Co-morbid insomnia and sleep apnea (COMISA) is a highly prevalent and debilitating disorder, which results in additive impairments to patients’ sleep, daytime functioning, and quality of life, and complex diagnostic and treatment decisions for clinicians. Although the presence of COMISA was first recognized by Christian Guilleminault and colleagues in 1973, it received very little research attention for almost three decades, until the publication of two articles in 1999 and 2001 which collectively reported a 30%–50% co-morbid prevalence rate, and re-ignited research interest in the field. Since 1999, there has been an exponential increase in research documenting the high prevalence, common characteristics, treatment complexities, and bi-directional relationships of COMISA. Recent trials indicate that co-morbid insomnia symptoms may be treated with cognitive and behavioral therapy for insomnia, to increase acceptance and use of continuous positive airway pressure therapy. Hence, the treatment of COMISA appears to require nuanced diagnostic considerations, and multi-faceted treatment approaches provided by multi-disciplinary teams of psychologists and physicians. In this narrative review, we present a brief overview of the history of COMISA research, describe the importance of measuring and managing insomnia symptoms in the presence of sleep apnea, discuss important methodological and diagnostic considerations for COMISA, and review several recent randomized controlled trials investigating the combination of CBTi and CPAP therapy. We aim to provide clinicians with pragmatic suggestions and tools to identify, and manage this prevalent COMISA disorder in clinical settings, and discuss future avenues of research to progress the field.

Chronotype differences in circadian rhythms of temperature, melatonin, and sleepiness as measured in a modified constant routine protocol Leon Lack, Michelle Bailey, Nicole Lovato, Helen WrightSchool of Psychology, Flinders University, Adelaide, South Australia, Australia Evening chronotypes typically have sleep patterns timed 2–3 hours later than morning chronotypes. Ambulatory studies have suggested that differences in the timing of underlying circadian rhythms as a cause of the sleep period differences. However, differences in endogenous circadian rhythms are best explored in laboratory protocols such as the constant routine. We used a 27-hour modified constant routine to measure the endogenous core temperature and melatonin circadian rhythms as well as subjective and objective sleepiness from hourly 15-minute sleep opportunities. Ten (8f) morning type individuals were compared with 12 (8f) evening types. All were young, healthy, good sleepers. The typical sleep onset, arising times, circadian phase markers for temperature and melatonin and objective sleepiness were all 2–3 hours later for the evening types than morning types. However, consistent with past studies the differences for the subjective sleepiness rhythms were much greater (5–9 hours). Therefore, the present study supports the important role of subjective alertness/sleepiness in determining the sleep period differences between morning and evening types and the possible vulnerability of evening types to delayed sleep phase disorder.Keywords: chronotype, constant routine, circadian rhythms, sleep propensity, subjective sleepiness

The purpose was to remedy the lack of experimental studies directly comparing the effects of brief and long daytime naps following nocturnal sleep restriction. Twelve young adult healthy sleepers participated in a repeated measures design comparing the effects of no nap, a 10-minute nap, and a 30-minute afternoon nap in each case following a night of 4.7 hours of total sleep time. Objective and subjective alertness measures and cognitive performance measures were taken before, then 5, 35, and 60 minutes after the termination of the nap. N/A N/A N/A In the no nap condition measures showed either no change or a decreases of alertness and performance across the testing period. Following the 10-minute nap there was an immediate improvement in subjective alertness and cognitive performance which was sustained for the hour of post nap testing. Immediately following the 30 minute nap most measures of alertness and performance declined but showed some recovery by the end of testing. Because the delayed benefits following the 30-minute nap may be due to sleep inertia, longer post-nap testing periods should be investigated. However, we conclude that the detrimental effects of sleep restriction were more rapidly and significantly ameliorated, at least within the hour following the nap, by a 10-minute afternoon nap.