Mutation of the Human Circadian Clock Gene CRY1 in Familial Delayed Sleep Phase Disorder.

Patterns of daily human activity are controlled by an intrinsic circadian clock that promotes ∼24 hr rhythms in many behavioral and physiological processes. This system is altered in delayed sleep phase disorder (DSPD), a common form of insomnia in which sleep episodes are shifted to later times misaligned with the societal norm. Here, we report a hereditary form of DSPD associated with a dominant coding variation in the core circadian clock gene CRY1, which creates a transcriptional inhibitor with enhanced affinity for circadian activator proteins Clock and Bmal1. This gain-of-function CRY1 variant causes reduced expression of key transcriptional targets and lengthens the period of circadian molecular rhythms, providing a mechanistic link to DSPD symptoms. The allele has a frequency of up to 0.6%, and reverse phenotyping of unrelated families corroborates late and/or fragmented sleep patterns in carriers, suggesting that it affects sleep behavior in a sizeable portion of the human population.

Rhythms of life: circadian disruption and brain disorders across the lifespan.

Many processes in the human body - including brain function - are regulated over the 24-hour cycle, and there are strong associations between disrupted circadian rhythms (for example, sleep-wake cycles) and disorders of the CNS. Brain disorders such as autism, depression and Parkinson disease typically develop at certain stages of life, and circadian rhythms are important during each stage of life for the regulation of processes that may influence the development of these disorders. Here, we describe circadian disruptions observed in various brain disorders throughout the human lifespan and highlight emerging evidence suggesting these disruptions affect the brain. Currently, much of the evidence linking brain disorders and circadian dysfunction is correlational, and so whether and what kind of causal relationships might exist are unclear. We therefore identify remaining questions that may direct future research towards a better understanding of the links between circadian disruption and CNS disorders.

Light, sleep and circadian rhythm in critical illness.

PURPOSE OF REVIEW: Sleep and circadian disruption (SCD) are associated with worse outcomes in the ICU population. We discuss sleep, circadian physiology, the role of light in circadian entrainment and its possible role in treating SCD, with special attention to the use of light therapies and ICU design. RECENT FINDINGS: The American Thoracic Society recently published an official research statement highlighting key areas required to define and treat ICU SCD. Recent literature has been predominantly observational, describing how both critical illness and the ICU environment might impair normal sleep and impact circadian rhythm. Emerging consensus guidance outlines the need for standardized light metrics in clinical trials investigating effects of light therapies. A recent proof-of-concept randomized controlled trial (RCT) showed improvement in delirium incidence and circadian alignment from ICU room redesign that included a dynamic lighting system (DLS). SUMMARY: Further investigation is needed to define the optimal physical properties of light therapy in the ICU environment as well as timing and duration of light treatments. Work in this area will inform future circadian-promoting design, as well as multicomponent nonpharmacological protocols, to mitigate ICU SCD with the objective of improving patient outcomes.

Sex Differences in Insomnia and Circadian Rhythm Disorders: A Systematic Review.

Insomnia and circadian rhythm disorders are increasingly common in modern society and lead to significant challenges for people's health and well-being. Some studies suggests that men and women differ in neurohormonal secretion, biological processes, and brain morphology. Thus, such differences may affect the etiology, manifestation, and course of sleep disorders, including insomnia and circadian rhythm. This systematic review aims to synthesize the existing literature on sex differences in insomnia and circadian rhythm disorders. PubMed, MEDLINE, Epistemonikos, and Cochrane databases were searched for articles published from inception until 5 September 2023, not older than five years. We performed a systematic search using MESH and non-MESH queries: (sex differences) or (male and female differences) or (men and women differences) or (men and women) AND (insomnia) or (sleep wake disorder*) or (sleep wake rhythm disorder*) or (circadian rhythm disorder*) or (sleep cycle disruption) or (sleep cycle disorder*). Out off 2833 articles screened, 11 studies were included. The prevalence of insomnia is higher among women, and their sleep is more regular and stable compared to men. Studies evaluating the impact of the stressful situation associated with the lockdown on women's and men's insomnia present discordant results concerning sex differences. Women's circadian rhythm was found to be more stable and less fragmented than men's. However, the progression of peak activity time with age was more pronounced in men. The current literature suggests that risk factors for insomnia and circadian rhythm disorders affect men and women differently. These include cerebrovascular and cardiometabolic factors, shift work, and infections. The long-term effects of insomnia seem to be more relevant for the male sex, shortening lifespan more than in women. By summarizing and analyzing existing studies, we highlight the need for further research to improve understanding of the interaction between sex and sleep.

[Consequences of chronodisruption on body weight regulation and metabolism]. / Konsequenzen von Chronodisruption auf Körpergewichtsregulation und Stoffwechsel.

