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.

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.

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.

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.

Relationships between circadian measures, depression, and response to antidepressant treatment: A preliminary investigation.

Few studies have examined relationships between circadian rhythms and unipolar major depressive disorder. Further, no study to date has examined circadian markers as predictors of response to depression treatment. In the present study, we examined associations between circadian timing and its alignment with sleep and depression severity in 30 adults with major depressive disorder who completed a randomized controlled trial of two weeks of time in bed (TIB) restriction administered adjunctive to fluoxetine, with a focus on sex differences. Thirty adults with major depressive disorder received 8 weeks of fluoxetine 20-40 mgs and were randomized to 8h TIB or 6h TIB for the first 2 weeks. Participants in the 6h TIB condition were further randomized to a delayed bedtime or advanced risetime group. Circadian measures included dim light melatonin onset (DLMO) and the difference between DLMO and midsleep point (i.e., phase angle difference). Depression was assessed using the Hamilton Rating Scale for Depression. For females, a phase delay after 2 weeks of fluoxetine and the experimental TIB manipulation was associated with a poorer response to fluoxetine, and depression severity was negatively correlated with phase angle difference, whereas males showed a positive correlation between depression severity and phase angle difference.

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.

Effects of Restricted Time in Bed on Antidepressant Treatment Response: A Randomized Controlled Trial.

OBJECTIVE: Antidepressant response onset is delayed in individuals with major depressive disorder (MDD). This study compared remission rates and time to remission onset for antidepressant medication delivered adjunctively to nightly time in bed (TIB) restriction of 6 hours or 8 hours for the initial 2 weeks. METHODS: Sixty-eight adults with DSM-IV-diagnosed MDD (mean ± SD age = 25.4 ± 6.6 years, 34 women) were recruited from September 2009 to December 2012 in an academic medical center. Participants received 8 weeks of open-label fluoxetine 20-40 mg and were randomized to 1 of 3 TIB conditions for the first 2 weeks: 8-hour TIB (n = 19); 6-hour TIB with a 2-hour bedtime delay (late bedtime, n = 24); or 6-hour TIB with a 2-hour rise time advance (early rise time, n = 25). Clinicians blinded to TIB condition rated symptom severity weekly. Symptom severity, remission rates, and remission onset as rated by the 17-item Hamilton Depression Rating Scale were the primary outcomes. RESULTS: Mixed effects models indicated lower depression severity for the 8-hour TIB compared to the 6-hour TIB group overall (F8, 226.9 = 2.1, P < .05), with 63.2% of 8-hour TIB compared to 32.6% of 6-hour TIB subjects remitting by week 8 (χ²1 = 4.9, P < .05). Remission onset occurred earlier for the 8-hour TIB group (hazard ratio = 0.43; 95% CI, 0.20-0.91; P < .03), with no differences between 6-hour TIB conditions. CONCLUSIONS: Two consecutive weeks of nightly 6-hour TIB does not accelerate or improve antidepressant response. Further research is needed to determine whether adequate sleep opportunity is important to antidepressant treatment response. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01545843.

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.

The role of fast and slow EEG activity during sleep in males and females with major depressive disorder.

Sleep difficulties are highly prevalent in depression, and appear to be a contributing factor in the development and maintenance of symptoms. However, despite the generally acknowledged relationship between sleep and depression, the neurophysiological substrates underlying this relationship still remain unclear. Two main hypotheses were tested in this study. The first hypothesis states that sleep in depression is characterized by inadequate generation of restorative sleep, as indexed by reduced amounts of slow-wave activity. Conversely, the second hypothesis states that poor sleep in depression is due to intrusions of fast-frequency activity that may be reflective of a hyperaroused central nervous system. This study aimed to test both hypotheses in a large sample of individuals with clinically validated depression, as well as to examine sex as a moderator. Results suggest that depression is better characterized by an overall decrease in slow-wave activity, which is related to elevated anxious and depressed mood the following morning. Results also suggest that females may be more likely to experience fast frequency activity related to depression symptom severity.

Reduction in delta activity predicted improved negative affect in Major Depressive Disorder.

While prior research has demonstrated a paradoxical antidepressant effect of slow-wave disruption (SWD), the specific dimensions of depression affected is still unclear. The current study aimed to extend this research by utilizing a dimensional approach in examining the antidepressant effects of SWD. Of particular interest is the affective dimension, as negative affect in depression is arguably the most salient characteristic of depression. This sample included 16 individuals with depression (10 female) recruited from the community. Participants slept in the lab for three nights (adaptation, baseline night, and SWD) with polysomnography, and completed measures of negative affect and depression severity the following morning. Results show that reduction in delta power was linearly associated with improved negative affect. Comparison of individual change scores revealed that half of the individuals showed improved negative affect, which is comparable to the reported 40-60% antidepressant response rate to sleep deprivation. Results suggest that vulnerability in the sleep homeostatic system may be a contributing individual differences factor in response to slow-wave disruption in depression.

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.

A preliminary study of slow-wave EEG activity and insulin sensitivity in adolescents.

