Even a Mild Sleep Restriction Can Impact Daytime Functioning in Children with ADHD and Their Typically Developing Peers.

OBJECTIVES/BACKGROUND: Correlational studies show that short sleep is associated with negative daytime outcomes in school-aged children, but there are few experimental sleep manipulation studies to assess whether this is a causal relation. The aim of this study was to determine the impact of mild, cumulative sleep restriction on daytime functioning of typically developing (TD) children and children with attention-deficit/hyperactivity disorder (ADHD). PARTICIPANTS: A total of 36 school-aged children (n = 18 TD; n = 18 ADHD), aged 6-11 years participated. METHODS: Children participated in two sleep conditions (order counter-balanced). The Restricted condition required a 1 h reduction of time in bed for one week, and the Controlled Typical condition was based on participant's average baseline sleep. At the end of each condition, participants attended the sleep lab for overnight polysomnography and daytime functioning assessments. RESULTS: Children successfully reduced time in bed by ~1 h. Due to compensatory changes, total sleep time (TST) was reduced by only ~20 min, as children fell asleep faster and spent less time awake after sleep onset during the Restricted compared to Controlled Typical condition. Many daytime functions were not affected by this very mild sleep restriction, however, both groups showed significant changes in performance on an objective attention task and on a parent-rated emotional lability measure after six nights of minimal reductions in TST. There were no significant differences between groups. CONCLUSIONS: Results suggest that a very mild sleep restriction can affect children's attention and emotional regulation, even with evidence of compensatory sleep mechanisms.

Sleep and Inhibitory Control Over Mood-Congruent Information in Emerging Adults With Depressive Disorder.

OBJECTIVE: Accumulating evidence has suggested bidirectionality between sleep problems and depression, but the underlying mechanism is unclear. We assessed the role of sleep in inhibitory control ability with emotional stimuli, which has been shown to be suboptimal among individuals with depression and proposed to perpetuate depressive symptoms. METHODS: Emerging adults (aged 18-25 years, 64.6% female) were screened for depressive and other mental disorders by structured clinical interview and questionnaire. Individuals with depressive disorders were assigned to have a polysomnography-monitored daytime sleep opportunity (Sleep-Dep, n = 20), whereas nondepressed individuals were randomized to either have daytime sleep (Sleep-Ctrl, n = 27) or stay awake (Wake-Ctrl, n = 18). Participants completed the Affective Go/No-Go Task two times, separated by experimental conditions. RESULTS: A factorial model with a between-subject factor (Sleep-Dep/Sleep-Ctrl/Wake-Ctrl) and a within-subject factor (test 1/test 2) was used to assess if the groups differed in inhibitory control across test sessions, as inferred by changes in d-prime and false alarm rates (FA). Results from mixed factorial models showed a significant interaction effect between time and group on FA in the block with neutral faces as the target and happy faces as the nontarget (F(2,61) = 5.15, pfdr = .045). Although Sleep-Dep had decreased FA after sleep (t(19) = 2.94, pfdr = .050), Sleep-Ctrl and Wake-Ctrl had no significant between-session changes (p values > .05). Postsleep improvement in FA in Sleep-Dep correlated with longer stage 2 sleep (r(20) = 0.788, pfdr < .001) and stage 2 fast spindle number at O1 (r(18) = 0.692, pfdr = .015). CONCLUSIONS: Sleep gain, particularly stage 2 sleep and related physiology, potentially enhances inhibitory control ability responding to emotional information among individuals with depressive disorders.

Exponential state transition dynamics in the rest-activity architecture of patients with bipolar disorder.

