Summary There is now an overwhelming preponderance of evidence that cognitive behavioural therapy for insomnia (CBT‐I) is effective, as effective as sedative hypnotics during acute treatment (4–8 weeks), and is more effective in long term (following treatment). Although the efficacy of CBT‐I in the treatment of chronic insomnia is well known, however there is little objective data on the effects of CBT‐I on sleep architecture and sleep EEG power densities. The present study evaluated, first, subjective change in sleep quality and quantity, and secondly the modifications occurring in polysomnography and EEG power densities during sleep after 8 weeks of CBT‐I. Nine free drug patients with psychophysiological insomnia, aged 33–62 years (mean age 47 ± 9.7 years), seven female and two male participated in the study. Self‐report questionnaires were administered 1 week before and 1 week after CBT‐I, a sleep diary was completed each day 1 week before CBT‐I, during CBT‐I and 1 week after CBT‐I. Subjects underwent two consecutive polysomnographic nights before and after CBT‐I. Spectral analysis was performed the second night following 16 h of controlled wakefulness. After CBT‐I, only scales assessing insomnia were significantly decreased, stages 2, REM sleep and SWS durations were significantly increased. Slow wave activity (SWA) was increased and the SWA decay shortened, beta and sigma activity were reduced. In conclusion CBT‐I improves both subjective and objective sleep quality of sleep. CBT‐I may enhance sleep pressure and improve homeostatic sleep regulation.

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The aim of the study was to elaborate a method to estimate the degree of cognitive impairment in Alzheimer’s disease from the EEG quantitative indicators. We examined 38 unmedicated patients with a diagnosis of Alzheimer’s disease, with various stages (mild, moderate, and severe) of dementia. The EEG recordings were evaluated both visually and by means of computer analysis. The EEG spectra and coherences in 6 frequency bands were calculated in 16 EEG derivations. Among various EEG indicators, a decrease in the alpha coherence and an increase in the delta coherence was found to be most significantly correlated to the degree of dementia. Combining 6 variables from the spectrum and coherence analysis by means of the multiple regression model, a high correlation (r = 0.87) between a set of EEG variables and the Mini-Mental State Examination score could be obtained. The results suggest that the EEG can supplement the clinical examination by providing an independent assessment of the degree of dementia. The results also suggest that the EEG coherences are of particular interest in dementia, being an indicator of the signal transfer between various parts of the brain cortex.

The %VLFI and LF/HF ratio provide indirect measures of sleep fragmentation, suggesting that HRV measures during sleep assess more the associated sleep fragmentation than the presence of a specific sleep disorder.

The extent to which sleep disorders are associated with impairment of health-related quality of life (HRQoL) is poorly described in the developing world. We investigated the prevalence and severity of various sleep disorders and their associations with HRQoL in an urban Georgian population. 395 volunteers (20–60 years) completed Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, STOP-Bang questionnaire, Insomnia Severity Index, Beck Depression Inventory-Short Form, and Short Form Health Survey (SF-12). Socio-demographic data and body mass index (BMI) were obtained. The prevalence of sleep disorders and their association with HRQoL was considerable. All SF-12 components and physical and mental component summaries (PCS, MCS) were significantly lower in poor sleepers, subjects with daytime sleepiness, apnea risk, or insomnia. Insomnia and apnea severity were also associated with lower scores on most SF-12 dimensions. The effect of insomnia severity was more pronounced on MCS, while apnea severity—on PCS. Hierarchical analyses showed that after controlling for potential confounding factors (demographics, depression, BMI), sleep quality significantly increased model’s predictive power with an R2 change (ΔR2) by 3.5% for PCS (adjusted R2 = 0.27) and by 2.9% for MCS (adjusted R2 = 0.48); for the other SF-12 components ΔR2 ranged between 1.4% and 4.6%. ESS, STOP-Bang, ISI scores, all exerted clear effects on PCS and MCS in an individual regression models. Our results confirm and extend the findings of studies from Western societies and strongly support the importance of sleep for HRQoL. Elaboration of intervention programs designed to strengthen sleep-related health care and thereof HRQoL is especially important in the developing world.

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BACKGROUND AND PURPOSEOpioids affect the circadian clock and may change the timing of many physiological processes. This study was undertaken to investigate the daily changes in sensitivity of the circadian pacemaker to an analgesic dose of morphine, and to uncover a possible interplay between circadian and opioid signalling. EXPERIMENTAL APPROACHA time-dependent effect of morphine (1 mg·kg −1 , i.p.) applied either during the day or during the early night was followed, and the levels of phosphorylated ERK1/2, GSK3β, c-Fos and Per genes were assessed by immunohistochemistry and in situ hybridization. The effect of morphine pretreatment on light-induced pERK and c-Fos was examined, and day/night difference in activity of opioid receptors was evaluated by [ KEY RESULTSMorphine stimulated a rise in pERK1/2 and pGSK3β levels in the suprachiasmatic nucleus (SCN) when applied during the day but significantly reduced both kinases when applied during the night. Morphine at night transiently induced Period1 but not Period2 in the SCN and did not attenuate the light-induced level of pERK1/2 and c-Fos in the SCN. The activity of all three principal opioid receptors was high during the day but decreased significantly at night, except for the δ receptor. Finally, we demonstrated daily profiles of pERK1/2 and pGSK3β levels in the rat ventrolateral and dorsomedial SCN. CONCLUSIONS AND IMPLICATIONSOur data suggest that the phase-shifting effect of opioids may be mediated via post-translational modification of clock proteins by means of activated ERK1/2 and GSK3β. Abbreviations

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