-10 F 31.4, F 32.1-3, F 33.1-3] were treated with various antidepressants of “doctor’s choice”. The change of the Hamilton depression scores between the first and fifth week of treatment provided evidence about response. Response to treatment was defined as a ≥ 50 % reduction of Hamilton score. Cordance values for the prefrontal theta-EEG were calculated from sleep EEG during the first week with active medication. Results: Results showed significant differences: 8 responders compared to 12 non-responders showed higher Cordance values in prefrontal EEG-sites (z-score -1,57 ± 0.79 versus -2,64 ± 0,69, p = 0.0055). Conclusion: These results suggest that Cordance derived from sleep EEG provides a biomarker for depression. 0741 DIFFERENCES IN SPONTANEOUS WAKING EEG BETWEEN CONTROLS AND SUBJECTS WITH DEPRESSION Guokas JJ, Landsness EC, Wanger TJ, Plante DT, Goldstein MR, Tononi G, Benca R Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA SLEEP, Volume 34, Abstract Supplement, 2011 A254
B. Clinical Sleep Science IX. Psychiatric and Behavioral Disorders and Sleep ing after sleep with subjects seated and eyes closed. The intervening sleep was recorded. Analyses used unpaired t-tests and Pearson correlations. Results: When examining global EEG power in the evening and morning, no differences were found between controls and MDD subjects. However, MDD subjects had a weaker low frequency power (2-8Hz) frontocentrally, both in the evening and morning. Next we examined the decline in waking power from evening to morning. Control subjects showed an overnight decline in low (1.5-7.5Hz) and high (9.5-37Hz) frequencies, whereas MDD subjects did not show a decline below 8 Hz, although they did decline in the 10-33Hz range. In controls, overnight change in waking theta and alpha power correlated to sleep SWA in the frontocentral region. In contrast, MDD subjects did not exhibit global or regional correlations of changes in waking theta and alpha power with sleep SWA. Conclusion: This study suggests that changes in waking EEG traces in healthy subjects that correlate with sleep homeostatic decline are altered in MDD. Further studies are needed to better assess altered sleep-wake homeostasis in depression and to determine if these findings are specific to subtypes of depression. Support (If Any): This research was funded by the National Institute of Mental Health (5P20MH077967 to GT and RB, F30MH082601 to EL) 0742 OVERNIGHT CHANGES IN AUDITORY EVOKED POTENTIAL AMPLITUDE REFLECT ALTERED SLEEP HOMEOSTASIS IN MAJOR DEPRESSION Goldstein MR 1 , Sarasso S 1 , Landsness EC 1 , Plante DT 1 , Hulse BK 2 , Laing HK 1 , Tononi G 1 , Benca R 1 1 Department of Psychiatry, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA, 2 Department of Biology, California Institute of Technology, Pasadena, CA, USA Introduction: Previous research has demonstrated that waking auditory evoked potential (AEP) amplitude declines after a night of sleep and that the overnight reduction in AEP amplitude correlates with the amount of sleep slow wave activity (SWA), suggesting that changes in the AEP waveform may reflect a homeostatic process related to sleep. Because major depressive disorder (MDD) may involve altered sleep homeostasis, we investigated overnight changes in AEPs and their relation to sleep SWA in MDD and matched controls. Methods: As part of a larger study on sleep homeostasis in depression, pre- and post-sleep single-tone, waking AEPs and all-night sleep recordings with 256-channel high-density EEG were analyzed for 11 righthanded, non-medicated MDD participants (8 female) and 11 age- and sex-matched controls. Overnight changes in amplitude and latency for N1 and P2 components were analyzed with paired t-tests for each group, while their relationships with sleep spectral power were calculated with a Pearson correlation. Results: A significant pre- to post-sleep decline in N1 amplitude was observed for healthy controls (p < .05), but not for the MDD group. Moreover, the overnight change in N1 amplitude correlated with sleep SWA (1-4.5Hz) only for the control group (p < .02); more SWA predicted a greater reduction in amplitude. No significant differences before and after sleep were detected for P2 amplitude, N1 latency, or P2 latency for