Effects of slow-wave activity on mood disturbance in major depressive disorder.

BACKGROUND: Studies have demonstrated that decreases in slow-wave activity (SWA) predict decreases in depressive symptoms in those with major depressive disorder (MDD), suggesting that there may be a link between SWA and mood. The aim of the present study was to determine if the consequent change in SWA regulation following a mild homeostatic sleep challenge would predict mood disturbance. METHODS: Thirty-seven depressed and fifty-nine healthy adults spent three consecutive nights in the sleep laboratory. On the third night, bedtime was delayed by 3 h, as this procedure has been shown to provoke SWA. The Profile of Mood States questionnaire was administered on the morning following the baseline and sleep delay nights to measure mood disturbance. RESULTS: Results revealed that following sleep delay, a lower delta sleep ratio, indicative of inadequate dissipation of SWA from the first to the second non-rapid eye movement period, predicted increased mood disturbance in only those with MDD. CONCLUSIONS: These data demonstrate that in the first half of the night, individuals with MDD who have less SWA dissipation as a consequence of impaired SWA regulation have greater mood disturbance, and may suggest that appropriate homeostatic regulation of sleep is an important factor in the disorder.

Modified Cognitive Behavioral Therapy for Insomnia in Depressed Adolescents: A Pilot Study.

Objective/Background: The purpose of the study was to pilot a five-week insomnia treatment in adolescents with major depressive disorder (MDD) and insomnia. This was an open-label trial of a modified-group cognitive behavioral therapy for insomnia (CBTI). Participants: Adolescents with MDD (n = 16; mean age = 17.3 +/- 1.7), characterized by the Children's Depression Rating Scale-Revised T-score ≥ 55 and insomnia, characterized by > 30 min to fall or return to sleep and an Insomnia Severity Index (ISI) score of ≥ 7 participated. Methods: Sleep diaries, actigraphy, weekly ISI, Quick Inventory of Depressive Symptomatology (QIDS), and Multidimensional Fatigue Inventory (MFI) were completed. Results: Paired t-tests comparing pre- and posttreatment revealed a decrease in sleep onset latency from 41 min +/- 14 min to 18 min +/- 8.9 min (t = 5.9, p = .004). Linear mixed modeling across sessions revealed that ISI (B = 11.0, SE = 0.94, p < .001), QIDS (B = 11.3, SE = 0.96, p < .001), and MFI (B = 30.0, SE = 4.4, p < .001) improved across treatment. Daily sleep diaries showed decreased wake during the night (B = 22.8, SE = 7.19, p = .008), increased sleep time (B = 382.4, SE = 71.89, p < .001), and increased quality of sleep (B = 3.7, SE = 0.37, p < .001). When asked whether group members would recommend this group, 27% responded "yes" and 73% responded "definitely yes." Conclusions: Additional controlled studies utilizing sleep-focused therapy in depressed adolescents with insomnia are warranted.

Insomnia as a Moderator of Response to Time in Bed Restriction for Augmenting Antidepressant Treatment: A Preliminary Investigation.

BACKGROUND: There are complex, bidirectional associations between major depressive disorder and insomnia. In the present study, we evaluated insomnia as a moderator of response to antidepressant therapy in the context of a sleep manipulation (time in bed restriction) for major depressive disorder. METHODS: Fifty-eight adults with major depressive disorder received 8 weeks of fluoxetine 20-40 mgs and were randomized to 8 hr time in bed (8h TIB) or 6 hr time in bed (6h TIB) for the first 2 weeks (participants in the 6h TIB condition were further randomized to a delayed bedtime (Late Bedtime) or advanced rise time (Early Rise Time) group). Insomnia was assessed at baseline using the Insomnia Severity Index. Depression symptom severity was determined by the clinician-rated 17-item Hamilton Rating Scale for Depression (HAMD-17), completed weekly. RESULTS: A group by time interaction was observed whereby HAMD-17 scores were higher for participants assigned to the 6h TIB group (without insomnia, weeks 3 through 7; with insomnia from week 3 through 6, ps < .05) relative to participants without insomnia assigned to the 8h TIB group. There were no differences in HAMD-17 scores for participants with insomnia in the 6h TIB group relative to the 8h TIB group. CONCLUSION: These preliminary findings suggest that response to fluoxetine may be hindered by TIB restriction in individuals without insomnia. Individuals with insomnia respond similarly to fluoxetine regardless of whether their TIB is restricted. Limitations include exclusive use of self-report measures to categorize insomnia, and small sample sizes in several of the subgroups.

