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Contexte La disparition de la nomenclature des troubles du sommeil dits primaires ou secondaires, rendue obsolète par le Manuel diagnostique et statistique des troubles mentaux (DSM-5), représente bien l’engouement académique actuel pour ce domaine de recherche. Il est de plus en plus reconnu que les troubles du sommeil sont plus que de simples conséquences d’un trouble psychiatrique et qu’ils peuvent persister malgré un traitement adéquat de la condition comorbide et même précéder ou exacerber cette dernière. Les troubles du sommeil dans les troubles psychotiques, très fréquents, sont donc devenus un sujet d’actualité, représentant une cible d’intervention jusqu’ici sous-estimée.Objectif Cet article vise à présenter l’état des connaissances actuelles sur la relation entre les troubles du sommeil et les troubles psychotiques ainsi que sur l’utilisation de la thérapie cognitivo-comportementale (TCC) pour traiter les troubles du sommeil dans ce contexte.Méthode L’article fait une recension narrative de la littérature pour décrire la relation bidirectionnelle entre la psychose et les troubles du sommeil, les corrélations cliniques et les traitements ciblant l’insomnie chez les patients psychotiques.Résultats Malgré la présence d’une relation entre les troubles du sommeil et les troubles psychotiques, les mécanismes neuronaux, hormonaux et socioculturels régissant cette relation demeurent encore incertains. Bien que l’association reliant les troubles du sommeil et les troubles psychotiques demeure à clarifier, les études démontrent qu’elle serait bidirectionnelle et peut engendrer un cercle vicieux où ces deux composantes s’aggravent mutuellement. Dans ce contexte de comorbidités, les modèles unifiés en TCC deviennent un traitement de choix, à condition d’adapter les protocoles de TCC pour insomnie (TCC-i) à une population avec trouble psychotique (TCC-ip).Conclusion Malgré la complexité de la relation entre les troubles psychotiques et ceux du sommeil, la TCC-i a été démontrée efficace pour traiter les troubles du sommeil dans une population psychotique et pourrait, dans certains cas, permettre d’alléger la symptomatologie psychotique. De futures études sur ce domaine pourraient permettre le développement de protocoles de thérapie cognitivo-comportementale pour les troubles du sommeil mieux adaptés à la population avec troubles psychotiques., Context Psychotic disorders are severe mental disorders that can cause a loss of contact with reality. Along with positive symptoms (delusions and hallucinations), they also encompass many other dysfunctions, such as sleep problems, which themselves can cause great distress and impairment in patients.Objective To review current literature on the relationship between sleep disorders and psychosis, on the clinical impact of such a relationship, and the psychological treatment of sleep disorders in the context of psychosis.Method Narrative overview of the literature synthesizing the findings about the relationship between psychosis and sleep disorders, and the psychological treatment of the latter, retrieved from searches of computerized databases, hand searches, and authoritative texts.Results Evidence shows a bidirectional relationship between psychosis and sleep disorders. Despite many hypotheses involving genetics, hormones, or neuronal functions regarding the nature of this association, the exact mechanism remains elusive. However, sleep-related problems are an interesting therapeutic target to improve quality of life and psychotic symptoms and respond well to psychological interventions.Conclusion Patients with psychotic disorders can benefit from CBT for insomnia, given a few adaptations to existing protocols. Additional studies are necessary to determine which patients are most likely to benefit from such interventions and to clarify the relationship between psychosis and sleep disorders, and the clinical implications of them co-existing.

Theoretical models of sleep and attention deficit hyperactivity disorder (ADHD) suggest that symptoms of ADHD are associated with daytime sleepiness, but it has received little support. The present study aimed at testing an alternative model involving the association of attentional instability with sleep instability, i.e., sleep stage transitions and arousals. Twelve ADHD and 15 healthy control (HC) boys aged between 8 and 12 years old underwent polysomnography recording and attentional testing. The microarousal index, the number of awakenings, and the number of stage shifts between stages 1, 2, 3, 4 and REM sleep throughout the night were computed as sleep stability parameters. Attentional functioning was assessed using the Continuous Performance Test-II. We found significantly higher sleep instability in ADHD compared to HC. Sleep arousals and stage transitions (micro arousal index, stage 4/3 and 2/4 transitions) in ADHD significantly correlated with lower attentional scores. No association whatsoever was found between sleep instability and attentional functioning in HC. The results show that sleep instability is associated with lower attentional performance in boys with ADHD, but not in HC. This could be compatible with a model according to which attention and sleep stability share a common neural substrate in ADHD.

We tested the hypothesis of an atypical scalp distribution of electroencephalography (EEG) activity during Rapid Eye Movement (REM) sleep in young autistic adults. EEG spectral activity and ratios along the anteroposterior axis and across hemispheres were compared in 16 neurotypical (NT) young adults and 17 individuals with autism spectrum disorder (ASD). EEG spectral power was lower in the ASD group over the bilateral central and right parietal (beta activity) as well as bilateral occipital (beta, theta, and total activity) recording sites. The NT group displayed a significant posterior polarity of intra-hemispheric EEG activity while EEG activity was more evenly or anteriorly distributed in ASD participants. No significant inter-hemispheric EEG lateralization was found. Correlations between EEG distribution and ASD symptoms using the Autism Diagnostic Interview-Revised (ADI-R) showed that a higher posterior ratio was associated with a better ADI-R score on communication skills, whereas a higher anterior ratio was related to more restricted interests and repetitive behaviors. EEG activity thus appears to be atypically distributed over the scalp surface in young adults with autism during REM sleep within cerebral hemispheres, and this correlates with some ASD symptoms. These suggests the existence in autism of a common substrate between some of the symptoms of ASD and an atypical organization and/or functioning of the thalamo-cortical loop during REM sleep.

Background An upsurge in dream and nightmare frequency has been noted since the beginning of the COVID-19 pandemic and research shows increases in levels of stress, depression and anxiety during this time. Growing evidence suggests that dream content has a bi-directional relationship with psychopathology, and that dreams react to new, personally significant and emotional experiences. The first lockdown experience was an acute event, characterized by a combination of several unprecedent factors (new pandemic, threat of disease, global uncertainty, the experience of social isolation and exposure to stressful information) that resulted in a large-scale disruption of life routines. This study aimed at investigating changes in dream, bad dream and nightmare recall; most prevalent dream themes; and the relationship between dreams, bad dreams, nightmares and symptoms of stress, depression and anxiety during the first COVID-19 lockdown (April-May 2020) through a national online survey. Methods 968 participants completed an online survey. Dream themes were measured using the Typical Dreams Questionnaire; stress levels were measured by the Cohen’s Perceived Stress Scale; symptoms of anxiety were assessed by Generalized Anxiety Disorder (GAD-7) scale; and symptoms of depression were assessed using the Quick Inventory of Depressive Symptomatology. Results 34% (328) of participants reported increased dream recall during the lockdown. The most common dream themes were centered around the topics of 1) inefficacy (e.g., trying again and again, arriving late), 2) human threat (e.g., being chased, attacked); 3) death; and 4) pandemic imagery (e.g., being separated from loved ones, being sick). Dream, bad dream and nightmare frequency was highest in individuals with moderate to severe stress levels. Frequency of bad dreams, nightmares, and dreams about the pandemic, inefficacy, and death were associated with higher levels of stress, as well as with greater symptoms of depression and anxiety. Conclusions Results support theories of dream formation, environmental susceptibility and stress reactivity. Dream content during the lockdown broadly reflected existential concerns and was associated with increased symptoms of mental health indices.