either group. Conclusion: These results support the notion that the overnight decline in N1 amplitude may reflect a sleep-related homeostatic process and suggest that MDD involves altered regulation of such homeostasis. Importantly, these findings indicate that single-tone AEPs, combined with high-density EEG, may provide a useful measure for investigating sleep homeostasis in depression. Subsequent research is required to corroborate these findings, and to examine the potential utility of AEPs in categorizing MDD in terms of subgroups and predicting treatment response. Support (If Any): This research was funded by the National Institute of Mental Health (5P20MH077967 to GT and RB, and F30MH082601 to EL). 0743 EFFECTS OF EARLY AND LATE PARTIAL SLEEP DEPRIVATION ON SLEEP AND SLOW-WAVE ACTIVITY (SWA) IN MAJOR DEPRESSIVE DISORDER Arnedt J, Swanson L, Bertram H, Mooney A, Dopp R, Hoffmann RF, Armitage R Psychiatry, University of Michigan, Ann Arbor, MI, USA Introduction: Acute total and partial sleep deprivation improve mood in more than half of major depressive disorder (MDD) patients, but relapse is common following recovery sleep and its practicality is limited in outpatient settings. We compared sleep PSG and SWA in MDD participants assigned to a more modest repeated early or late partial sleep deprivation (6 hours TIB) vs. no sleep deprivation (8 hours TIB) in conjunction with antidepressant medication. Methods: Twenty-two subjects meeting DSM-IV criteria for MDD (25.2 ± 6.7 years of age, 9 women, baseline HAMD-17 score 20.2 ± 1.8) have participated to date. Subjects received 8 weeks of fluoxetine 20-40 mg and were randomized to two weeks of no sleep deprivation (NSD, n=7), early partial sleep deprivation (E-PSD, 2-hour delay of bedtime, n=7) or late partial sleep deprivation (L-PSD, 2-hour advance of rise time, n=8). Following an 8-hour at-home sleep schedule, subjects underwent PSG at baseline, on the first and last experimental nights, and on the first recovery night (8 hours TIB). Results: No group differences were found on baseline sleep variables. Total sleep time was reduced in the E-PSD and L-PSD groups compared to NSD on experimental nights vs. baseline (p < .001). Stage N3% increased in the E-PSD group and decreased in the L-PSD and NSD groups (p < .03). REM latency and Stage N1% were elevated and SWA power was decreased on the last experimental night compared to baseline and the first experimental night (p < .001). REM% increased during recovery sleep in the L-PSD group while Stage N2% increased in the E-PSD and NSD groups. Conclusion: The sleep manipulations increased SWS and SWA in the E-PSD group, while fluoxetine increased Stage N1 and prolonged REM latency in all three groups. We are evaluating how the sleep manipulations combined with fluoxetine influence self- and clinician-rated mood. Support (If Any): NIH R01 MH077690 (JT Arnedt) 0744 OBJECTIVE VS. SUBJECTIVE MEASUREMENTS OF SLEEP IN DEPRESSED INSOMNIACS: FIRST NIGHT EFFECT OR REVERSE FIRST NIGHT EFFECT? McCall C 1 , Bowes RC 2,3 , McCall W 4 1 Wake Forest University School of Medicine, Winston-Salem, NC, USA, 2 Department of Clinical Research, Campbell University School of Pharmacy, Buies Creek, NC, USA, 3 Consultant, Philips Respironics, Fuquay Varina, NC, USA, 4 Department of Psychiatry and Behavioral Medicine, Wake Forest University Health Sciences, Winston-Salem, NC, USA Introduction: Many individuals experience worse sleep during their first night in a sleep laboratory compared to succeeding laboratory nights. This “first night effect” is typically characterized by increased sleep onset and REM latency, less REM stage sleep, and lower sleep efficiency. In contrast, other studies have observed a “reverse” first night effect, in which individuals sleep better the first night at the laboratory compared to later nights. Studies investigating laboratory adaptation effects have typically focused on comparing the first night in the laboratory with successive nights in the same environment. This study compared sleep in the laboratory with sleep at home, before and after laboratory monitoring, in depressed insomniacs undergoing treatment. A255 SLEEP, Volume 34, Abstract Supplement, 2011
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