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Depression, anxiety, sleep disturbances and poor relationship functioning often co-occur with the confluence of these factors contributing to greater suicide risk. This study investigated whether the pathways between depression, anxiety, sleep disturbances, and relationship functioning differentiated patients with suicide attempt history from those with suicidal ideation history. Patients seeking partial hospital treatment for severe psychiatric symptoms (N = 180) completed interviews assessing psychiatric and suicidal symptom histories, and self-report measures of sleep behaviors, anxiety, depression, and relationship functioning. Multiple sleep behaviors were examined: duration, sleep onset latency, and bedtime. Bias-corrected bootstrap mediation and moderated mediation analyses with suicide attempt as the moderator were used to evaluate pathways between variables. Among patients with ideation and attempt history, (1) sleep onset latency significantly mediated the association between depression and relationship functioning and that between anxiety and relationship functioning; (2) relationship functioning significantly mediated the association between depression and sleep onset latency and that between anxiety and sleep onset latency. These pathways were not significant among patients with suicidal ideation only. No other sleep behaviors were related to study variables. The reciprocal relationship between disrupted sleep onset latency and poor relationship functioning was specifically linked to more severe psychiatric symptoms among acute patients with suicide attempt histories.

This study investigated sleep subtypes in schizophrenia, and their response to Cognitive Behavioural Therapy for Insomnia (CBT-I) treatment. Sleep profiling was conducted using latent class analysis on baseline Pittsburgh Sleep Quality Index data (N = 74 outpatients with schizophrenia who were poor sleepers, 52% male, mean age = 41.4 years). Of these, 40 took part in CBT-I treatment. Analyses revealed three sleep subtypes based on total sleep time (TST), sleep efficiency (SE), and sleep onset latency (SOL) parameters: Cluster 1 ('classic severe insomnia', 44.6%), Cluster 2 ('insomnia with normal sleep duration', 37.8%), and Cluster 3 ('insomnia with hypersomnia', 17.6%). Gains analysis of pre- and post-treatment data from CBT-I participants revealed improvements in sleep and psychopathology in all three clusters, although there were some group differences in the areas and magnitude of improvement. Cluster 1 showed the greatest benefits with longer TST and improved SE. Cluster 2 showed a comparatively blunted treatment response although TST moved closer to recommended sleep guidelines. Cluster 3 showed significant reductions in TST. Altogether, this is the first demonstration of different sleep profiles in schizophrenia and their influence on treatment response to CBT-I. It also supports the notion that therapies should be tailored to the person and their insomnia presentation.

Sleep disturbance may be the most often endorsed symptom of posttraumatic stress disorder (PTSD). Much of this research is based on subjective reports from trauma survivors; however, objective measures of sleep-related impairment have yielded findings inconsistent with self-report data. More studies investigating subjective and objective assessments concordantly are needed to understand sleep impairment in PTSD. The current study examined PTSD-related sleep disturbance in a female interpersonal violence cohort with full PTSD diagnoses (N = 51) assessing subjective (global and daily diary measures) and objective (actigraphy) sleep measures concurrently. PTSD severity was positively associated with global, subjective reports of sleep impairment and insomnia. Subjective measures of sleep (including global sleep impairment, insomnia, and daily sleep diary reports of total sleep time, sleep efficiency, and sleep onset latency) were moderately to strongly correlated. However, no significant correlations between subjective and objective reports of sleep impairment were found in this cohort. Analyses demonstrated an overall elevation in subjectively reported sleep impairment when compared to objective measurement assessed concurrently. Findings demonstrate a lack of agreement between subjective and objective measurements of sleep in a PTSD-positive female cohort, suggesting objective and subjective sleep impairments are distinct sleep parameters that do not necessarily directly co-vary.

Sleep disorder is a risk factor for several systemic inflammation-related diseases and there are extensive data showing that schizophrenia is associated with chronic low-grade systemic inflammation. This study investigated the associations between sleep quality and inflammatory markers in patients with schizophrenia, which has not been examined before. Sleep quality (total sleep time, sleep efficiency, sleep onset latency, total activity counts, wake after sleep onset, number of awakening, and average length of awakening) was measured using actigraphy in 199 schizophrenia inpatients. The state of inflammation was measured using blood concentration of white blood cells (WBC) and neutrophils, together with neutrophil-lymphocyte ratio (NLR), and platelet-lymphocyte ratio (PLR). The results showed that total sleep time was negatively associated with NLR and PLR, and sleep efficiency was negatively associated with neutrophil counts and NLR. Sleep onset latency, total activity counts, wake after sleep onset, and number of awakening were positively associated with WBC and neutrophil counts. The average length of awakening was positively associated with NLR and PLR. This is the first report to suggest that improving sleep quality may modulate the state of inflammation in patients with schizophrenia.