Background/aims Insomnia is highly prevalent in children with neurodevelopmental disorders (NDDs), yet little research exists on sleep treatment access, utilization, and provision in this population. This study explores barriers and facilitators to access, use, and provision of treatment for sleep problems as experienced by parents of children with NDDs, including Autism Spectrum Disorder (ASD), Attention-Deficit/Hyperactivity Disorder (ADHD), Cerebral Palsy (CP) and Fetal Alcohol Spectrum Disorder (FASD), and health care professionals who work with children with these conditions. Method Transcripts from online focus groups and interviews, conducted separately with parents of children with NDDs (n = 43) and health care professionals (n = 44), were qualitatively analyzed using content analysis for key themes. Results Barriers included limited access to/availability of treatment, lack of knowledge/training, NDD-specific factors (e.g., symptoms, medications, and comorbidities), parent factors (e.g., capacity to implement treatment, exhaustion), and the challenging, intensive nature of sleep treatment. Facilitators included positive beliefs and attitudes, education, support, and ability to modify treatments for NDD symptoms. Barriers and facilitators were similar across all four NDDs. Conclusions Results highlight a need for more education about sleep in NDDs and to develop accessible interventions, as well as the potential of a transdiagnostic approach to sleep treatment in this population.

Background The endogenous cannabinoid system mediates the psychoactive effects of cannabis in the brain. It has been argued that this system may play a key role in the pathophysiology of schizophrenia. While some studies have consistently shown that the levels of anandamide, an endogenous cannabinoid ligand, are increased in the cerebrospinal fluid of schizophrenia patients, inconsistent results have been observed in studies measuring anandamide levels in the periphery. Here, we sought to determine if the assessment of peripheral anandamide levels in patients evaluated in a psychiatric emergency setting would show robust increases. Methods One hundred seven patients with a schizophrenia-spectrum disorder from the psychiatric emergency settings of the Institut Universitaire en Sante Mentale de Montreal and 36 healthy volunteers were included in the study. A subsample of thirty patients were assessed at two time points: at the emergency and at their discharge from the hospital. Anxious and depressive symptoms, sleep and substance use were assessed using self-report questionnaires. In addition to anandamide, the levels of oleoylethanolamide (OEA), an anorexigenic fatty-acid ethanolamide, were also measured, since the prevalence of the metabolic syndrome is increased in schizophrenia. Plasma levels of anandamide and OEA were measured using liquid chromatography and mass spectrometry. Results Plasma anandamide and OEA levels were significantly increased in schizophrenia patients, relative to controls (Cohen's d=1.0 and 0.5, respectively). Between-group differences remained significant after controlling for metabolic measures. No differences were observed between schizophrenia patients with and without a comorbid substance use disorder at baseline. Importantly, the levels of both endocannabinoids significantly decreased after discharge from the emergency setting. Conclusion The current results add to the growing body of evidence of endocannabinoid alterations in schizophrenia. The strong elevation of plasma anandamide levels in schizophrenia patients assessed in the psychiatric emergency setting suggests that anandamide and OEA area potential biomarkers of the psychological turmoil associated with this context.

Children with neurodevelopmental disorders (NDD) are at high risk for sleep problems, especially insomnia. It is currently not known whether behavioural sleep interventions developed for typically developing (TD) children are effective for children with NDD, and if interventions need to be modified for each diagnostic group. The aim of this systematic review was to identify and evaluate commonalities, trends in outcomes, and the methodological quality of parent-delivered behavioural sleep interventions for children with NDD, specifically Attention-Deficit/Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), Cerebral Palsy, and Fetal Alcohol Spectrum Disorder. Nine databases were searched. A total of 40 studies met eligibility criteria. The majority of studies were conducted with ASD and ADHD populations. Common sleep problems were evident across the NDD populations. The most frequently reported included bedtime resistance, night-waking, early morning awakening, and co-sleeping. The most common interventions used were implementation of healthy sleep practices, reinforcement, graduated extinction, and faded bedtime. All studies reported at least one behavioural treatment component as effective. Commonalities across NDD populations, as well as the TD population, for both sleep problems reported and behavioural interventions implemented, suggest the feasibility of developing a transdiagnostic behavioural sleep intervention suitable for children with a range of NDD.

Delta EEG activity (0.75-3.75 Hz) during non-Rapid eye movement (NREM) sleep reflects the thalamo-cortical system contribution to memory consolidation. The functional integrity of this system is thought to be compromised in the Autism spectrum disorder (ASD). This lead us to investigate the topography of NREM sleep Delta EEG activity in young adults with ASD and typically-developed individuals (TYP). The relationship between Delta EEG activity and sensory-motor procedural information was also examined using a rotary pursuit task. Two dependent variables were computed: a learning index (performance increase across trials) and a performance index (average performance for all trials). The ASD group showed less Delta EEG activity during NREM sleep over the parieto-occipital recording sites compared to the TYP group. Delta EEG activity dropped more abruptly from frontal to posterior regions in the ASD group. Both groups of participants learned the task at a similar rate but the ASD group performed less well in terms of contact time with the target. Delta EEG activity during NREM sleep, especially during stage 2, correlated positively with the learning index for electrodes located all over the cortex in the TYP group, but only in the frontal region in the ASD group. Delta EEG activity, especially during stage 2, correlated positively with the performance index, but in the ASD group only. These results reveal an atypical thalamo-cortical functioning over the parieto-occipital region in ASD. They also point toward an atypical relationship between the frontal area and the encoding of sensory-motor procedural memory in ASD. Autism Res 2018, 11: 613-623. © 2018 International Society for Autism Research, Wiley Periodicals, Inc. Lay summary Slow EEG waves recorded from the scalp during sleep are thought to facilitate learning and memory during daytime. We compared these EEG waves in young autistic adults to typically-developing young adults. We found less slow EEG waves in the ASD group and the pattern of relationship with memory differed between groups. This suggests atypicalities in the way sleep mechanisms are associated with learning and performance in a sensory-motor procedural memory task in ASD individuals.

Over time, the sleep disturbances experienced by people with bipolar disorder (BD) can lead to a progressive accumulation of sleep debt with widespread adverse consequences on mental and physical health. This review looks at recent studies that have examined bipolar disorder in relation to sleep and cardiovascular dysfunctions. Sleep loss not only alters basal cardiometabolic features but also stress-related cardiometabolic responses, putting individuals with chronic sleep difficulties at higher risk for vascular events. Abnormalities of sleep parameters and circadian rhythms in individuals with BD point towards the necessity of sleep assessments in order to create the most effective therapeutic strategies. Risk factors and pathophysiological mechanisms inherent to BD such as extreme affective liability, obesity, diabetes, hypertension, hyperlipidemia, proinflammatory background, and psychotropic medications put patients at a higher risk for cardiovascular problems. In addition to their direct effects on cardiometabolic health, psychoactive substances commonly used by this population may also trigger diverse sleep problems and disrupt sleep processes involved in cardiovascular regulation. Overall, it is proposed that sleep loss and dysfunction in circadian rhythms related to BD can trigger or amplify cardiometabolic dysfunctions, thus adding a burden to the clinical picture. We conclude with promising avenues for optimal management and treatment strategies.