OBJECTIVE: Our goal was to model the temporal dynamics of sleep-wake transitions, represented by transitions between rest and activity obtained from actigraphic data, in patients with bipolar disorder using a probabilistic state transition approach. METHODS: We collected actigraphic data for 14 days from 20 euthymic patients with bipolar disorder, who had been characterized clinically, demographically, and with respect to their circadian preferences (chronotype). We processed each activity record to generate a series of transitions in both directions between the states of rest (R) and activity (A) and plotted the estimated transition probabilities (pRA and pAR). Each 24-hour period was also divided into a rest phase consisting of the eight consecutive least active hours in each day and an active phase consisting of the 16 consecutive most active hours in each day. We then calculated separate transition probabilities for each of these phases for each participant. We subsequently modeled the rest phase data to find the best fit for rest-activity transitions using maximum likelihood estimation. We also examined the association of transition probabilities with clinical and demographic variables. RESULTS: The best-fit model for rest-activity transitions during the rest phase was a mixture (bimodal) of exponential functions. Of those patients with rapid cycling, 75% had an evening-type chronotype. Patients with bipolar II disorder taking antidepressants had a lower probability of transitioning back to rest than those not on antidepressants [mean ± SD = 0.050 ± 0.006 versus 0.141 ± 0.058, F(1,15) = 3.40, p < 0.05]. CONCLUSIONS: The dynamics of transitions between rest and activity in bipolar disorder can be accounted for by a mixture (bimodal) of exponential functions. Patients taking antidepressants had a reduced probability of sustaining and returning to sleep.

Concordance of actigraphy with polysomnography in children with and without attention-deficit/hyperactivity disorder.

This study sought to: (1) compare actigraphy-derived estimated sleep variables to the same variables based on the gold-standard of sleep assessment, polysomnography; (2) examine whether the correlations between the measures differ between children with attention-deficit/hyperactivity disorder and typically developing children; and (3) determine whether these correlations are altered when children with attention-deficit/hyperactivity disorder are treated with medication. Participants (24 attention-deficit/hyperactivity disorder; 24 typically developing), aged 6-12 years, completed a 1-week baseline assessment of typical sleep and daytime functioning. Following the baseline week, participants in the attention-deficit/hyperactivity disorder group completed a 4-week blinded randomized control trial of methylphenidate hydrochloride, including a 2-week placebo and 2-week methylphenidate hydrochloride treatment period. At the end of each observation (typically developing: baseline; attention-deficit/hyperactivity disorder: baseline, placebo and methylphenidate hydrochloride treatment), all participants were invited to a sleep research laboratory, where overnight polysomnography and actigraphy were recorded concurrently. Findings from intra-class correlations and Bland-Altman plots were consistent. Actigraphy was found to provide good estimates (e.g. intra-class correlations >0.61) of polysomnography results for sleep duration for all groups and conditions, as well as for sleep-onset latency and sleep efficiency for the typically developing group and attention-deficit/hyperactivity disorder group while on medication, but not for the attention-deficit/hyperactivity disorder group during baseline or placebo. Based on the Bland-Altman plots, actigraphy tended to underestimate for sleep duration (8.6-18.5 min), sleep efficiency (5.6-9.3%) and sleep-onset latency, except for attention-deficit/hyperactivity disorder during placebo in which actigraphy overestimated (-2.1 to 6.3 min). The results of the current study highlight the importance of utilizing a multimodal approach to sleep assessment in children with attention-deficit/hyperactivity disorder.

NPAS3 variants in schizophrenia: a neuroimaging study.

BACKGROUND: This research is a one-site neuroimaging component of a two-site genetic study involving patients with schizophrenia at early and later stages of illness. Studies support a role for the neuronal Per-Arnt-Sim 3 (NPAS3) gene in processes that are essential for normal brain development. Specific NPAS3 variants have been observed at an increased frequency in schizophrenia. In humans, NPAS3 protein was detected in the hippocampus from the first trimester of gestation. In addition, NPAS3 protein levels were reduced in the dorsolateral prefrontal cortex of some patients with schizophrenia. Npas3 knockout mice display behavioural, neuroanatomical and structural changes with associated severe reductions in neural precursor cell proliferation in the hippocampal dentate gyrus. This study will evaluate the hypothesis that the severe reductions in neural precursor cell proliferation in the dentate gyrus will be present to some degree in patients carrying schizophrenia-associated NPAS3 variants and less so in other patients. METHODS/DESIGN: Patients enrolled in the larger genetic study (n = 150) will be invited to participate in this neuroimaging arm. The genetic data will be used to ensure a sample size of 45 participants in each genetic subgroup of patients (with and without NPAS3 variants). In addition, we will recruit 60 healthy controls for acquisition of normative data. The following neuroimaging measures will be acquired from the medial temporal region: a) an index of the microcellular environment; b) a macro-structural volumetric measure of the hippocampus; and c) concentration levels of N-acetylaspartate, a marker of neuronal health. DISCUSSION: This study will help to establish the contribution of the NPAS3 gene and its variants to brain tissue abnormalities in schizophrenia. Given the genetic and phenotypic heterogeneity of the disorder and the large variation in outcomes, the identification of biological subgroups may in future support tailoring of treatment approaches in order to optimize recovery.