Slow-wave disruption enhances the accessibility of positive memory traces.

The purpose of this study was to explore the effects of slow-wave disruption on positive and negative word recognition in a sample of healthy control participants and those with major depressive disorder. Prior to sleep, participants learned a set of emotional and neutral words during an encoding task by responding whether or not the word described them. Following baseline sleep, participants underwent one night of selective slow-wave disruption by auditory stimuli. Accuracy and reaction time to a recognition word set, including both positive and negative words, was assessed in the morning. Repeated-measures ANOVA revealed a significant interaction between word valence and condition, with positive words recognized significantly faster than negative words after disruption, in only healthy control participants. There were no significant results in those with major depressive disorder, or with regard to accuracy. These results may add to the increasing body of literature suggesting a hedonic bias to positive stimuli following sleep disruption.

Examining the effects of sleep delay on depressed males and females and healthy controls.

Individuals with major depressive disorder typically exhibit sleep electroencephalograpy abnormalities which have been shown to vary by sex. Recent research has shown that depressed males display deficits in slow wave sleep and delta electroencephalograph (EEG) activity that are not apparent in depressed females. This may suggest that males and females with depression vary with respect to their homeostatic regulation of sleep. Utilizing archival data, the present study examined the effects of a 3-h sleep delay, which represents a mild sleep challenge, on slow wave activity in healthy controls and individuals with depression. All participants slept in the laboratory for three sequential nights. On the third night in the laboratory, the participants' bedtime was delayed by 3 h. Slow wave activity was calculated utilizing power spectral analysis and compared across groups. Following the sleep delay, males with depression exhibited the lowest slow wave activity compared to all other groups. These results may suggest that males with depression are at a greater risk for homeostatic dysregulation than females, and may require specialized intervention.

Representativeness of obstetric patients who participate in perinatal depression research: findings from the Women's Mental Health and Infants Program (WMHIP) integrated dataset.

The aims of this study were to evaluate the feasibility of integrating archival datasets from depression projects involving pregnant women recruited from obstetric clinics and then assess the representativeness of the integrated dataset. Datasets from six studies were standardized and integrated. Chi-square, t-, and Wilcoxon rank-sum tests were used to compare characteristics between women who completed a depression screening questionnaire (DSQ) and were (1) eligible and ineligible for research participation and (2) eligible women who accepted and declined participation. The integrated dataset comprises 9,112 pregnant women, of whom 71.0 % (n = 6,472) were ineligible for participation because their DSQ scores indicated no-to-minimal depressive symptoms (NDS). Among the 23.9 % (2,176) of women identified as eligible, in part, because their DSQ scores indicated elevated levels of depressive symptoms (EDS), 29.6 % (644) of women participated (P-EDS) and 47.6 % (1,036) of women did not participate (D-EDS). While the NDS and EDS groups were significantly different on almost all variables, the P-EDS and D-EDS groups were significantly different on only a few variables. Compared to the D-EDS group, the P-EDS group was earlier in pregnancy and, on the Edinburgh Postnatal Depression Screen, was more likely to endorse impaired "ability to laugh" and "enjoy oneself", and endorse at greater severity "ability to laugh." It is a reasonable and feasible strategy to integrate thematically similar datasets to increase statistical power. Additionally, typical recruitment strategies for minimal risk perinatal depression research at obstetric clinics, during routine prenatal care visits, appear to produce an externally valid study cohort.

Sleep-disordered breathing in major depressive disorder.