Better Nights, Better Days (BNBD) is a 5-session online intervention designed to treat insomnia in 1–10-year-old children (Corkum et al. 2016). Obstructive sleep apnea (OSA) and insomnia commonly occur in children and, after surgical treatment for OSA, it is estimated that up to 50% of children may continue to suffer from insomnia symptoms. Access to insomnia interventions following OSA treatment is limited as there are few programs available, few trained practitioners to deliver these programs, and limited recognition that these problems exist. The current study involved the usability testing of an internet-based parent-directed session of BNBD tailored towards the needs of children (ages 4–10 years) who experience residual insomnia symptoms after treatment of OSA. This new session was added to the BNBD program. Participants (n = 43) included 6 parents, 17 sleep experts, and 20 front-line healthcare providers who completed and provided feedback on the new session. Participants completed a feedback questionnaire, with both quantitative and qualitative questions, after reviewing the session. Quantitative responses analyzed via descriptive statistics suggested that the session was primarily viewed as helpful by most participants, and open-ended qualitative questions analyzed by content analyses generated a mix of positive and constructive feedback. The results provide insights on how to optimally tailor the BNBD program to meet the needs of the target population and suggest that testing the session on a larger scale would be beneficial., Highlights • A new OSA-tailored session for the eHealth program Better Nights, Better Days (BNBD) was evaluated by stakeholders. • Quantitative and qualitative feedback suggests that stakeholders generally viewed the new session as helpful and provided feedback. • The current study assesses the usability of the first eHealth intervention tailored for children with insomnia symptoms after treatment for OSA.

Caspase-3 activation in the limbic system and depressive-like symptoms are observed after an acute myocardial infarction (MI) and studies suggest that inflammation may play a significant role. Combined treatment with the probiotic strains Bifidobacterium longum and Lactobacillus helveticus in rats has been shown to attenuate caspase-3 activation and depressive-like behaviour together with a reduction in pro-inflammatory cytokines. The present study was designed to determine the respective contribution of these two strains on caspase-3 activity in the limbic system and on depressive-like behaviour. Sprague-Dawley rats were assigned to one of four groups: Vehicle, L. helveticus R0052, B. longum R0175 and L. salivarius HA-118, administered orally for 14 days (109CFU daily) before inducing MI by occlusion of the left anterior descending artery for 40 min followed by 14 days of reperfusion. Animals were then tested for socialisation, passive avoidance and forced swim test to assess depressive-like behaviour. At day 18 the animals were sacrificed; infarct size was estimated, plasma C-reactive protein concentration and brain caspase-3 activity were measured. Results indicated that infarct size did not vary across the different treatments. Rats treated with B. longum spent more time socializing, learned more rapidly the passive avoidance test and spent less time immobile in the forced swim test compared to the vehicle groups. Caspase-3 activity and plasma C-reactive protein concentrations were reduced in the lateral and medial amygdala as well as in the dentate gyrus of B. longum-supplemented animals. The only significant effect in the two groups receiving Lactobacilli compared to vehicle was that rats receiving L. salivarius learned more rapidly in the step-down passive avoidance test. In conclusion, most of the beneficial effects that we previously reported with the combination of two probiotic strains in our experimentation regarding post-myocardial infarction depression are related to Bifidobacterium longum.

Autism spectrum (AS) is a neurodevelopmental condition associated with poor sleep, which impairs daytime functioning. Most studies of sleep in autism have been based on subjective measures, notably parental reports. A few studies have used objective, laboratory polysomnography (PSG) measures, but often include confounding factors such as intellectual disability, sleep problems, other psychiatric illnesses, and medication. To address these limitations, we examined the relationship between sleep and behavior in prototypical AS of typical level of intelligence and non-autistic children not complaining of sleep problems. We examined sleep variables with The Children’ Sleep Habit Questionnaire (CSHQ) and a daily sleep agenda, both filled out by parents, and by PSG. These subjective and objective measures both revealed that sleep latency was longer in AS than in non-autistic children. Furthermore, AS children also showed less slow-wave sleep (SWS: stages 3 + 4), fewer sleep spindles and fewer K-complexes than non-autistic children. REM sleep, including eye movement density, was similar between the two groups. The proportion of light sleep, (stage 1 non-REM sleep) was negatively correlated with IQ (Wechsler and Raven matrices) in both groups of participants. A large amount of SWS predicted low levels of internalizing behavior in both groups and typical social functioning as determined by ADOS in AS children. These results indicate that autistic children not complaining of sleep problems may nonetheless be affected by poor sleep, which in turn influences their daytime functioning.

Purpose of Review Melatonin is used to treat sleep difficulties associated with autism spectrum disorder (ASD). There are growing evidence that melatonin could have an effect on other symptoms than sleep, such as anxiety, depression, pain, and gastrointestinal dysfunctions. Interestingly, these symptoms frequently are found as comorbid conditions in individuals with ASD. We aimed to highlight the potential effect of melatonin on these symptoms. Recent Findings Animal and human studies show that melatonin reduces anxiety. Regarding the effect of melatonin on pain, animal studies are promising, but results remain heterogeneous in humans. Both animal and human studies have found that melatonin can have a positive effect on gastrointestinal dysfunction. Summary Melatonin has the potential to act on a wide variety of symptoms associated with ASD. However, other than sleep difficulties, no studies exist on melatonin as a treatment for ASD comorbid conditions. Such investigations should be on the research agenda because melatonin could improve a multitude of ASD comorbidities and, consequently, improve well-being.

Objective: This exploratory study measured the impact of comorbid anxiety disorders on sleep in children with ADHD and tested the effect of cognitive-behavioral therapy (CBT) on these measures. Method: Fifty-seven children (8-12 years old) were assessed with the Child Sleep Habits Questionnaire. Four groups were formed: ADHD ( n = 20), ADHD + Anxiety ( n = 20), Anxiety ( n = 8), and Healthy Controls ( n = 9). A subgroup of 10 children with ADHD + Anxiety underwent CBT for anxiety. Results: The results showed that sleep difficulties were better associated with anxiety than with ADHD. CBT reduced sleep onset latency and marginally decreased the total amount of sleep problems. Conclusion: The present study demonstrates that comorbid anxiety in ADHD children is linked with specific sleep disturbances and is sensitive to CBT aimed at reducing anxiety.

The relationship between intelligence measures and 2 EEG measures of non-rapid eye movement sleep, sleep spindles and Sigma activity, was examined in 13 typically-developing (TD) and 13 autistic children with normal IQ and no complaints of poor sleep. Sleep spindles and Sigma EEG activity were computed for frontal (Fp1, Fp2) and central (C3, C4) recording sites. Time in stage 2 sleep and IQ was similar in both groups. Autistic children presented less spindles at Fp2 compared to the TD children. TD children showed negative correlation between verbal IQ and sleep spindle density at Fp2. In the autistic group, verbal and full-scale IQ scores correlated negatively with C3 sleep spindle density. The duration of sleep spindles at Fp1 was shorter in the autistic group than in the TD children. The duration of sleep spindles at C4 was positively correlated with verbal IQ only in the TD group. Fast Sigma EEG activity (13.25-15.75 Hz) was lower at C3 and C4 in autistic children compared to the TD children, particularly in the latter part of the night. Only the TD group showed positive correlation between performance IQ and latter part of the night fast Sigma activity at C4. These results are consistent with a relationship between EEG activity during sleep and cognitive processing in children. The difference between TD and autistic children could derive from dissimilar cortical organization and information processing in these 2 groups.