A blunting of heart rate (HR) reduction during sleep has been reported to be associated with increased all-cause mortality. An increased incident of cardiovascular events has been observed in patients with insomnia but the relationship between nighttime HR and insomnia remains unclear. Here we investigated the HR patterns during the sleep onset period and its association with the length of sleep onset latency (SOL). Nineteen sleep-onset insomniacs (SOI) and 14 good sleepers had their sleep analyzed. Linear regression and nonlinear Hilbert-Huang transform (HHT) of the HR slope were performed in order to analyze HR dynamics during the sleep onset period. A significant depression in HR fluctuation was identified among the SOI group during the sleep onset period when linear regression and HHT analysis were applied. The magnitude of the HR reduction was associated with both polysomnography-defined and subjective SOL; moreover, we found that the linear regression and HHT slopes of the HR showed great sensitivity with respect to sleep quality. Our findings indicate that HR dynamics during the sleep onset period are sensitive to sleep initiation difficulty and respond to the SOL, which indicates that the presence of autonomic dysfunction would seem to affect the progress of falling asleep.

Anxiety affects millions of people and has been shown to co-occur in combination with sleep disturbances, generating heavy medical costs and a huge socio-medico-economic burden. Sleep-studies in anxiety disorders are inconsistent and the effects of state and trait anxiety are unexplored. We selected 1083 patients from the database of a hospital sleep laboratory. The patients had polysomnography for different sleep disorders; their sleep initiation (sleep onset latency), sleep maintenance (total sleep time), non-rapid eye movement sleep-, and rapid eye movement sleep parameters; as well as their State-Trait Anxiety Inventory and Beck depression scale were measured. In order to be included in our study, individuals needed to score in the low or high range on the State and/or Trait Subscales of the State-Trait Anxiety Inventory. We found that both state and trait anxiety affected non-rapid eye movement sleep parameters. Sleep onset latency changes predominantly associated to state anxiety while rapid eye movement parameters related to trait anxiety.

Studies of the correlation of subjective and objective sleep measures in depressed patients have produced mixed results so far. Further, they were carried out in sleep laboratories and tended to obtain one-off assessments, thus not taking into account the effect of treatment. We investigated forty (40) patients over the course of 8-week treatment of depression with either paroxetine or nefazodone. We used home polysomnography at baseline, nights 3 and 10, and week 8 of treatment, with extensive assessments of subjective sleep, the morning after each sleep recording. The patients were able to judge accurately their total sleep time and sleep onset latency, both before and during treatment. However, they were inaccurate in estimating the number of times they woke up during the night. Sleep satisfaction correlated negatively with Stage 1 sleep at baseline. Sleep quality was represented by a combination of subjective parameters measuring the ease of initiation and maintenance of sleep, and it appeared to derive from slow wave sleep and sleep continuity as seen in polysomnography. The partial discrepancy between subjective and objective measures suggests that a cognitive element is combined with the biological element to produce the sleep problems reported by depressed patients.

Sleep abnormalities have been consistently observed in patients with schizophrenia. Elevated levels of corticotropin releasing factor (CRF) and prostaglandins (PGs) in the cerebrospinal fluid (CSF) of patients with schizophrenia have been reported, and these neurochemical substances, known to modulate sleep in experimental animals, may play a role in these sleep abnormalities. In this study, we measured PGD2, PGE2, PGF2alpha and CRF levels in the CSF of 14 unmedicated schizophrenic patients and 14 age- and sex-matched control subjects. Polysomnographic recordings were also carried out for each subject. As expected, the sleep of the schizophrenic subjects significantly differed from that of the controls; schizophrenic subjects had a longer sleep onset latency, slept less, spent fewer minutes in stage 2 sleep and had a lower sleep efficiency. We could not, however, detect any differences in CSF CRF and PG levels between normal and schizophrenic subjects, nor could we find any correlation between CSF variables and sleep parameters in the schizophrenic subjects and the non-psychiatric controls. These results do not favor the hypothesis of a role for CRF or PGs in the pathophysiology of sleep disturbances in schizophrenia.