Individuals with major depressive disorder often experience obstructive sleep apnea. However, the relationship between depression and less severe sleep-disordered breathing is unclear. This study examined the rate of sleep-disordered breathing in depression after excluding those who had clinically significant sleep apnea (>5 apneas∙h⁻¹). Archival data collected between 1991 and 2005 were used to assess the prevalence of sleep-disordered breathing events in 60 (31 depressed; 29 healthy controls) unmedicated participants. Respiratory events were automatically detected using a program developed in-house measuring thermal nasal air-flow and chest pressure. Results show that even after excluding participants with clinically significant sleep-disordered breathing, individuals with depression continue to exhibit higher rates of sleep-disordered breathing compared with healthy controls (depressed group: apnea-hypopnea index mean = 0.524, SE = 0.105; healthy group: apnea-hypopnea index mean = 0.179, SE = 0.108). Exploratory analyses were also conducted to assess for rates of exclusion in depression studies due to sleep-disordered breathing. Study exclusion of sleep-disordered breathing was quantified based on self-report during telephone screening, and via first night polysomnography. Results from phone screening data reveal that individuals reporting depression were 5.86 times more likely to report a diagnosis of obstructive sleep apnea than presumptive control participants. Furthermore, all of the participants excluded for severe sleep-disordered breathing detected on the first night were participants with depression. These findings illustrate the importance of understanding the relationship between sleep-disordered breathing and depression, and suggest that screening and quantification of sleep-disordered breathing should be considered in depression research.

An open pilot of cognitive-behavioral therapy for insomnia in women with postpartum depression.

Sleep disturbances and depression are commonly experienced by postpartum women. We evaluated the preliminary efficacy of a modified version of cognitive-behavioral therapy for insomnia on mood, sleep, and fatigue in postpartum women with insomnia and depression in an open pilot study. Twelve postpartum women participated in five weekly individual treatment sessions. Statistically significant improvements were observed in sleep diary-rated sleep efficiency and total wake time, and subjective mood, insomnia severity, sleep quality, and fatigue. Further evaluation of the treatment using a controlled design is warranted.

Screening for depression, sleep-related disturbances, and anxiety in patients with adenocarcinoma of the pancreas: a preliminary study.

PURPOSE: Screening for depression, sleep-related disturbances, and anxiety in patients with diagnosed adenocarcinoma of the pancreas. MATERIALS AND METHODS: Patients were evaluated at initial consultation and subsequent visits at the multidisciplinary pancreatic cancer clinic at our University Cancer Center. Cross-sectional and longitudinal psychosocial distress was assessed utilizing Personal Health Questionnaire 9 (PHQ9) to screen for depression and monitor symptoms, the Penn State Worry Questionnaire (PSWQ) for generalized anxiety, and the University of Michigan Sleep Questionnaire to monitor sleep symptoms. RESULTS: Twenty-two patients diagnosed with pancreatic cancer participated during the 6-month pilot study with longitudinal followup for thirteen patients. In this study, mild-to-moderate depressive symptoms, anxiety, and potential sleep problems were common. The main finding of the study was 23% of the patients who were part of this pilot project screened positive for moderately severe major depressive symptoms, likely anxiety disorder or a potential sleep disorder during the study. One patient screened positive for moderately severe depressive symptoms in longitudinal followup. CONCLUSIONS: Depression, anxiety, and sleep problems are evident in patients with pancreatic cancer. Prospective, longitudinal studies, with larger groups of patients, are needed to determine if these comorbid symptoms impact outcome and clinical course.

Sleep homeostasis in alcohol-dependent, depressed and healthy control men.

Visually scored and power spectral analyses (PSA) of polysomnography (PSG) recordings reveal abnormalities in alcohol dependence (AD) and major depressive disorder (MDD), including deficiencies in slow wave activity (SWA) during non-rapid eye movement (NREM) sleep. SWA parameters reflect the integrity of the homeostatic sleep drive, which have not been compared in those with AD or MDD. Ten men with AD were compared with 10 men with MDD and 10 healthy controls (HCs), all aged 20-40 years. They maintained an 11 pm to 6 am sleep schedule for 5-7 days, followed by 3 consecutive nights of PSG in the laboratory: night 1 for adaptation/screening; night 2 for baseline recordings; and night 3 as the challenge night, delaying sleep until 2 am. SWA was quantified with PSA across 4 NREM periods. Men with AD generated the least SWA at baseline. In response to sleep delay, HC men showed the expected SWA enhancement and a sharper exponential decline across NREM periods. Both the MDD and the AD groups showed a significantly blunted SWA response to sleep delay. Men with MDD had the least SWA in the first NREM period (impaired accumulation of sleep drive), whereas men with AD had the slowest SWA decay rate (impaired dissipation of sleep drive). These results suggest that both SWA generation and its homeostatic regulation are impaired in men with either AD or MDD. Finding interventions that selectively improve these different components of sleep homeostasis should be a goal of treatment for AD and MDD.