INTRODUCTION: The prevalence of overweight and obesity has increased dramatically. At the same time, lack of sleep has become a part of the modern lifestyle, as well as shift and night work. As a result, chronodisruption, i. e. a change in physiological processes that are controlled by the internal clock, becomes commonplace. Epidemiological data show that too short but also too long sleep are associated with an increased risk of obesity, also seen for night shift work. Overweight and obesity are associated with metabolic syndrome and data likewise report an increased risk by both short and long sleep. It has not yet been conclusively clarified how chronodisruption influences the metabolic risks. Clinical experimental studies report on neuroendocrine and circadian mechanisms and it has been shown that lack of sleep increases the hunger-promoting hormone ghrelin as well as subjective feelings of hunger and increases leptin levels. Lack of sleep also increases hedonic hunger and food-related reward signals. Through preventive measures, chronodisruption and thus, the risk of obesity can be counteracted. The extent to which smartwatches and fitness trackers, which according to the manufacturer can measure and analyze sleep, provide an objective picture of sleep has not been sufficiently investigated. However, smartwatches and fitness trackers can - probably - increase awareness of sleep in the modern society.

Circadian gene × environment perturbations influence alcohol drinking in Cryptochrome-deficient mice.

Alcohol use disorder (AUD) is a widespread addiction disorder with severe consequences for health. AUD patients often suffer from sleep disturbances and irregular daily patterns. Conversely, disruptions of circadian rhythms are considered a risk factor for AUD and alcohol relapses. In this study, we investigated the extent to which circadian genetic and environmental disruptions and their interaction alter alcohol drinking behaviour in mice. As a model of genetic circadian disruption, we used Cryptochrome1/2-deficient (Cry1/2-/- ) mice with strongly suppressed circadian rhythms and found that they exhibit significantly reduced preference for alcohol but increased incentive motivation to obtain it. Similarly, we found that low circadian SCN amplitude correlates with reduced alcohol preference in WT mice. Moreover, we show that the low alcohol preference of Cry1/2-/- mice concurs with high corticosterone and low levels of the orexin precursor prepro-orexin and that WT and Cry1/2-/- mice respond differently to alcohol withdrawal. As a model of environmentally induced disruption of circadian rhythms, we exposed mice to a "shift work" light/dark regimen, which also leads to a reduction in their alcohol preference. Interestingly, this effect is even more pronounced when genetic and environmental circadian perturbations interact in Cry1/2-/- mice under "shift work" conditions. In conclusion, our study demonstrates that in mice, disturbances in circadian rhythms have pronounced effects on alcohol consumption as well as on physiological factors and other behaviours associated with AUD and that the interaction between circadian genetic and environmental disturbances further alters alcohol consumption behaviour.

Deciphering the Interacting Mechanisms of Circadian Disruption and Alzheimer's Disease.

Alzheimer's disease (AD) is one of the crucial causative factors for progressive dementia. Neuropathologically, AD is characterized by the extracellular accumulation of amyloid beta plaques and intracellular neurofibrillary tangles in cortical and limbic regions of the human brain. The circadian system is one of the many affected physiological processes in AD, the dysfunction of which may reflect in the irregularity of the sleep/wake cycle. The interplay of circadian and sleep disturbances inducing AD progression is bidirectional. Sleep-associated pathological alterations are frequently evident in AD. Understanding the interrelation between circadian disruption and AD may allow for earlier identification of AD pathogenesis as well as better suited approaches and potential therapies to combat dementia. In this article, we examine the existing literature related to the molecular mechanisms of the circadian clock and interacting mechanisms of circadian disruption and AD pathogenesis.

Ageing shift workers' sleep and working-hour characteristics after implementing ergonomic shift-scheduling rules.

We studied whether implementing binding ergonomic shift-scheduling rules change ageing (≥45 years) social and healthcare employees' (mean age 52.5 years, 95% women) working-hour characteristics (e.g. weekly working hours, number and length of night shifts, and short shift intervals) and sleep. We compared an intervention group (n = 253) to a control group (n = 1,234) by survey responses (baseline 2007/2008, follow-up 2012) and objective working-hour characteristics (intervention group n = 159, control group n = 379) from 91 days preceding the surveys. Changes in working-hour characteristics were analysed with repeated measures general linear models. The fully adjusted model (sociodemographics and full-/part-time work) showed that proportion of short shift intervals (<11 hr, p = .033) and weekend work (p = .01) decreased more in the intervention than in the control group. Changes in sleep outcomes were analysed with generalised logit model to binomial and multinomial variables. The fully adjusted model (sociodemographics, full-/part-time work, job strain, health behaviours, and perceived health) revealed higher odds in the intervention group for long sleep (≥9 hr; odds ratio [OR] 5.53, 95% confidence interval [CI] 2.21-13.80), and lower odds of short sleep (<6 hr; OR 0.72, 95% CI 0.57-0.92), having at least two sleep difficulties often (OR 0.55, 95% CI 0.43-0.70), and more specifically difficulties in falling asleep (OR 0.56, 95% CI 0.41-0.77), waking up several times per night (OR 0.43, 95% CI 0.34-0.55), difficulties in staying asleep (OR 0.64, 95% CI 0.49-0.82), and non-restorative sleep (OR 0.70, 95% CI 0.54-0.90) than the control group. In conclusion, implementation of ergonomic shift-scheduling rules resulted in minor changes in ageing employees' objective working hours and a consistent buffering effect against worsening of sleep.

