Search

Cortical hyperarousal is higher in insomnia sufferers (INS) than in good sleepers (GS) and could be related to an alteration in sleep protection mechanisms, like reduced density or altered characteristics in sleep spindles. The deficient sleep protection mechanisms might in turn enhance underestimation of sleep. This study’s objective was to document sleep spindles characteristics in INS compared with GS and to investigate their potential role in sleep consolidation and misperception. Seventeen individuals with paradoxical insomnia (PARA-I), 24 individuals with psychophysiological insomnia (PSY-I), and 29 GS completed four consecutive polysomnographic nights in laboratory. Sleep spindles were detected automatically during stage 2 and SWS (3-4) on night 3. Number, density, duration, frequency, and amplitude of sleep spindles were calculated. A misperception index was used to determine the degree of discrepancy between subjective and objective total sleep times. Kruskal-Wallis H tests and post hoc tests revealed that PARA-I had significantly shorter sleep spindles than GS but that PSY-I and GS did not differ on spindles length. A standard multiple regression model revealed that neither sleep spindles characteristics nor objective sleep measures were predictive of sleep misperception. A longer duration of spindles could reflect a higher gating process but this hypothesis still needs to be confirmed in replication studies. [ABSTRACT FROM AUTHOR]

Our objective was to investigate the physiological mechanisms involved in the sleep restriction treatment of insomnia. A multiple baseline across subjects design was used. Sleep of five participants suffering from insomnia was assessed throughout the experimentation by sleep diaries and actigraphy. Ten nights of polysomnography were conducted over five occasions. The first two-night assessment served to screen for sleep disorders and to establish a baseline for dependent measures. Three assessments were undertaken across the treatment interval, with the fifth and last one coming at follow-up. Daily cortisol assays were obtained. Sleep restriction therapy was applied in-lab for the first two nights of treatment and was subsequently supervised weekly. Interrupted time series analyses were computed on sleep diary data and showed a significantly decreased wake time, increasedsleep efficiency, and decreased total sleep time. Sleepiness at night seems positively related to sleep variables, polysomnography data suggest objective changes mainly for stage 2, and power spectral analysis shows a decrease in beta-1 and -2 powers for the second night of treatment. Cortisol levels seem to be lower during treatment. These preliminary results confirmpart of the proposed physiological mechanisms and suggest that sleep restriction contributes to a rapid decrease in hyperarousal insomnia. [ABSTRACT FROM AUTHOR]