Although patients with insomnia often show a discrepancy between self-reported and objective sleep parameters, the role of and change in this phenomenon during treatment remain unclear. The present study aimed to assess the effect of cognitive behavioural therapy for insomnia on subjective and objective sleep discrepancy of total sleep time, sleep-onset latency and wake after sleep onset. The total sleep time discrepancy was also assessed across the entire therapy. The second aim was to examine the treatment outcome of two insomnia groups differing in sleep perception. Thirty-six adults with insomnia (mean age = 46.7 years, SD = 13.9; 22 females) were enrolled in the final analyses. Patients underwent a 6-week group cognitive behavioural therapy for insomnia programme. Sleep diary and actigraphy measurements were obtained during the therapy. Patients who underestimated total sleep time (n = 16; underestimating group) were compared with patients who accurately perceived or overestimated total sleep time (n = 20; accurate/overestimating group). After cognitive behavioural therapy for insomnia, a significant decrease of total sleep time and sleep-onset latency discrepancy was observed without a change in wake after sleep onset discrepancy in the total sample. Only the underestimating group reported decreased sleep-onset latency discrepancy after the treatment, whereas total sleep time discrepancy significantly changed in both groups. The underestimating group showed a significant decrease of total sleep time discrepancy from Week 1 to Week 2 when the sleep restriction was implemented, whereas the accurate/ overestimating group showed the first significant change at Week 4. In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different therapeutic components could play important roles in each group. components could play important roles in each group.

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Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin’s antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep.