PURPOSE:Comorbid insomnia and cancer-related cognitive impairment (CRCI) are experienced by up to 26% of individuals diagnosed with cancer. This study examined the efficacy and durability of cognitive behavioral therapy for insomnia (CBT-I) on perceived CRCI in cancer survivors. METHODS:Atlantic Canadian cancer survivors with insomnia and CRCI were randomly assigned to receive seven weekly virtual CBT-I sessions (n = 63) or placed in a waitlist control group (n = 69) to receive treatment after the waiting period. Participants completed assessments at baseline, 1 month (mid-treatment), and 2 months (post-treatment). Age- and education-adjusted mixed-effects models using intention-to-treat principles assessed change at post-treatment. Data from both groups were then pooled to assess the durability of effects at 3 and 6 months. A mediation analysis examined whether change in insomnia symptoms mediated the effect of CBT-I on cognitive outcomes. RESULTS:The mean age of the sample was 60 years, 77% were women, and breast cancer was the most common diagnosis (41%). The treatment group reported an 11.35-point reduction in insomnia severity, compared with a 2.67-point reduction in the waitlist control group ( < .001). The treatment group had a greater overall improvement than the waitlist control on perceived cognitive impairment ( < .001; = 0.75), cognitive abilities ( < .001; = 0.92), and impact on quality of life ( < .001; = 1.01). These improvements were maintained at follow-up. Change in insomnia symptoms fully mediated the effect of CBT-I on subjective cognitive outcomes. CONCLUSION:Treating insomnia with CBT-I produces clinically meaningful and durable improvements in CRCI. There is an urgent need increase access to evidence-based treatment for insomnia in cancer centers and the community.

Sleep improves cognitive performance, yet little is known about the neural mechanisms of this improvement. We performed multielectrode recording in macaque visual and dorsolateral prefrontal cortex while animals performed a visual discrimination task before and after non-rapid eye movement (NREM) sleep. Although sleep induces synchronized fluctuations in population activity across cortical areas, the post-sleep population activity became more desynchronized relative to the pre-sleep state. The changes after sleep were correlated with an increase in information encoded in population activity in each area and improved behavioral performance. Electrically stimulating visual cortex at 4 hertz emulated the beneficial effects of sleep on network and perceptual performance. A large-scale neural network model indicated that asymmetric depression of local intracortical synapses is consistent with the observed changes in neural activity after sleep.

The daily alternation between sleep and wakefulness is one of the most dominant features of our lives and is a manifestation of the intrinsic 24 h rhythmicity underlying almost every aspect of our physiology. Circadian rhythms are generated by networks of molecular oscillators in the brain and peripheral tissues that interact with environmental and behavioural cycles to promote the occurrence of sleep during the environmental night. This alignment is often disturbed, however, by contemporary changes to our living environments, work or social schedules, patterns of light exposure, and biological factors, with consequences not only for sleep timing but also for our physical and mental health. Characterised by undesirable or irregular timing of sleep and wakefulness, in this Series paper we critically examine the existing categories of circadian rhythm sleep-wake disorders and the role of the circadian system in their development. We emphasise how not all disruption to daily rhythms is driven solely by an underlying circadian disturbance, and take a broader, dimensional approach to explore how circadian rhythms and sleep homoeostasis interact with behavioural and environmental factors. Very few high-quality epidemiological and intervention studies exist, and wider recognition and treatment of sleep timing disorders are currently hindered by a scarcity of accessible and objective tools for quantifying sleep and circadian physiology and environmental variables. We therefore assess emerging wearable technology, transcriptomics, and mathematical modelling approaches that promise to accelerate the integration of our knowledge in sleep and circadian science into improved human health.

Insomnia is highly prevalent in clinical practice, occurring in up to 50% of primary care patients. Insomnia can present independently or alongside other medical conditions or mental health disorders and is a risk factor for the development and exacerbation of these other disorders if not treated. In 2016, the American College of Physicians recommended that insomnia be specifically targeted for treatment. The recommended first-line treatment for insomnia, whether the underlying cause has been identified or not, is cognitive behavioural therapy for insomnia (CBT-I). Currently, there is no global consensus regarding which pharmacological treatment has the best efficacy or risk-benefit ratio. Both CBT-I and pharmacological intervention are thought to have similar acute effects, but only CBT-I has shown durable long-term effects after treatment discontinuation. Administering a combined treatment of CBT-I and medication could decrease the latency to treatment response, but might diminish the durability of the positive treatment effects of CBT-I.