Myocardial infarction (MI) induces an inflammatory process that is associated with increased apoptosis in the limbic system of rats and the development of post-MI depressive symptoms. Resolvin D1 (RvD1), an omega-3 fatty acid metabolite, is known for its pro-resolution properties; it reduces infarct size and attenuates post-MI depression-like symptoms. The present study was designed to determine if a single RvD1 dose could abate caspase-3 activation, a marker of apoptosis, in the limbic system. Male Sprague-Dawley rats underwent 40 min of myocardial ischemia, followed by 24-h reperfusion. Five min before MI, the animals received a single intra-cardiac RvD1 injection (0.01, 0.1 or 0.3 μg) or vehicle (saline). Infarct size was assessed and caspase-3 activity measured in the amygdala and hippocampus. Rats receiving 0.1 or 0.3 μg RvD1 showed significantly decreased infarct size. Caspase-3 activity was significantly attenuated in the lateral amygdala and dentate gyrus with 0.1 μg RvD1 and in the CA1 region of the hippocampus and medial amygdala with 0.3 μg RvD1. In conclusion, RvD1 could reduce infarct size and caspase-3 activity in the amygdala and hippocampus.

Sleep-wake patterns are rarely examined in adolescents with borderline personality disorder (BPD) or bipolar disorder (BD). Within a developmental perspective, this study explores the sleep-wake cycle of adolescents aged 12-17 years with BPD or BD and healthy controls (HC) during periods with and without entrainment by school/work schedules. Eighteen euthymic BPD, six euthymic BD, and 20 HC adolescents wore wrist actigraphy during nine consecutive days to assess sleep-wake patterns. During school/work days, BPD adolescents spent more time awake when they were in bed compared to HC and BD adolescents (p = 0.039). On schedule-free days, BPD and BD youths spent more time in bed compared to HC adolescents (p = 0.015). BPD adolescents woke up over 1 h later compared to HC (p = 0.003). Total sleep time was more variable between nights in BPD adolescents compared to the HC group (p = 0.031). Future research should explore if sleep-wake pattern disruptions are a cause or a consequence of BPD symptomatology in adolescents. Addressing sleep-wake pattern during clinical assessment and treatment of BPD adolescents may potentially reduce their symptoms; this therapeutic effect still needs to be evaluated.

Studies suggest a sympathetic-parasympathetic disequilibrium in children with autism spectrum disorder (ASD), compared to typically developing (TD) children. The autonomic nervous system (ANS) shows profound modification with age but studies in ASD adults are lacking. The ANS is also influenced by vigilance states such as wakefulness and sleep. The aim of this study is to explore differences in ANS activity in typically developing (TD) and ASD individuals during sleep and wakefulness, as a function of age.Four groups of participants (17 adults with ASD, 16 TD adults, 13 children with ASD and 13 TD children) were recorded for two consecutive nights in a sleep laboratory. Electrocardiogram (ECG) was sampled during wakefulness (before and after sleep) and during stage N2 and REM sleep. Groups were compared on their heart rate variability parameters (LFnu, HFnu, LF/HF ratio) in each vigilance state.Results show that ASD adults had lower HFnu in the morning than TD adults (p 0.05). During REM sleep, adults had higher LF/HF ratio than children, regardless of their clinical status (p 0.05).Results of this study show autonomic distinctiveness during wakefulness specifically in ASD adults, suggesting a lower parasympathetic activity in the morning. Whether this characteristic represents a developmental feature or is related to lower sleep quality remains to be clarified.

Insomnia, which is related to daytime deficits and is a common problem for children with neurodevelopmental disorders (NDDs), is often successfully treated with behavioral strategies. However, there are barriers to accessing these treatments, and there has been little research examining what these interventions need to be usable and effective. The goal of this study was to gain consensus from experts in the field on the key components of an eHealth, parent-implemented, intervention program aimed at improving sleep in children with attention-deficit/hyperactivity disorder, autism spectrum disorder, cerebral palsy, and fetal alcohol spectrum disorder. This was achieved using the Delphi method, which involves asking participants to respond to open-ended questions about a topic of interest and then, in iterative rounds, to rate the recommendations that were made by the group. In the current study, participants (27 responders in the first round, 21 in the second, and 18 in the third) rated a total of 131 recommendations. Of those 131 recommendations, 52 items had high importance and high consensus and were deemed to be priority items to consider for creating an eHealth, parent-delivered, behaviorally-based intervention for insomnia in children with NDD. Furthermore, 75% (n = 84) of the 112 recommendations from the first round were believed to be applicable across all 4 NDD groups, thus providing evidence of the potential for a transdiagnostic intervention.

In 2008, the National Institute of Mental Health (NIMH) announced that in the next few decades, it will be essential to study the various biological, psychological and social "signatures" of mental disorders. Along with this new "signature" approach to mental health disorders, modifications of DSM were introduced. One major modification consisted of incorporating a dimensional approach to mental disorders, which involved analyzing, using a transnosological approach, various factors that are commonly observed across different types of mental disorders. Although this new methodology led to interesting discussions of the DSM5 working groups, it has not been incorporated in the last version of the DSM5. Consequently, the NIMH launched the "Research Domain Criteria" (RDoC) framework in order to provide new ways of classifying mental illnesses based on dimensions of observable behavioral and neurobiological measures. The NIMH emphasizes that it is important to consider the benefits of dimensional measures from the perspective of psychopathology and environmental influences, and it is also important to build these dimensions on neurobiological data. The goal of this paper is to present the perspectives of DSM5 and RDoC to the science of mental health disorders and the impact of this debate on the future of human stress research. The second goal is to present the "Signature Bank" developed by the Institut Universitaire en Sante Mentale de Montreal (IUSMM) that has been developed in line with a dimensional and transnosological approach to mental illness.

We hypothesized that inflammation induced by myocardial ischemia plays a central role in depression-like behavior after myocardial infarction (MI). Several experimental approaches that reduce inflammation also result in attenuation of depressive symptoms. We have demonstrated that Resolvin D1 (RvD1), a metabolite of omega-3 polyunsaturated fatty acids (PUFA) derived from docosahexaenoic acid, diminishes infarct size and neutrophil accumulation in the ischemic myocardium. The aim of this study is to determine if a single RvD1 injection could alleviate depressive symptoms in a rat model of MI. MI was induced in rats by occlusion of the left anterior descending coronary artery for 40 min. Five minutes before ischemia or after reperfusion, 0.1 μg of RvD1 or vehicle was injected in the left ventricle cavity. Fourteen days after MI, behavioral tests (forced swim test and socialization) were conducted to evaluate depression-like symptoms. RvD1 reduced infarct size in the treated vs. the vehicle group. Animals receiving RvD1 also showed better performance in the forced swim and social interaction tests vs. vehicle controls. These results indicate that a single RvD1 dose, given 5 min before occlusion or 5 min after the onset of reperfusion, decreases infarct size and attenuates depression-like symptoms.

This study aimed at characterizing the functional stability of sleep in schizophrenia by quantifying dissociated stages of sleep (DSS), and to explore their correlation with psychopathology. The sleep of 10 first-break, drug-naive young adults with schizophrenia and 10 controls was recorded. Four basic DSS patterns were scored: 1) the transitional EEG-mixed intermediate stage (EMIS); 2) Rapid-eye-movement (REM) sleep without rapid eye movement (RSWR); 3) REM sleep without atonia (RSWA); and 4) non-REM sleep with rapid eye movements. An intermediate sleep (IS) score was calculated by summing EMIS and RSWR scores, and the durations of intra-REM sleep periods IS (IRSPIS) and IS scored “at the expense” of REM sleep (ISERS) were determined. Patients were administered the Brief Psychiatric Rating Scale (BPRS) at the time of recording. Proportions of each DSS variables over total sleep time and proportions of IRSPIS and ISERS over REM sleep duration were compared between patients and controls. Correlation coefficients between DSS variables and BPRS total scores were calculated. The proportion of total DSS did not differ between patients and controls. Among DSS subtypes, RSWA was significantly increased in patients while other comparisons showed no significant differences. Significant positive correlations were found between BPRS scores and proportions of DSS, IS, RSWR, IRSPIS and ISERS over total sleep and REM sleep durations. These results demonstrate the functional instability of REM sleep in first-break, drug naive young adults with schizophrenia and unveil a pattern reminiscent of REM sleep behavior disorder. The significant correlation suggests that schizophrenia and REM sleep share common neuronal control mechanisms.

Poor sleep is a common feature in autism even though patients themselves do not necessarily complain. The impact of poor sleep on daytime cognitive functioning in autism is not well-known and we therefore investigated whether sleep in autism correlates with daytime cognitive performance. A battery of non-verbal tasks was administered, in the morning after a second night of sleep in the laboratory, to 17 young adults with autism and normal intelligence, and 14 typically developed individuals matched for age and IQ; none of the participants complained about sleep problems. Two dimensions of attention (sustained and selective) and 4 types of memory (working, declarative, sensory-motor and cognitive procedural) were tested. Individuals with autism showed clear signs of poor sleep. Their performance differed from the controls in response speed but not in accuracy. Signs of poor sleep in the autism group were significantly correlated with either normal performance (selective attention and declarative memory) or performance inferior to that of the controls (sensory-motor and cognitive procedural memories). Both groups presented a significant negative correlation between slow-wave sleep (SWS) and learning a sensory-motor procedural memory task. Only control participants showed a positive association between SWS duration and number of figures recalled on the declarative memory task. Correlation patterns differed between groups when sleep spindles were considered: they were negatively associated with number of trials needed to learn the sensory-motor procedural memory task in autism and with reaction time and number of errors on selective attention in the controls. Correlation between rapid eye movements (REMs) in REM sleep and cognitive procedural memory was not significant. We conclude that some signs reflecting the presence of poor sleep in adults with high-functioning autism correlate with various aspects of motor output on non-verbal performance tasks. The question is raised whether poor sleep in non-complaining persons with autism should be treated.

Myocardial infarction (MI) has dramatic mid- and long-term consequences at the physiological and behavioral levels, but the mechanisms involved are still unclear. Our laboratory has developed a rat model of post-MI syndrome that displays impaired cardiac functions, neuronal loss in the limbic system, cognitive deficits and behavioral signs of depression. At the neuronal level, caspase-3 activation mediates post-MI apoptosis in different limbic regions, such as the amygdala – peaking at 3 days post-MI. Cognitive and behavioral impairments appear 2-3 weeks post-MI and these correlate statistically with measures of caspase-3 activity. The protocol described here is used to induce MI, collect amygdala tissue and measure caspase-3 activity using spectrofluorometry. To induce MI, the descending coronary artery is occluded for 40 min. The protocol for evaluation of caspase-3 activation starts 3 days after MI: the rats are sacrificed and the amygdala isolated rapidly from the brain. Samples are quickly frozen in liquid nitrogen and kept at -80 °C until actual analysis. The technique performed to assess caspase-3 activation is based on cleavage of a substrate (DEVD-AMC) by caspase-3, which releases a fluorogenic compound that can be measured by spectrofluorometry. The methodology is quantitative and reproducible but the equipment required is expensive and the procedure for quantifying the samples is time-consuming. This technique can be applied to other tissues, such as the heart and kidneys. DEVD-AMC can be replaced by other substrates to measure the activity of other caspases.

Proinflammatory cytokines play a central role in depression-like behaviour and apoptosis in the limbic system after myocardial infarction (MI). A PUFAn-3 diet or the combination ofLactobacillus helveticusR0052 andBifidobacterium longumR0175 probiotics, when given before the ischaemic period, reduce circulating proinflammatory cytokines as well as apoptosis in the limbic system. The present study was designed to determine if the same nutritional interventions maintain their beneficial effects when started after the onset of the reperfusion period and attenuate depression-like behaviour observed after MI. MI was induced by the occlusion of the left anterior descending coronary artery for 40 min in rats. After the onset of reperfusion, animals were fed with a high- or low-PUFAn-3 diet, combined or not with one billion live bacteria ofL. helveticusandB. longum. At 3 d post-MI, caspase-3 enzymatic activities and terminal 2′-deoxyuridine, 5′-triphosphate (dUTP) nick-end labelling (TUNEL)-positive cells were decreased in the CA1, dentate gyrus (DG) and amygdala with the high-PUFAn-3 diet, as compared to the three other diets. Probiotics attenuated caspase-3 activity and TUNEL-positive cells in the DG and the medial amygdala. At 2 weeks post-MI, depression-like behaviour was observed in the low-PUFAn-3 diet without probiotics-group, and this behaviour was attenuated with the high-PUFAn-3 diet or/and probiotics. These results indicate that a high-PUFAn-3 diet or the administration of probiotics, starting after the onset of reperfusion, are beneficial to attenuate apoptosis in the limbic system and post-MI depression in the rat.

Summary Background Borderline personality disorder (BPD) represents 2% of the general population, 10% of outpatient psychiatry facilities, 20% of inpatients and nearly 41% of patients seen in Emergency Room for attempted suicide. Also, 10% complete suicide and 64–66% have comorbid substance dependence. In addition, several studies report sleep subjective complaints in patients with BPD, and research has explored objective sleep disturbances. Objective To examine the results of previous studies in polysomnography in BPD to better characterize the objective sleep disturbances in this population. Data sources and study selection A review of the literature on MedLine and PsycINFO using the term “borderline personality disorder”, “sleep” and “polysomnography” allowed the review of 15 original articles on sleep assessed by PSG in subjects adults with BPD, published between 1980 and may 2010. Results Compared with healthy subjects, a decreased onset delay of rapid eye movements (REM) sleep and an increased REM density have been observed in BPD. In addition BPD shares with major depression the following disturbances: increase in onset latency, decreased total sleep time and efficiency. Limitations Differences between studies regarding sex, age, mood state at the time of the study and psychiatric comorbidity influence the results, which explains the disparity in findings. Conclusion There are objective disturbances associated with BPD according to polysomnographic studies.