Hypocretins/orexins are newly identified peptides of hypothalamic origin. Hypocretin deficiency is involved in the sleep disorder narcolepsy, suggesting the importance of hypocretin neurotransmission for the regulation of sleep. Hypocretin is known to excite midbrain dopaminergic neurons and to induce hyperactivity and stereotypy in animals. Altered hypocretin neurotransmission might therefore be involved in schizophrenia, since an involvement of dopaminergic mechanisms and an association with sleep disturbance are well demonstrated in patients with schizophrenia. Hypocretin is also known to affect the hypothalamic-pituitary-adrenal axis by stimulating the release of corticotropin releasing hormone (CRH). In the current study, we measured CSF hypocretin levels in 12 controls and 13 patients with chronic schizophrenia associated with moderate sleep disturbance, such as longer sleep onset latency, decreased total sleep time and decreased sleep efficacy. No difference in CSF hypocretin levels between schizophrenia and control subjects was found. CSF hypocretin levels were positively correlated with CSF CRH levels in the patient, control and combined subject populations, but the correlation did not reach statistical significance in any population. The hypocretin levels in schizophrenic patients were, however, positively and significantly correlated with sleep latency, one of the most consistent sleep abnormalities seen in schizophrenia. This correlation was not significant in controls, and no other significant correlation between CSF hypocretin levels and any measure of sleep architecture in either patients or controls was observed. Further studies of whether CNS hypocretin neurotransmission is involved in sleep and neuroendocrine abnormalities seen in patients with schizophrenia and other psychiatric conditions are warranted.

A significant association between rapid eye movement (REM) sleep latency and the number of non-REM/REM sleep cycles was found 15 years ago in a large retrospective study. The present prospective study further explored this intra-sleep relationship and analyzed the links between these two variables and the mean cycle duration. It was based on a carefully selected group of healthy control subjects whose sleep was polysomnographically recorded at home for 4 sequential nights. The latency of REM sleep was inversely correlated with the number of cycles and positively correlated with the mean cycle duration, both in individual nights and on means of 4 nights. The present study demonstrated that variations in the number of cycles or the mean cycle duration between the nights are far less important than the substantial differences observed between subjects. Present outcomes support the study of sleep cycle periods and frequencies in those psychiatric disorders where REM sleep latencies have been found to be shorter, and they suggest that these variables be included in sleep studies in which cycles are compared with each other.

To examine the relationship of clinical symptoms to sleep architecture, polysomnography and clinical ratings were carried out in 20 male psychiatric in-patients who met Research Diagnostic Criteria for schizophrenia. Clinical symptoms were assessed by the Brief Psychiatric Rating Scale (BPRS). Four BPRS sub-factors, i.e., 'Thinking Disturbance', 'Withdrawal/Retardation', 'Hostility/Suspiciousness', and 'Anxiety/Depression' were correlated with five components of sleep architecture, namely, sleep onset latency, total sleep time, total slow wave sleep minutes (the summation of visually scored stages 3 and 4), total REM minutes, and REM latency. Partial correlations were computed to control for the effects of age. Of the 20 correlation coefficients computed, only one was statistically significant after Bonferroni correction, namely, sleep onset latency was positively correlated with the 'Thinking Disturbance' factor. This finding is consistent with studies showing that psychotic exacerbation is associated with reduced sleep efficiency. In contrast to this cross-sectional design, longitudinal studies are more likely to clarify the relationship of sleep architecture to changes in clinical state.

Ten adolescents with major depression and 10 age-matched controls were studied with polysomnography for 3 consecutive nights. The sleep records were analyzed for variables pertaining to sleep continuity (total sleep time, sleep efficiency, sleep onset latency, number of awakenings, and number of stage shifts), sleep architecture (Stages 1, 2, 3, and 4), and rapid eye movement (REM) sleep (total) REM sleep time, number of REM periods, REM latency, and REM density). The experimental and control groups were compared on 14 variables with the t test for independent groups. The results indicated that none of the sleep variables differed significantly between the two groups. These results confirm earlier findings indicating that the abnormalities in REM latency and REM density that characterize adults with major depression are absent in adolescents suffering from major depression. Developmental and diagnostic variables are discussed as possible explanations for the sleep differences between adolescents and adults with depressive disorders.

Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.

Sleep polygraphic recordings were performed during 3 consecutive nights in 12 inpatients with generalized anxiety disorder (GAD) in comparison with age- and sex-matched groups of patients with major depressive disorder (MDD) and normal subjects. GAD patients differed significantly from those with MDD. A lower number of awakenings and stage shifts in night 1 and the mean of the 3 nights and a shorter rapid eye movement (REM) duration in night 1 but longer REM latency in the mean of the 3 nights were observed in GAD in comparison to MDD. GAD patients also showed a significantly longer sleep onset latency and shorter duration of total sleep time and Stage 2 than control subjects. Electroencephalographic sleep recordings, as well as other laboratory tests, may help the clinician to differentiate anxiety from depressive disorders.