Manipulating sleep duration alters emotional functioning and cognitive performance in children.

OBJECTIVE: To examine the impact of sleep duration on emotional functioning and cognitive performance in children. METHODS: 32 children (8-12 years) wore actigraphs for 3 weeks. Following a week of typical sleep, each child was randomly assigned to go to bed 1 hr earlier for 4 nights (Long Sleep) or 1 hr later for 4 nights (Short Sleep) relative to their typical bedtime. Each child then completed the opposite condition. After each week, emotional and cognitive functioning were assessed using objective and subjective measures. RESULTS: Results revealed impaired functioning in the Short- relative to the Long-Sleep condition on measures of positive affective response, emotion regulation, short-term memory, working memory, and aspects of attention. CONCLUSIONS: Results suggest that even modest differences in sleep duration over just a few nights can have significant consequences for children's daytime functioning. These findings demonstrate the important impact of sleep duration on children's daytime functioning.

Sleep Architecture and EEG Power Spectrum Following Cumulative Sleep Restriction: A Comparison between Typically Developing Children and Children with ADHD.

No studies have looked at the effects of cumulative sleep restriction (CSR) on sleep architecture or the power spectrum of sleep EEG (electroencephalogram) in school-age children, as recorded by PSG (polysomnography). This is true for both typically developing (TD) children and children with ADHD (attention deficit/hyperactivity disorder), who are known to have more sleep difficulties. Participants were children (ages 6-12 years), including 18 TD and 18 ADHD, who were age- and sex-matched. The CSR protocol included a two-week baseline and two randomized conditions: Typical (six nights of sleep based on baseline sleep schedules) and Restricted (one-hour reduction of baseline time in bed). This resulted in an average of 28 min per night difference in sleep. Based on ANOVAs (analysis of variance), children with ADHD took longer to reach N3 (non-rapid eye movement), had more WASO (wake after sleep onset) (within the first 5.1 h of the night), and had more REM (rapid eye movement) sleep than TD children regardless of condition. During CSR, ADHD participants had less REM and a trend toward longer durations of N1 and N2 compared to the TD group. No significant differences in the power spectrum were found between groups or conditions. In conclusion, this CSR protocol impacted some physiological aspects of sleep but may not be sufficient to cause changes in the power spectrum of sleep EEG. Although preliminary, group-by-condition interactions suggest that the homeostatic processes in children with ADHD may be impaired during CSR.

Assessing research competency development in Canadian psychiatry residency programs: A systematic review and future directions.

Objective: We aimed to conduct a systematic review to identify curricular and educational interventions to build research competency among Canadian psychiatry residents and fellows transitioning to the competency-by-design framework. Methods: The PRISMA guidelines were followed, searching five databases from their inception to February 2023 for relevant evaluation-type studies exploring research competency among psychiatry residents and fellows. We appraised thestudy's quality using the Joanna Briggs Institute's risk of bias tool for observational designs. Results: Overall, 36 original articles met our inclusion criteria. Surveys (n = 10) showed that participation in scholarly research, quality improvement, or educational projects relevant to psychiatry is needed in most residency programs. However, these vary significantly across programs; few need direct research experience for residency completion. The interventions spanned four categories: externally funded comprehensive research training programs (n = 5); resident research tracks (n = 11); workshops and seminars (n = 7); and specific modules (n = 3). Reported outcomes included overall program ratings, research output, and career trajectory. The quality of most studies was low because of the lack of controls or validated metrics for evaluating outcomes. Conclusions: While many studies have explored best practices in research curricula, the current literature does not inform competency-based models for Canadian psychiatry residency programs incorporating research training requirements. Further description is needed from Canadian psychiatric training bodies regarding appropriate curricula, milestones, and metrics for evaluating research competencies.

Olfactory Function and Diffusion Tensor Imaging as Markers of Mild Cognitive Impairment in Early Stages of Parkinson's Disease.