Sleep disturbance is common in autism spectrum disorders (ASD) and melatonin is widely prescribed in such cases despite a lack of guidelines. The aim of this paper is to provide a systematic review of efficacy and safety of exogenous melatonin for treating disordered sleep in individuals with ASD. We performed a Pubmed(®) documentary search enlarged by a manual review of references, which finally supplied 12 citations (4 case reports, 3 retrospective studies, 2 open-label clinical trials, and 3 placebo-controlled trials). As a whole, we found that the literature supports the existence of a beneficial effect of melatonin on sleep in individuals with ASD, with only few and minor side effects. However, considering the small number of studies and their methodological limits, these conclusions cannot yet be regarded as evidence-based. Randomized controlled trials and long-term follow-up data are still lacking to better assess efficacy and safety of exogenous melatonin for disordered sleep in individuals with ASD.

We have observed that, after myocardial infarction (MI), rats display apoptosis in the limbic system that can be prevented by pentoxifylline (PTX), a proinflammatory cytokine inhibitor. We have hypothesized that reduction of apoptosis in the limbic system can attenuate the depressive behaviour occurring post-MI. The present study was, therefore, designed to assess the outcome of PTX on depressive behaviour manifesting after MI. Myocardial ischaemia, induced for 40 min in male Sprague-Dawley rats, was followed by reperfusion (MI groups). Sham groups were subjected to the same protocol without occlusion. PTX (10 mg/kg/day) or saline was administered intraperitoneally 15 min before ischaemia, and then every day until sacrifice. Two weeks after ischaemia, depression was evaluated by the forced swim test and the sucrose preference test. At the end of the experiment, the animals were sacrificed, and myocardial infarct size was examined along with plasma IL-1β concentrations. MI rats drank less sucrose in the sucrose preference test and were more immobile in the forced swim test than the sham controls. PTX reversed these behaviours in the MI group to a level similar to that in the untreated sham group, without affecting infarct size. PTX reduced plasma IL-1β concentrations in both sham and MI rats. We conclude that PTX administration significantly reverses the depressive-like behaviour seen after MI in rats.

Myocardial infarction (MI) in rats is followed by a behavioral syndrome similar to human post-MI depression. We tested the effects of escitalopram, a selective serotonin reuptake inhibitor, on this syndrome. MI was induced in 19 Sprague-Dawley rats by occluding the left anterior descending coronary artery for 40min, followed by reperfusion. A sham-operated group of 20 rats was submitted to the same protocol without coronary artery occlusion. Fifteen minutes after the onset of reperfusion, escitalopram (10mg/kg/day, i.p.) or saline was infused continuously through osmotic minipumps. After 2weeks of treatment, the rats were tested for behavioral despair and anhedonia by the forced swimming and sucrose preference tests, respectively. They were then sacrificed, and blood levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), PGE(2) and corticosterone were measured. In a separate cohort of 24 rats, sleep was recorded after 2weeks of post-MI treatment with escitalopram or saline. In MI rats, behavioral despair and anhedonia were blocked by escitalopram but prolonged sleep latency, low total sleep time and short latency to paradoxical sleep (PS) were not; escitalopram decreased PS in sham controls. Plasma TNF-α, PGE(2), and corticosterone levels were higher in MI rats than in the controls. Escitalopram lowered TNF-α, IL-1β, and PGE(2) levels in both groups of rats while IL-6 showed no differences whatsoever. Escitalopram reverses post-MI behavioral syndrome in rats through a mechanism that could involve a reduction of pro-inflammatory cytokines and PGE(2). It has limited effects on sleep disorders in MI rats but reduces PS in control rats.

Autism is a developmental disorder with a neurobiological aetiology. Studies of the autistic brain identified atypical developmental trajectories that may lead to an impaired capacity to modulate electroencephalogram activity during sleep. We assessed the topography and characteristics of non-rapid eye movement sleep electroencephalogram slow waves in 26 boys aged between 6 and 13 years old: 13 with an autism spectrum disorder and 13 typically developing. None of the participants was medicated, intellectually disabled, reported poor sleep, or suffered from medical co-morbidities. Results are derived from a second consecutive night of polysomnography in a sleep laboratory. Slow waves (0.3-4.0 Hz; >75 µV) were automatically detected on artefact-free sections of non-rapid eye movement sleep along the anteroposterior axis in frontal, central, parietal and occipital derivations. Slow wave density (number per minute), amplitude (µV), slope (µV s-1 ) and duration (s) were computed for the first four non-rapid eye movement periods. Slow wave characteristics comparisons between groups, derivations and non-rapid eye movement periods were assessed with three-way mixed ANOVAs. Slow wave density, amplitude, slope and duration were higher in anterior compared with most posterior derivations in both groups. Children with autism spectrum disorder showed lower differences in slow waves between recording sites along the anteroposterior axis than typically developing children. These group differences in the topography of slow wave characteristics were stable across the night. We propose that slow waves during non-rapid eye movement sleep could be an electrophysiological marker of the deviant cortical maturation in autism linked to an atypical functioning of thalamo-cortical networks.

Patients with schizophrenia may have sleep disorders even when clinically stable under antipsychotic treatments. To better understand this issue, we measured sleep characteristics between 1999 and 2003 in 150 outpatients diagnosed with Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) schizophrenia or schizoaffective disorder and 80 healthy controls using a sleep habits questionnaire. Comparisons between both groups were performed and multiple comparisons were Bonferroni corrected. Compared to healthy controls, patients with schizophrenia reported significantly increased sleep latency, time in bed, total sleep time and frequency of naps during weekdays and weekends along with normal sleep efficiency, sleep satisfaction, and feeling of restfulness in the morning. In conclusion, sleep-onset insomnia is a major, enduring disorder in middle-aged, non-hospitalized patients with schizophrenia that are otherwise clinically stable under antipsychotic and adjuvant medications. Noteworthy, these patients do not complain of sleep-maintenance insomnia but report increased sleep propensity and normal sleep satisfaction. These results may reflect circadian disturbances in schizophrenia, but objective laboratory investigations are needed to confirm subjective sleep reports.

Many clinical, laboratory and non-laboratory studies have examined dream content reported by patients with schizophrenia but findings have been variable and inconsistent. Using both questionnaire-based measures and laboratory REM sleep awakenings, we investigated dream content in 14 patients with schizophrenia (mean age = 25.5 ± 3.2 years) under atypical antipsychotic medication and 15 healthy controls (mean age = 22.3 ± 4.2 years). The relationship between eye movement density during REM sleep and dream content was also explored. Questionnaire data revealed that when compared to controls, patients with schizophrenia report experiencing a greater number of nightmares but no significant differences were found on other measures including overall dream recall, presence of recurrent dreams, and frequency of specific emotions. 39 dream reports were collected from each group following awakenings from REM sleep. Laboratory dream narratives from the patients were shorter and, after controlling for report length, most significant differences in dream content between the two groups disappeared with the exception of a greater proportion of unknown characters in the participant group. Patients with schizophrenia spontaneously rated their dream reports as being less bizarre than did controls, despite a similar density of bizarre elements as scored by external judges. Finally, both groups had a comparable density of rapid eye movements during REM sleep but a significant positive correlation between eye-movement density and dream content variables was only found in controls. Taken together, the findings suggest that dream content characteristics in schizophrenia may reflect neurocognitive processes, including emotional processing, specific to this disorder.