Maternal mood and sleep in children of women at risk for perinatal depression.

Few studies have examined relationships between perinatal depression and sleep in offspring beyond very early childhood. Eighty-five women classified as high risk for major depressive disorder during pregnancy completed measures of mood and their child's sleep 4-7 years postpartum. Mothers with Beck Depression Inventory-II (BDI-II) scores ≥20 reported more sleep problems in their child, and child sleep disruption was a reasonable predictor of maternal BDI-II. More research is needed to determine causal relationships between perinatal depression and sleep in offspring.

Early developmental changes in sleep in infants: the impact of maternal depression.

OBJECTIVES: This study evaluated whether sleep over the first 6 months of life was more disturbed in infants born to mothers who were depressed compared with infants from nondepressed mothers. DESIGN: Actigraphy was recorded for 7 consecutive days starting at 2 weeks postpartum and monthly thereafter until 6 months of age. Mothers completed daily sleep/wake diaries. Sleep data at 2 weeks and 6 months postpartum are presented here. SETTING: The home environment. PARTICIPANTS: Eighteen healthy, full-term infants, 9 males and 9 females. Seven infants were born to women with no personal or family history of depression; 11 infants were born to women diagnosed with depression or with elevated levels of depression symptoms. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Total sleep time, sleep latency, sleep efficiency, and number and duration of sleep episodes were computed for nocturnal and daytime sleep in each 24-hour block. Data were coded for risk group (1 = low risk, 2 = high risk), and repeated-measures multivariate analysis of variance contrasted changes in sleep measures at Week 2 and Week 24, between risk groups. The high-risk infants took longer to fall asleep, had lower sleep efficiencies, and had more sleep bouts in the nocturnal sleep period than did low-risk infants. These effects persisted at 6 months postpartum. CONCLUSIONS: Maternal depression is associated with significant sleep disturbance in infancy at 2 weeks postpartum that continues through 24 weeks. It remains to be determined if sleep disturbance in infancy confers a greater risk of developing early-onset depression in childhood.

Power spectral analysis of sleep EEG in twins discordant for chronic fatigue syndrome.

OBJECTIVE: The purpose of the study was to evaluate quantitative sleep electroencephalogram (EEG) frequencies in monozygotic twins discordant for chronic fatigue syndrome. METHODS: Thirteen pairs of female twins underwent polysomnography. During the first night, they adapted to the sleep laboratory, and during the second night, their baseline sleep was assessed. Visual stage scoring was conducted on sleep electroencephalographic records according to standard criteria, and power spectral analysis was used to quantify delta through beta frequency bands, processed in 6-s blocks. Data were averaged across sleep stage within each twin and coded for sleep stage and the presence or absence of chronic fatigue syndrome (CFS). A completely within-subjects repeated measure multivariate analysis of variance evaluated twin pairs by frequency band by sleep stage interactions and simple effects. The relationship between alpha and delta EEG was also assessed across twin pairs. RESULTS: No significant differences in spectral power in any frequency band were found between those with CFS and their nonfatigued cotwins. Phasic alpha activity, coupled with delta was noted in five subjects with CFS but was also present in 4/5 healthy twins, indicating this finding likely reflects genetic influences on the sleep electroencephalogram rather than disease-specific sleep pathology. CONCLUSIONS: The genetic influences on sleep polysomnography and microarchitecture appear to be stronger than the disease influence of chronic fatigue syndrome, despite greater subjective sleep complaint among the CFS twins. EEG techniques that focus on short duration events or paradigms that probe sleep regulation may provide a better description of sleep abnormalities in CFS.

Relationships between the number of ultradian cycles and key sleep variables in outpatients with major depressive disorder.

The regulation of the alternation between rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) is still a matter of much debate. It is also an important topic for psychiatric research, since both sleep components show anomalies in Major Depressive Disorders (MDD) and related syndromes. In previous studies on healthy controls, we showed preferential links of the number of ultradian cycles with REMS-related variables rather than with NREMS-related variables. REMS Latency (RL), for example, was shown to be inversely related to the number of cycles. The present study replicates these analyses in a group of 29 patients with MDD (age range: 23-56; 16 females), after two adaptation nights. Results showed significant correlations between the number of cycles and REMS, and between the number of cycles and RL, whereas correlations with NREMS were not significant. This indirectly supports regulation hypotheses considering REMS as the main focus of the oscillation, inhibiting and interrupting NREMS. Also, when the RL is shorter, there are more ultradian cycles than when the RL is long. This adds an interesting element in the elucidation of the physiological meaning of anomalies of RL.

A preliminary investigation of the role of slow-wave activity in modulating waking EEG theta as a marker of sleep propensity in major depressive disorder.

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.

Sleep architecture in adolescents hospitalized during a suicidal crisis.

OBJECTIVE/BACKGROUND: Rates of suicide attempts in Canadian youths are concerning. Adolescence is a sensitive period for the emergence of both sleep and mood problems, two major risk factors for suicidality. This naturalistic study aimed to define the sleep profile of adolescents under the combined influence of suicidality, depression and pharmacotherapy during hospitalization for a suicidal crisis. PATIENTS/METHODS: Seventeen suicidal adolescents (15.0 + 1.2years, 82% females) with major depression were recruited from a Canadian pedopsychiatric inpatient unit. Seventeen non-depressed adolescents were retrospectively collated from another database (15.0 + 1.1years, 83% females). None of the participants had a history of sleep disorders or significant medical conditions. RESULTS: Compared to controls, suicidal adolescents had a longer sleep onset latency (Z = -4.5, p < 0.001), longer REM latency (Z = -3.2, p = 0.001), higher percentage of NREM1 sleep t(33) = -2.6, p = 0.020), and higher REM density (Z = -2.8, p = 0.004) than controls. Higher REM density correlated with higher CDI-II scores (r = 0.55, p = 0.27) A significant interaction indicated that the two groups had similar NREM3 percentages in the first two-thirds of the night, but that the suicidal group had significantly lower NREM3 percentage than the controls in the last third of the night (F(2,66) = 3.4, p = 0.041). CONCLUSIONS: Significant sleep abnormalities were observed during hospitalization for a suicidal crisis in a sample of depressed and mostly medicated adolescents. This included sleep initiation and REM sleep latency abnormalities, shallower sleep and high REM density. Future studies should decipher the relative effects of depression, suicidality and medication on sleep. These findings stress the need to address sleep disturbances in the management of suicidality in adolescents.

Salivary melatonin onset in youth at familial risk for bipolar disorder.

Melatonin secretion and polysomnography (PSG) were compared among a group of healthy adolescents who were at high familial risk for bipolar disorder (HR) and a second group at low familial risk (LR). Adolescent participants (n = 12) were a mean age 14 ± 2.3 years and included 8 females and 4 males. Saliva samples were collected under standardized condition light (red light) and following a 200 lux light exposure over two consecutive nights in a sleep laboratory. Red Light Melatonin onset (RLMO) was defined as saliva melatonin level exceeding the mean of the first 3 readings plus 2 standard deviations. Polysomnography was also completed during each night. HR youth, relative to LR, experienced a significantly earlier melatonin onset following 200 lux light exposure. Polysomnography revealed that LR youth, relative to HR, spent significantly more time in combined stages 3 and 4 (deep sleep) following red light exposure. Additionally, regardless of the group status (HR or LR), there was no significant difference in Red Light Melatonin Onset recorded at home or in the laboratory, implying its feasibility and reliability.

The impact of a 4-hour sleep delay on slow wave activity in twins discordant for chronic fatigue syndrome.