Parkinson's disease (PD) is a neurodegenerative disorder that is typified by motor signs and symptoms but can also lead to significant cognitive impairment and dementia Parkinson's Disease Dementia (PDD). While dementia is considered a nonmotor feature of PD that typically occurs later, individuals with PD may experience mild cognitive impairment (PD-MCI) earlier in the disease course. Olfactory deficit (OD) is considered another nonmotor symptom of PD and often presents even before the motor signs and diagnosis of PD. We examined potential links among cognitive impairment, olfactory functioning, and white matter integrity of olfactory brain regions in persons with early-stage PD. Cognitive tests were used to establish groups with PD-MCI and with normal cognition (PD-NC). Olfactory functioning was examined using the University of Pennsylvania Smell Identification Test (UPSIT) while the white matter integrity of the anterior olfactory structures (AOS) was examined using magnetic resonance imaging (MRI) diffusion tensor imaging (DTI) analysis. Those with PD-MCI demonstrated poorer olfactory functioning and abnormalities based on all DTI parameters in the AOS, relative to PD-NC individuals. OD and microstructural changes in the AOS of individuals with PD may serve as additional biological markers of PD-MCI.

Aberrant corticospinal tract characteristics in prodromal PD: A diffusion tensor imaging study.

Introduction: Parkinson's disease (PD) is typically diagnosed when motor symptoms first occur. However, PD-related non-motor symptoms may appear several years before diagnosis. REM sleep behaviour disorder (RBD) and olfactory deficits (hyposmia) are risk factors, but they are not specific for predicting progression towards PD. Other PD-related markers, for example brain imaging markers, may help to identify preclinical PD in hyposmic RBD patients. Studies have reported abnormal structural characteristics in the corticospinal tract (CST) of PD patients, but it is unclear whether hyposmic RBD patients have similar abnormalities that may help to predict PD in these individuals. This study examined whether CST abnormalities may be a potential marker of PD risk by using diffusion tensor imaging (DTI) measures. Methods: Twenty hyposmic RBD patients, 31 PD patients, and 29 healthy controls (HCs) were studied. DTI data were collected on a 1.5 T MRI scanner and CST characteristics (FA, MD, AD, and RD) were evaluated using probabilistic tractography (with seed regions in the bilateral primary motor cortex and mediolateral cerebral peduncles). Olfactory function was assessed with the University of Pennsylvania Smell Identification Test (UPSIT). Results: Hyposmic RBD patients showed significantly higher mean diffusivity (MD) values of the right CST compared to HCs but did not differ from PD patients. PD patients showed a trend of higher MD values compared to HCs. Conclusions: Altered diffusivity in the CST seems to be associated with RBD. The combination of RBD, hyposmia, and CST alterations may be related to later development of PD with comorbid RBD.

Augmenting Mental Health Support for Patients Accessing Different Degrees of Formal Psychiatric Care through a Supportive Text Messaging Program: Protocol for a Randomized Controlled Trial.

Patients feel more vulnerable when accessing community mental health programs for the first time or after being discharged from psychiatric inpatient units. Long wait times for follow-up appointments, shortage of mental health professionals, lack of service integration, and scarcity of tailored support can weaken their connection to the health care system. As a result, patients can present low adherence, dissatisfaction with treatment, and recurrent hospitalizations. Finding solutions to avoid unnecessary high-cost services and providing tailored and cost-effective mental health interventions may reduce the health system burden and augment patient support. We propose implementing an add-on, supportive text messaging service (Text4Support), developed using cognitive-behavioural therapy (CBT) principles to augment mental health support for patients attending to or being discharged from psychiatric care in Nova Scotia, Canada. This randomized controlled trial aims to investigate the effectiveness of Text4Support in improving mental health outcomes and overall mental well-being compared with usual care. We also will examine the intervention's impact on health services utilization and patient satisfaction. The results from this study will provide evidence on stepped and technology-based mental health care, which will contribute to generating new knowledge about mental health innovations in various clinical contexts, which is not only helpful for the local context but to other jurisdictions in Canada and abroad that are seeking to improve their health care.

The Text4HealthyAging Program: An Evidence-Based Text Messaging Innovation to Support Healthy Urban Aging in Canada and Australia.

