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The pathogenesis, pathophysiology, and pharmacotherapy of sleep bruxism (SB) are still not fully understood. We investigated symptomatology, objective and subjective sleep and awakening quality of middle-aged bruxers compared with controls and acute effects of clonazepam 1 mg compared with placebo by polysomnography and psychometry. Twenty-one drug-free bruxers spent 3 nights in the sleep lab, 21 age- and sex-matched controls 2 nights. Clinically, bruxers exhibited deteriorated PSQI, SAS, SDS and IRLSSG measures, polysomnographically impaired sleep maintenance, increased movement time, stage shift index, periodic leg movements (PLM) and arousals and psychometrically deteriorated subjective sleep and awakening quality, evening/morning well-being, drive, mood, drowsiness, attention variability, memory, and fine motor activity. As compared with placebo, clonazepam significantly decreased the SB index in all patients (mean: −42 ± 15%). Sleep efficiency, maintenance, latency, awakenings and nocturnal wake time, the stage shift index, S1, PLM, the arousal index, subjective sleep and awakening quality, and fine motor activity improved. [ABSTRACT FROM AUTHOR]

Interrater variability of sleep stage scorings has an essential impact not only on the reading of polysomnographic sleep studies (PSGs) for clinical trials but also on the evaluation of patients’ sleep. With the introduction of a new standard for sleep stage scorings (AASM standard) there is a need for studies on interrater reliability (IRR). The SIESTA database resulting from an EU-funded project provides a large number of studies ( n = 72; 56 healthy controls and 16 subjects with different sleep disorders, mean age ± SD: 57.7 ± 18.7, 34 females) for which scorings according to both standards (AASM and R&K) were done. Differences in IRR were analysed at two levels: (1) based on quantitative sleep parameter by means of intraclass correlations; and (2) based on an epoch-by-epoch comparison by means of Cohen’s kappa and Fleiss’ kappa. The overall agreement was for the AASM standard 82.0% (Cohen’s kappa = 0.76) and for the R&K standard 80.6% (Cohen’s kappa = 0.68). Agreements increased from R&K to AASM for all sleep stages, except N2. The results of this study underline that the modification of the scoring rules improve IRR as a result of the integration of occipital, central and frontal leads on the one hand, but decline IRR on the other hand specifically for N2, due to the new rule that cortical arousals with or without concurrent increase in submental electromyogram are critical events for the end of N2. [ABSTRACT FROM AUTHOR]

Utilizing polysomnography (PSG) and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients (mean age 50 ± 14) with nonorganic insomnia (F 51.0) related to dysthymia (F 34.1) as compared with 11 age- and sex-matched normal controls. Patients demonstrated decreased sleep efficiency and sleep stage S2 as well as increased sleep latency to S1, S2 and S3, wakefulness within the total sleep period, number of awakenings, S1 and REM sleep. There was no intergroup difference in REM latency. Subjective sleep quality and the total score of the Self-Assessment Scale for Sleep and Awakening Quality (SSA) were deteriorated as were evening and morning well-being, mood, affectivity and drowsiness. Noopsychic measures showed deteriorated numerical memory, fine motor activity and reaction time variability. In a placebo-controlled crossover design study, the acute effects of 100 mg trazodone[sup 1] , a serotonin reuptake inhibitor with a sedative action due to 5HT[sub 2] and α[sub 1] receptor blockade, were investigated in the patients. As compared with placebo, trazodone induced an increase in slow-wave sleep (S3 + 4), a lengthening of REM latency, a decrease in REM sleep and a normalization of the periodic leg movement (PLM) index. In the morning, there was a minimal increase in somatic complaints and a decrease in critical flicker frequency and systolic blood pressure. In conclusion, our study demonstrated that dysthymia induced significant changes in objective and subjective sleep and awakening quality, which were counteracted by 100 mg trazodone, thus suggesting a key-lock principle in the treatment of nonorganic insomnia related to dysthymia with this drug.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

AbstractThe goal of our study was to investigate different aspects of sleep, namely the sleep-wake cycle and sleep stages, in the vegetative state/unresponsive wakefulness syndrome (VS/UWS), and minimally conscious state (MCS). A 24-h polysomnography was performed in 20 patients who were in a UWS (n=10) or in a MCS (n=10) because of brain injury. The data were first tested for the presence of a sleep-wake cycle, and the observed sleep patterns were compared with standard scoring criteria. Sleep spindles, slow wave sleep, and rapid eye movement sleep were quantified and their clinical value was investigated. According to our results, an electrophysiological sleep-wake cycle was identified in five MCS and three VS/UWS patients. Sleep stages did not always match the standard scoring criteria, which therefore needed to be adapted. Sleep spindles were present more in patients who clinically improved within 6 months. Slow wave sleep was present in eight MCS and three VS/UWS patients but never in the ischemic etiology. Rapid eye movement sleep, and therefore dreaming that is a form of consciousness, was present in all MCS and three VS/UWS patients. In conclusion, the presence of alternating periods of eyes-open/eyes-closed cycles does not necessarily imply preserved electrophysiological sleep architecture in the UWS and MCS, contrary to previous definition. The investigation of sleep is a little studied yet simple and informative way to evaluate the integrity of residual brain function in patients with disorders of consciousness with possible clinical diagnostic and prognostic implications. [ABSTRACT FROM AUTHOR]