OBJECTIVES: Chronic fatigue syndrome (CFS) has been associated with altered amounts of slow wave sleep, which could reflect reduced delta electroencephalograph (EEG) activity and impaired sleep regulation. To evaluate this hypothesis, we examined the response to a sleep regulatory challenge in CFS. DESIGN: The first of 3 consecutive nights of study served as laboratory adaptation. Baseline sleep was assessed on the second night. On the third night, bedtime was delayed by 4 hours, followed by recovery sleep. Total available sleep time was held constant on all nights. SETTING: A research sleep laboratory. PARTICIPANTS: 13 pairs of monozygotic twins discordant for CFS. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Power spectral analysis quantified slow wave activity (SWA) in the 0.5-3.9 Hz band in successive NREM periods (stage 2, 3, or 4) on each night. To ensure comparability, analyses were restricted to the first 4 NREM periods on each night. Data were coded for NREM period and twin pair. Repeated-measures analysis of variance (ANOVA) contrasted sleep delay effects across NREM periods between twin pairs. A second ANOVA calculated the SWA in each NREM period in recovery sleep relative to baseline SWA. The 2 groups of twins were similar on baseline SWA power. After sleep delay, CFS twins exhibited significantly less SWA power in the first NREM period of recovery sleep and accumulated a smaller percentage of SWA in the first NREM period than their co-twins. CONCLUSIONS: CFS is associated with a blunted SWA response to sleep challenge, suggesting that the basic sleep drive and homeostatic response are impaired.

An open trial of cognitive-behavioral treatment for insomnia comorbid with alcohol dependence.

OBJECTIVE: We evaluated the efficacy of cognitive-behavioral treatment for insomnia in recovering alcoholic patients in an open pilot study. METHODS: Seven abstinent alcoholic patients (3 women, mean age 38.6+/-10.8 years) recruited from outpatient and residential treatment facilities met the Diagnostic and Statistic Manual of Mental Disorders - Fourth edition (DSM-IV) criteria for insomnia comorbid with alcohol dependence and participated in eight individual treatment sessions. Participants were free of other medical, psychiatric, and sleep disorders. Daily sleep diaries were completed beginning two weeks before treatment until two weeks after treatment. Measures of sleep, daytime functioning, and drinking were collected. RESULTS: Diary-rated sleep latency [F(2,10)=14.4, p<.001], wake after sleep onset [F(2,10)=7.7, p=.009], and sleep efficiency [F(2,10)=28.3, p<.001] improved as did patient-rated and clinician-rated Insomnia Severity Index (ISI) and the Dysfunctional Beliefs and Attitudes about Sleep - Short Form (DBAS-SF). Compared to pre-treatment, significant post-treatment improvements were found on scales measuring depression and anxiety symptoms, fatigue, and quality of life. No one relapsed to alcohol during treatment. CONCLUSIONS: Cognitive-behavioral insomnia therapy may benefit recovering alcoholics with mild to moderate insomnia by improving sleep and daytime functioning. Effects on relapse remain to be determined. Findings need to be interpreted cautiously due to the uncontrolled design and lack of follow-up assessments.

Neurophysiological correlates of suicidal ideation in major depressive disorder: Hyperarousal during sleep.

BACKGROUND: Suicide is a major public health concern, and a barrier to reducing the suicide rate is the lack of objective predictors of risk. The present study considers whether quantitative sleep electroencephalography (EEG) may be a neurobiological correlate of suicidal ideation. METHODS: Participants included 84 (45 female, mean age=26.6) adults diagnosed with major depressive disorder (MDD). The item that measures thoughts of death or suicide on the Quick Inventory of Depressive Symptomatology (QIDS) was used to classify 47 participants as low suicidal ideation (24 females, mean age=26.1) and 37 as high suicidal ideation (21 females, mean age=27.3). Data were obtained from archival samples collected at the University of Michigan and University of Texas Southwestern Medical Center between 2004 and 2012. Sleep EEG was quantified using power spectral analysis, and focused on alpha, beta, and delta frequencies. RESULTS: Results indicated that participants with high compared to low suicidal ideation experienced 1) increased fast frequency activity, 2) decreased delta activity, and 3) increased alpha-delta sleep after adjusting for age, sex, depression, and insomnia symptoms. LIMITATIONS: Limitations include the exclusion of imminent suicidal intent, a single suicidal ideation item, and cross-sectional archival data. CONCLUSIONS: This is one of the first studies to provide preliminary support that electrophysiological brain activity during sleep is associated with increased suicidal ideation in MDD, and may point toward central nervous system (CNS) hyperarousal during sleep as a neurobiological correlate of suicidal ideation.