Age-friendly cities are crucial to achieve the WHO goal of healthy aging. Such cities promote opportunities for health, participation, and security, thus enhancing quality of life as people age. Older people commonly experience psychosocial challenges such as anxiety, depression, substance abuse, loss of autonomy, grief, fear, and loneliness. Australian and Canadian cities continue to seek innovation to improve healthy urban aging and create more age-friendly environments for older adults. There is increasing evidence on the effectiveness and feasibility of mobile technology in health promotion and closing psychological treatment gaps. Older adults have been demonstrated to engage frequently with mobile devices, particularly text messaging. In this article, we conceptualize the Text4HealthyAging, an evidence-based text messaging innovation to support healthy urban aging in Canadian and Australian cities.

Sleep Variables as Predictors of Treatment Effectiveness and Side Effects of Stimulant Medication in Newly Diagnosed Children with Attention-Deficit/Hyperactivity Disorder.

OBJECTIVE: There is a growing body of research on the impact of stimulant medication on sleep in children with attention-deficit/hyperactivity disorder (ADHD). Negative sleep side effects are a common reason for nonadherence or for discontinuing a course of treatment. However, there is no published evidence as to whether pretreatment sleep can predict responses to treatment and the emergence of side effects. METHOD: In this study, baseline sleep variables were used to predict therapeutic effect (i.e., reduction of ADHD symptoms) and side effects (both sleep and global side effects) in a sample of newly diagnosed, medication-naive children (n = 50). RESULTS: The results of hierarchical regression analysis showed that parent-reported shorter sleep duration before medication treatment significantly predicted better response to treatment, independent of pretreatment ADHD symptoms. Baseline sleep features did not significantly predict global (nonsleep) side effects but did predict increased sleep side effects during treatment. CONCLUSION: These results indicate that baseline sleep variables may be helpful in predicting therapeutic response to medication and sleep disturbance as a side effect of stimulant medication.

Altered circadian activity and sleep/wake rhythms in the stable tubule only polypeptide (STOP) null mouse model of schizophrenia.

Sleep and circadian rhythm disruptions commonly occur in individuals with schizophrenia. Stable tubule only polypeptide (STOP) knockout (KO) mice show behavioral impairments resembling symptoms of schizophrenia. We previously reported that STOP KO mice slept less and had more fragmented sleep and waking than wild-type littermates under a light/dark (LD) cycle. Here, we assessed the circadian phenotype of male STOP KO mice by examining wheel-running activity rhythms and EEG/EMG-defined sleep/wake states under both LD and constant darkness (DD) conditions. Wheel-running activity rhythms in KO and wild-type mice were similarly entrained in LD, and had similar free-running periods in DD. The phase delay shift in response to a light pulse given early in the active phase under DD was preserved in KO mice. KO mice had markedly lower activity levels, lower amplitude activity rhythms, less stable activity onsets, and more fragmented activity than wild-type mice in both lighting conditions. KO mice also spent more time awake and less time in rapid eye movement sleep (REMS) and non-REMS (NREMS) in both LD and DD conditions, with the decrease in NREMS concentrated in the active phase. KO mice also showed altered EEG features and higher amplitude rhythms in wake and NREMS (but not REMS) amounts in both lighting conditions, with a longer free-running period in DD, compared to wild-type mice. These results indicate that the STOP null mutation in mice altered the regulation of sleep/wake physiology and activity rhythm expression, but did not grossly disrupt circadian mechanisms.

MRI-related anxiety levels change within and between repeated scanning sessions.

Magnetic resonance imaging (MRI) scans frequently trigger state anxiety in individuals being scanned. It is not known, however, whether levels of MRI-related anxiety change over the course of a single scan or across repeated scanning experiences. Since changes in state anxiety are known to affect regional brain activity in healthy volunteers, systematic changes in levels of MRI-related anxiety could confound findings from neuroimaging studies. We assessed anxiety levels in eleven healthy male volunteers during a control period and during two MRI scanning sessions. Anxiety levels were highest during the first MRI scan, dropping to control levels or below by the second scan. In addition, anxiety fluctuated within scanning sessions, particularly during the first scan, with levels high at the beginning of the session, decreasing during mid-scan and then increasing again toward the end of the session. These results suggest that habituation in an MRI simulator before participating in a neuroimaging study could help to decrease fluctuations in MRI-related anxiety. Moreover, in studies that address several experimental questions within a single scanning session, experimental designs could be adapted to avoid potential confounds from within-scan variation in scanner-related anxiety.