Myocardial infarction (MI) stimulates the release of pro-inflammatory substances that induce apoptosis in the limbic system. Pro-inflammatory cytokines are considered as the root cause of apoptosis, although the mechanism is not fully explained and/or understood at this time. In addition, depression may induce gastrointestinal perturbations that maintain the elevated levels of pro-inflammatory cytokines. It has been shown that some specific probiotic formulations may reduce gastrointestinal problems induced by stress and the pro/anti-inflammatory cytokine ratio. Therefore, we hypothesised that probiotics, when given prophylactically, may diminish the apoptosis propensity in the limbic system following a MI. Male adult Sprague–Dawley rats were given probiotics (Lactobacillus helveticusandBifidobacterium longumin combination) or placebo in their drinking-water for four consecutive weeks. A MI was then induced in the rats by occluding the left anterior coronary artery for 40 min. Rats were killed following a 72 h reperfusion period. Infarct size was not different in the two groups. Bax/Bcl-2 (pro-apoptotic/anti-apoptotic) ratio and caspase-3 (pro-apoptotic) activity were reduced in the amygdala (lateral and medial), as well as in the dentate gyrus in the probiotics group when compared with the placebo. Akt activity (anti-apoptotic) was increased in these same three regions. No significant difference was observed in Ca1 and Ca3 for the different markers measured. In conclusion, the probioticsL. helveticusandB. longum, given in combination as preventive therapy, reduced the predisposition of apoptosis found in different cerebral regions following a MI.

Adolescents with anxiety disorders often report sleep disturbance. To dissociate the effects of both sets of symptoms (anxiety vs. sleep disturbances) on clinical markers we recorded evening and morning wake EEG activity in 13 anxious adolescents without sleep complaints and compared results to 15 matched healthy controls. Evening EEG activity did not differ between the two groups; in the morning, patients showed a significantly higher activity than controls at central (0.75–10 Hz and 13–20 Hz) and occipital (2.5–7.75 Hz) electrodes. Trait anxiety scores of anxious participants correlated with central electrodes delta activity and occipital electrodes delta and theta activity. State anxiety correlated with delta activity on central electrodes, particularly in the low frequency range. Conclusion The evening EEG results are not consistent with presence of central nervous system (CNS) hyperarousal in adolescents with anxiety disorders not complaining of sleep disorders. The morning EEG results could point toward a marker of CNS malfunctioning in pediatric anxiety disorders.

The relationship between emotional dream content and Alpha and Beta REM sleep EEG activity was investigated in typical individuals and in Autistic Spectrum Disorders (ASD). Dream narratives of persons with ASD contained fewer emotional elements. In both groups, emotions correlated positively with slow Alpha (8.0-10.0 Hz) spectral power over parieto-occipital and left central regions, as well as with a right occipital EEG asymmetry. Slow Alpha activity in ASD individuals was lower over midline and parasagittal areas and higher over lateral areas compared to controls. Both groups displayed a right-biased slow Alpha activity for midparietal and occipital (significantly higher in control) sites. Results indicate that Alpha EEG activity may represent a neurophysiological substrate associated with emotional dream content. Distinctive Alpha EEG patterns and asymmetries suggest that dream generation implies different brain connectivity in ASD.

Reperfused myocardial infarction induces an inflammatory response that is responsible for local and systemic alterations. Among these, apoptosis observed in the amygdala following myocardial infarction has been pointed out as a consequence of such an inflammatory process. We hypothesized that inhibition of the inducible inflammatory enzyme Cox-2 during the reperfusion period may attenuate the apoptotic process in the amygdala. Anaesthetized rats were subjected to left anterior descending coronary artery occlusion for 40 min, followed by reperfusion. The Cox-2 antagonist Celecoxib (3 mg/kg i.p.) was administered 10 min after the onset of the reperfusion period. After 72 h of reperfusion, infarct size was determined and the lateral and medial amygdala were dissected from the brain. Infarct size was similar between untreated and Celecoxib-treated animals (40-45% of the area at risk). Cox-2 expression was significantly reduced in both parts of the amygdala in the Celecoxib group. Apoptosis regression was observed in the amygdala of the Celecoxib group as shown by decreased number of TUNEL positive cells and by decreased of caspase-3 activation. Bax/Bcl-2 ratio was not significantly altered by Celecoxib while Akt activation was increased in the lateral amygdala but not in the medial amygdala. This data indicates that inhibition of Cox-2 by Celecoxib is associated with regression of apoptosis in the amygdala following myocardial infarction.

Dream questionnaires were completed by 28 young adults with autism spectrum disorder (ASD) participants. Seventy-nine typically developed individual served as the control group. In a subset of 17 persons with ASD and 11 controls matched for verbal IQ, dream narratives were obtained following REM sleep awakenings in a sleep laboratory. Questionnaires revealed that participants with ASD, compared to controls, had fewer recollections of dreaming, fewer bad dreams and fewer emotions. In the sleep laboratory, dream content narratives following REM sleep awakenings were shorter in ASD participants than in controls. ASD participants also reported fewer settings, objects, characters, social interactions, activities, and emotions. It is concluded that these characteristics of dreaming in ASD may reflect neurocognitive dimensions specific to this condition.

Although new atypical antipsychotic agents have been found to improve overall cognitive function in patients with schizophrenia (SZ), some aspects of memory, attention and executive functions still remain impaired. Acetylcholinesterase (AChE) inhibitors, such as rivastigmine, have been shown to improve cognition in other disorders, particularly Alzheimer's disease. Dysfunctions in cholinergic systems, especially in the prefrontal cortex, have been identified in SZ, suggesting that cholinesterase inhibitors may be effective in treating cognitive deficits in this disease.Using a randomized crossover design, we assessed SZ patients with stable symptoms and poor cognitive functioning. Fifty-eight patients with memory deficits, according to subjective complaints or based on clinicians' observations, were assessed with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and Subjective Scale to Investigate Cognition in Schizophrenia (SSTICS). Only 24 of these subjects met the inclusion criteria. Twenty patients took part in the study (four dropped out). All subjects meeting the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for SZ were maintained on their current antipsychotic medication (18 atypicals and two typicals) and were randomly assigned to treatment with rivastigmine. Dosage was a function of tolerability, beginning at 3 mg/day and progressively increasing to 9 mg/day. Subjects were given the Cambridge Neuropsychological Test Automated Battery (CANTAB) at baseline and 3 and 6 months.The results revealed no significant improvement in any of the cognitive variables investigated following rivastigmine treatment and symptom severity scores remained unchanged over all recorded time periods.Rivastigmine treatment did not appear to enhance cognition in SZ patients with important cognitive impairments. This finding needs to be interpreted with care and requires substantiation with larger sample size studies with patients treated with cognitive enhancer for longer periods.

The relationship between sleep architecture and attentional performance was evaluated in neuroleptic-naive patients with schizophrenia and healthy controls. Participants were recorded in a sleep laboratory for two consecutive nights after which selective and sustained attention performance was tested. In both groups of participants, Spearman's rho statistics revealed a negative correlation between reaction time on the selective attention task and sleep spindle density. Only control participants showed a negative correlation between reaction time and duration of stage 2 sleep and a positive correlation between reaction time and duration of stage 1 ("light") sleep. Only persons with schizophrenia showed a negative correlation between reaction time and duration of stage 4 ("deep") sleep. In the sustained attention task, we found no correlation between reaction time and sleep for control participants while persons with schizophrenia showed a negative correlation between reaction time and duration of stage 4 sleep. It is proposed that EEG sleep spindle activity is associated with automatic attentional processing, while stage 2 sleep continuity in healthy individuals and percentage of stage 4 in patients with schizophrenia are associated with voluntary processes. These results support the existence of a relationship between non-rapid-eye-movement sleep and cognitive performance in healthy individuals as well as in persons with schizophrenia.