OBJECTIVE: The objective was to evaluate the relationship between the time course of slow wave EEG activity (SWA) during NREM sleep and insulin sensitivity in adolescents. METHODS: Nine normal weight and nine overweight (BMI>85th percentile) adolescents (13-18 years of age) participated. None of the participants had a history of sleep disordered breathing, confirmed by sleep study. Participants maintained a regularized sleep wake cycle for five days followed by overnight polysomnography in the lab or at home. An oral glucose tolerance test (OGTT) was administered after a 12h fast and within two weeks of the sleep study. Whole body insulin sensitivity (WBISI) and homeostasis model assessment (HOMA-IR) determined insulin resistance. Power spectral analysis quantified slow-wave EEG activity (.05-3.9 Hz) and exponential regression evaluated SWA across successive NREM periods. RESULTS: Those who were insulin resistant and had low insulin sensitivity had less Stages 2, 3 and 4 of NREM sleep, more Stage 1, but did not sleep less than those with low resistance and high sensitivity. SWA power was significantly lower in the first NREM period and the decay rate of SWA across NREM sleep was significantly slower in the low insulin sensitivity group. Similar results were obtained after removing the influence of BMI and Tanner score. CONCLUSIONS: Insulin sensitivity in adolescents is related to SWA power and its time course, not total sleep time, regardless of BMI.

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.

Exercise for adolescents with depressive disorders: a feasibility study.

Objectives. Adolescence is associated with increased depressive symptoms and decreased aerobic exercise, yet the relationship between exercise and clinical depression among adolescents requires further examination. This study assessed the feasibility of a 12-week intervention designed to increase exercise for adolescents with depressive disorders: Will a teenager with depression exercise? Methods. Participants were 13 adolescents with depression reporting low levels of aerobic exercise. They completed a 12-week intervention (15 supervised exercise sessions and 21 independent sessions). Exercise was measured through the aerobic exercise Questionnaire, actigraphy, and heart-rate monitoring. Depression was measured with the Children's Depression Rating Scale, Revised, and Quick Inventory of Depressive Symptomatology, Self-Report. Results. All participants who started the intervention completed the protocol, attending all supervised exercise sessions. Actigraphy verified 81% adherence to the protocol's independent sessions. Analysis of secondary outcomes showed a significant increase in exercise levels and a significant decrease in depression severity. Initially, ten participants were overweight or obese, and three were healthy weight. After 12 weeks of exercise, the number of participants in the healthy-weight category doubled. Conclusions. Adolescents suffering from depression can complete a rigorous protocol requiring structured increases in aerobic exercise. Participants showed significant increases in exercise, and significant decreases in depressive symptoms.

Ultra-slow delta power in chronic fatigue syndrome.

The role of sleep in patients diagnosed with chronic fatigue syndrome is not fully understood. Studies of polysomnographic and quantitative sleep electroencephalographic (EEG) measures have provided contradictory results, with few consistent findings in patients with Chronic Fatigue Syndrome (CFS). For the most part, it appears that delta EEG activity may provide the best discrimination between patients and healthy controls. A closer examination of delta activity in the very slow end of the frequency band is still to be considered in assessing sleep in CFS. The present preliminary study compared absolute and relative spectral power in conventional EEG bands and ultra-slow delta (0.5-0.8Hz) between 10 young female patients with the CFS and healthy controls without psychopathology. In absolute measures, the ultra-slow delta power was lower in CFS, about one-fifth that of the control group. Other frequency bands did not differ between groups. Relative ultra-slow delta power was lower in patients than in controls. CFS is associated with lower ultra-slow (0.5-0.8Hz) delta power, underscoring the importance of looking beyond conventional EEG frequency bands. From a neurophysiological standpoint, lower ultra-slow wave power may indicate abnormalities in the oscillations in membrane potential or a failure in neural recruitment in those with CFS.

Time course of EEG slow-wave activity in pre-school children with sleep disordered breathing: a possible mechanism for daytime deficits?

BACKGROUND: Daytime deficits in children with sleep disordered breathing (SDB) are theorized to result from hypoxic insult to the developing brain or fragmented sleep. Yet, these do not explain why deficits occur in primary snorers (PS). The time course of slow wave EEG activity (SWA), a proxy of homeostatic regulation and cortical maturation, may provide insight. METHODS: Clinical and control subjects (N=175: mean age 4.3±0.9 y: 61% male) participated in overnight polysomnography (PSG). Standard sleep scoring and power spectral analyses were conducted on EEG (C4/A1; 0.5-<3.9Hz). Univariate ANOVA's evaluated group differences in sleep stages and respiratory parameters. Repeated-measures ANCOVA evaluated group differences in the time course of SWA. RESULTS: Four groups were classified: controls (OAHI ≤ 1 event/h; no clinical history); PS (OAHI ≤ 1 event/h; clinical history); mild OSA (OAHI=1-5 events/h); and moderate to severe OSA (MS OSA: OAHI>5 events/h). Group differences were found in the percentage of time spent in NREM Stages 1 and 4 (p<0.001) and in the time course of SWA. PS and Mild OSA children had higher SWA in the first NREM period than controls (p<0.05). All SDB groups had higher SWA in the fourth NREM period (p<0.01). CONCLUSIONS: These results suggest enhanced sleep pressure but impaired restorative sleep function in pre-school children with SDB, providing new insights into the possible mechanism for daytime deficits observed in all severities of SDB.