The Effects of Extended-Release Stimulant Medication on Sleep in Children with ADHD.

OBJECTIVE: Although stimulant medications, such as methylphenidate hydrochloride (MPH), are effective at reducing the core symptoms of Attention-Deficit/Hyperactivity Disorder (ADHD), they may also disrupt children's sleep. This study aimed to investigate the acute impact of extended-release MPH on sleep using both actigraphy and polysomnography (PSG). METHOD: Participants were 26 medication-naïve newly and rigorously diagnosed children with ADHD (23 males; 3 females) with a mean age of 8 years, 8 months (SD = 24.5mos) who were enrolled in a clinically-administered crossover medication trial with 2 conditions: 2 weeks of placebo and 2 weeks of MPH treatment. The effect of condition on sleep variables as measured by actigraphy (primary outcome) and PSG (secondary outcome) was analyzed using repeated measures MANOVAs. RESULTS: Based on actigraphy data, total sleep time was significantly reduced by 30 minutes and sleep onset latency was significantly increased by 30 minutes in the MPH condition compared to the placebo condition (p<0.001). No differences were found in sleep efficiency. No statistically significant differences were found for the same variables assessed by PSG; however, the means were in the same direction as the actigraphy data. There was a significant increase in the relative percentage of stage N3 sleep by 3.2% during MPH treatment (p<0.05). CONCLUSIONS: Increased sleep onset latency resulting in reduced total sleep time, which has been linked to poorer daytime functioning, is a potential adverse effect of stimulant medication which may require management to optimize outcome.

OBJECTIF: Bien que les médicaments stimulants comme le chlorhydrate de méthylphénidate (MPH) soient efficaces pour réduire les principaux symptômes du trouble de déficit de l'attention avec hyperactivité (TDAH), ils peuvent également perturber le sommeil des enfants. La présente étude visait à rechercher l'effet précis du MPH à libération prolongée sur le sommeil à l'aide d'une actigraphie et d'une polysomnographie (PSG). MÉTHODE: Les participants étaient 26 enfants naïfs de médicaments ayant nouvellement et rigoureusement reçu un diagnostic de TDAH (23 garçons; 3 filles) d'âge moyen de 8 ans et 8 mois (ET = 24,5 mois) qui étaient inscrits dans un essai croisé cliniquement administré sur la médication selon 2 conditions: 2 semaines de placebo et deux semaines de traitement par MPH. L'effet de la condition sur les variables du sommeil telles que mesurées par l'actigraphie (résultat principal) et la PSG (résultat secondaire) a été analysé par des mesures répétées MANOVA. RÉSULTATS: Selon les données de l'actigraphie, le temps de sommeil total était significativement réduit de 30 minutes et la latence d'endormissement était significativement accrue de 30 minutes dans la condition MPH comparativement à la condition placebo (p < 0,001). Aucune différence n'a été notée pour l'efficacité du sommeil. Aucune différence statistiquement significative n'a été observée pour les mêmes variables évaluées par la PSG; cependant, les moyennes suivaient la même direction que les données de l'actigraphie. Il y avait une augmentation significative de 3,2 % du pourcentage relatif au stade N3 du sommeil durant le traitement par MPH (p < 0,05). CONCLUSIONS: La latence d'endormissement accrue entraînant un temps de sommeil total réduit, qui est lié à un mauvais fonctionnement de jour, est un effet indésirable potentiel des médicaments stimulants, qui peut nécessiter une prise en charge afin d'optimiser le résultat.

Estradiol and progesterone modulate spontaneous sleep patterns and recovery from sleep deprivation in ovariectomized rats.