Studies have reported beneficial effects of cholinergic enhancers, e.g., rivastigmine, on memory in schizophrenia but others have not. Possibly, these discrepancies are related to the lack of specificity of the tests used. This study investigated the effect of rivastigmine on memory in schizophrenia using event-related potentials (ERPs). Eighteen patients treated with atypical antipsychotic received rivastigmine adjuvant therapy in a randomized, crossover design. They were assessed at baseline (T1) and on two subsequent occasions (T2 and T3), where one half of the subjects were taken rivastigmine and the other half not. ERPs were recorded during a recognition memory task on each session. Behavioral and ERP data were analyzed using mixed ANOVA models first at T1 to detect potential group differences and for the trial (T1–T2) to determine the influence of rivastigmine, i.e., session×group interactions. The results showed no group difference at T1 except a trend for one group to be less efficient than the other on RT measures. When controlling for this difference the results on the trial data showed a trend for a benefit of rivastigmine on the RT memory effect. ERP analysis revealed that rivastigmine affects the amplitudes of two components elicited within 150–300 ms over posterior (reduced N2b) and frontal sites (enhanced P2a). It also enhances the magnitude of the memory (old/new) effect on two later components over posterior (N400) and frontal sites (F-N400). These results suggest that rivastigmine improves selective attention by enhancing interference inhibition processes (P2a) and lowering the reactivity to incoming stimulus (N2b). It also improves the integration of information with knowledge (N400) and with its context (F-N400). Generally, this study showed that the beneficial effect of rivastigmine on memory is not unitary but rather comes from its action at different time points within information processing cascade.

It has been observed that a cytokine synthesis inhibitor, pentoxifylline, prevents the apoptotic processes taking place in the amygdala following myocardial infarction. However, it is unknown if the cardioprotective effect of A(2A) adenosine receptor agonist, CGS21680, which reduces cytokine synthesis, would lead to such amygdala apoptosis regression. Thus, this study was designed to investigate whether cardioprotective A(2A) adenosine receptor activation reduces apoptosis in the amygdala following myocardial infarction. Anesthetized rats were subjected to left anterior descending coronary artery occlusion for 40 min, followed by 72 h of reperfusion. The A(2A) agonist CGS21680 (0.2 mug/kg/min i.v.) was administered continuously for 120 min, starting (1) five minutes prior to instituting reperfusion (Early) or (2) five minutes after the beginning of reperfusion (Late). After reperfusion, myocardial infarct size was determined and the amygdala was dissected from the brain. Infarct size was reduced significantly in the Early compared to the Control group (34.6 +/- 1.8% and 52.3 +/- 2.8% respectively; p0.05), with no difference compared to the Late group (40.1 +/- 6.1%). Apoptosis regression was documented in the amygdala of the Early group by an enhanced phosphatidylinositol 3-kinase-Akt pathway activation and Bcl-2 expression concurrently to a caspase-3 activation limitation and reduction in TUNEL-positive cells staining. On the other hand, amygdala TUNEL-positive cell numbers were not reduced in the Late group. Moreover, TNFalpha was significantly reduced in the amygdala of the Early group compared to the Control and Late groups. These results indicate that A(2A) adenosine receptor stimulation is associated with apoptosis regression in the amygdala following myocardial infarction.

BACKGROUND: Myocardial infarction (MI) contains a risk factor for developing episodes of Major Depressive Disorder (MDD). Apoptosis is commonly observed in the reperfused myocardial infarcted heart, and recent findings suggest the existence of apoptosis in MDD. Cytokines, which are released by ischemic myocardium and which may induce apoptosis, have been proposed as a possible cause for MDD. METHODS: Myocardial infarction was produced in anesthetized rats by a 40-minute occlusion of the left anterior descending coronary artery followed by 72 hours of reperfusion. Determination of apoptosis was done in the amygdala, hippocampus and vermis of MI and Sham rats treated or not with pentoxyfilline (PTX), a cytokine synthesis inhibitor (10 mg/kg/day intraperitoneal). RESULTS: Compared to Sham rats, the amygdala of MI rats showed significantly reduced P13K activity, increased Bax/Bcl-2 ratio, caspase-3 activity, and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling)-positive cells. The effect of MI on apoptosis was completely reversed in presence of PTX. No statistical difference was observed in the hippocampus and the vermis in the different groups for any of the biochemical measurements. CONCLUSIONS: These results indicated that MI induce apoptosis in amygdala by a cytokine-sensitive mechanism and may explain the MDD observed following myocardial infarction.

Objective The aim of this study was to investigate the involvement of temporo-occipital regions in the pathophysiology of autistic spectrum disorders (ASD) by using REM sleep and waking EEG. Methods The EEG recordings of 9 persons with ASD and 8 control participants were recorded using a 12-electrode montage. Spectral analysis (0.75–19.75 Hz) was performed on EEG activity recorded upon two activated states: REM sleep and wakefulness. Results During REM sleep, persons with ASD showed a selective, significantly lower absolute beta (13.0–19.75 Hz) spectral amplitude over the primary (O 1 , O 2 ) and associative (T 5 , T 6 ) cortical visual areas compared to controls. Persons with ASD showed significantly higher absolute theta (4.0–7.75 Hz) spectral amplitude over the left frontal pole region (Fp1) compared to controls during evening wakefulness, but not during morning wakefulness. Significance The results of waking EEG are consistent with previously reported observations of neuropsychological signs of frontal atypicalities in ASD; results from REM sleep are the first EEG evidence to support the hypothesis of abnormal visuoperceptual functioning in ASD. Altogether, these results point toward atypical thalamo-cortical mechanisms subserving the neural processing of information in ASD.

Background Myocardial infarction (MI) is associated with apoptosis in the amygdala and, ultimately, with clinical signs of depression. Different treatments have proven to be beneficial in preventing depression, including combination of the probiotics Lactobacillus helveticus and Bifidobacterium longum for prophylaxis. We have speculated previously that the benefit of these probiotics is due to their anti-inflammatory properties, and evidence suggests that an intact vagus nerve is important for this effect to occur. This study was designed to ascertain vagus nerve involvement in the beneficial influence of probiotics on caspase activities in our post-MI animal model of depression. Methods Probiotics and/or vehicle were administered daily to male adult rats, 14 days before MI and until euthanasia. Vagotomy was performed in subgroups of rats 40 min before MI. They were sacrificed after 3 days of reperfusion, and MI size was assessed along with caspase-3 and -8 activities in the amygdala. Key Results Probiotics had no effect on infarct size but vagotomy increased it. Caspase-3 and caspase-8 activities in the amygdala were higher in MI than in sham-operated rats, and this outcome was reversed by probiotics. The beneficial influence of probiotics was abolished by vagotomy. Conclusions & Inferences Our data indicate that the effect of probiotics on caspase activities in the amygdala after MI depends on an intact vagus nerve.