STUDY OBJECTIVES: Women undergo hormonal changes both naturally during their lives and as a result of sex hormone treatments. The objective of this study was to gain more knowledge about how these hormones affect sleep and responses to sleep loss. DESIGN: Rats were ovariectomized and implanted subcutaneously with Silastic capsules containing oil vehicle, 17 beta-estradiol and/or progesterone. After 2 weeks, sleep/wake states were recorded during a 24-h baseline period, 6 h of total sleep deprivation induced by gentle handling during the light phase, and an 18-h recovery period. MEASUREMENTS AND RESULTS: At baseline and particularly in the dark phase, ovariectomized rats treated with estradiol or estradiol plus progesterone spent more time awake at the expense of non-rapid eye movement sleep (NREMS) and/or REMS, whereas those given progesterone alone spent less time in REMS than ovariectomized rats receiving no hormones. Following sleep deprivation, all rats showed rebound increases in NREMS and REMS, but the relative increase in REMS was larger in females receiving hormones, especially high estradiol. In contrast, the normal increase in NREMS EEG delta power (an index of NREMS intensity) during recovery was attenuated by all hormone treatments. CONCLUSIONS: Estradiol promotes arousal in the active phase in sleep-satiated rats, but after sleep loss, both estradiol and progesterone selectively facilitate REMS rebound while reducing NREMS intensity. These results indicate that effects of ovarian hormones on recovery sleep differ from those on spontaneous sleep. The hormonal modulation of recovery sleep architecture may affect recovery of sleep related functions after sleep loss.

Effects of overnight sleep restriction on brain chemistry and mood in women with unipolar depression and healthy controls.

BACKGROUND: Partial or total overnight sleep deprivation produces immediate mood improvement in about 50% of patients with depression, but not in healthy controls. Our objectives were to compare the neurochemical changes that accompanied partial overnight sleep deprivation in healthy and depressed participants, and to compare baseline neurochemical profiles and overnight neurochemical changes between those depressed participants who did and did not respond to sleep loss with mood improvement. METHODS: We studied 2 brain regions (left dorsal prefrontal area and pons) in 12 women with unipolar depression and in 15 healthy women using proton magnetic resonance spectroscopy acquired at 1.5 T. The scans took place at baseline and 24 hours later after a night with sleep restricted to a maximum of 2.5 hours (22:30-01:00). We assessed 3 neurochemical signals (referenced to internal water): N-acetylaspartate (NAA), choline compounds (Cho) and creatine-plus-phosphocreatine (tCr). RESULTS: In both groups combined, sleep restriction caused a 20.1% decrease in pontine tCr (F(1-16) = 5.07, p = 0.039, Cohen's d = 0.54) and an 11.3% increase in prefrontal Cho (F(1-21) = 5.24, p = 0.033, Cohen's d = 0.46). Follow-up tests revealed that prefrontal Cho increases were significant only among depressed participants (17.9% increase, t(9) = -3.35, p = 0.008, Cohen's d = 1.06). Five depressed patients showed at least 30% improvement in mood, whereas 6 showed no change or worsening in mood after sleep restriction. Baseline pontine Cho levels distinguished subsequent responders from nonresponders to sleep restriction among depressed participants (z = 2.61, p = 0.008). LIMITATIONS: A limitation of this study is the relatively small sample size. CONCLUSION: Sleep restriction altered levels of pontine tCr and prefrontal Cho in both groups combined, suggesting effects on phospholipid and creatine metabolism. Baseline levels of pontine Cho were linked to subsequent mood responses to sleep loss, suggesting a role for pontine phospholipid metabolism in mood effects of sleep restriction.

Sleep in Offspring of Parents With Mood Disorders.

Background: Sleep problems in childhood are an early predictor of mood disorders among individuals at high familial risk. However, the majority of the research has focused on sleep disturbances in already diagnosed individuals and has largely neglected investigating potential differences between weeknight and weekend sleep in high-risk offspring. This study examined sleep parameters in offspring of parents with major depressive disorder or bipolar disorder during both weeknights and weekends. Methods: We used actigraphy, sleep diaries, and questionnaires to measure several sleep characteristics in 73 offspring aged 4-19 years: 23 offspring of a parent with major depressive disorder, 22 offspring of a parent with bipolar disorder, and 28 control offspring. Results: Offspring of parents with major depressive disorder slept, on average, 26 min more than control offspring on weeknights (95% confidence interval, 3 to 49 min, p = 0.027). Offspring of parents with bipolar disorder slept, on average, 27 min more on weekends than on weeknights compared to controls, resulting in a significant family history × weekend interaction (95% confidence interval, 7 to 47 min, p = 0.008). Conclusions: Sleep patterns in children and adolescents were related to the psychiatric diagnosis of their parent(s). Future follow-up of these results may clarify the relations between early sleep differences and the risk of developing mood disorders in individuals at high familial risk.