Optimising sleep and performance during night float: A systematic review of evidence and implications for graduate medical education trainees.

Graduate medical education (GME) training commonly requires residents and fellows to engage in night float shift work. This review aims to assess the effectiveness of interventions for trainees when preparing for, completing, and recovering from working night float shifts. We reviewed all available studies published prior to September 2019 using PubMed, Scopus, CINAHL, the Cochrane library, PsycINFO, and Google Scholar databases. We included all original, primary research articles assessing either non-pharmacological or pharmacological interventions on the chronobiological and physiological effects of night float shift work among GME trainees. Five studies (n = 179 patients) met inclusion criteria. Interventions included melatonin in the morning before sleep after night float shifts, napping during night float shifts, modafinil after a night of sleep deprivation, and caffeinated energy drinks after 6 consecutive night float shifts. Melatonin improved one measure of attention. A 2-hr nap was associated with improved speed related to task switching. Modafinil improved performance in tests of cognition. Caffeinated energy drinks led to improvement in select driving performance variables and reaction time. Effect sizes for outcome variables were calculated. Heterogeneity among the studies precluded combining the data in a meta-analysis. According to GRADE criteria, the quality of the evidence in these studies was low or very low. Our findings suggest GME trainees may benefit from utilising a limited number of interventions when preparing for or recovering from night float shift work. More investigation is needed to identify interventions that could help GME trainees adapt to and recover from working night float shifts.

Disrupted nocturnal melatonin in autism: Association with tumor necrosis factor and sleep disturbances.

Sleep disturbances, abnormal melatonin secretion, and increased inflammation are aspects of autism spectrum disorder (ASD) pathophysiology. The present study evaluated the daily urinary 6-sulfatoxymelatonin (aMT6s) excretion profile and the salivary levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in 20 controls and 20 ASD participants, as well as correlating these measures with sleep disturbances. Although 60% of ASD participants showed a significant night-time rise in aMT6s excretion, this rise was significantly attenuated, compared to controls (P < .05). The remaining 40% of ASD individuals showed no significant increase in nocturnal aMT6s. ASD individuals showed higher nocturnal levels of saliva TNF, but not IL-6. Dysfunction in the initiation and maintenance of sleep, as indicated by the Sleep Disturbance Scale for Children, correlated with night-time aMT6s excretion (r = -.28, P < .05). Dysfunction in sleep breathing was inversely correlated with aMT6s (r = -.31, P < .05) and positively associated with TNF level (r = .42, P < .01). Overall such data indicate immune-pineal axis activation, with elevated TNF but not IL-6 levels associated with disrupted pineal melatonin release and sleep dysfunction in ASD. It is proposed that circadian dysregulation in ASD is intimately linked to heightened immune-inflammatory activity. Such two-way interactions of the immune-pineal axis may underpin many aspects of ASD pathophysiology, including sleep disturbances, as well as cognitive and behavioral alterations.

Simulated night shift work induces circadian misalignment of the human peripheral blood mononuclear cell transcriptome.

Misalignment of the endogenous circadian timing system leads to disruption of physiological rhythms and may contribute to the development of the deleterious health effects associated with night shift work. However, the molecular underpinnings remain to be elucidated. Here, we investigated the effect of a 4-day simulated night shift work protocol on the circadian regulation of the human transcriptome. Repeated blood samples were collected over two 24-hour measurement periods from eight healthy subjects under highly controlled laboratory conditions before and 4 days after a 10-hour delay of their habitual sleep period. RNA was extracted from peripheral blood mononuclear cells to obtain transcriptomic data. Cosinor analysis revealed a marked reduction of significantly rhythmic transcripts in the night shift condition compared with baseline at group and individual levels. Subsequent analysis using a mixed-effects model selection approach indicated that this decrease is mainly due to dampened rhythms rather than to a complete loss of rhythmicity: 73% of transcripts rhythmically expressed at baseline remained rhythmic during the night shift condition with a similar phase relative to habitual bedtimes, but with lower amplitudes. Functional analysis revealed that key biological processes are affected by the night shift protocol, most notably the natural killer cell-mediated immune response and Jun/AP1 and STAT pathways. These results show that 4 days of simulated night shifts leads to a loss in temporal coordination between the human circadian transcriptome and the external environment and impacts biological processes related to the adverse health effects associated to night shift work.

Short sleep duration and high exposure to quick returns are associated with impaired everyday memory in shift workers.

PURPOSE: To investigate the relationship between self-reported everyday memory problems the last month, and: (a) shift work schedule, (b) night shifts and quick returns worked the last year, and (c) sleep duration the last month. METHODS: In all, 1,275 nurses completed the Everyday Memory Questionnaire - revised, and answered questions about shift work exposure and sleep duration. We performed multiple linear regression analyses with memory score as dependent variable, and the shift work exposure variables as well as sleep duration as predictors, while adjusting for potential confounders. FINDINGS: High exposure to quick returns (ß = .10, p < .05) and short sleep duration (ß = .10, p < .05) were both positively associated with memory problems, whereas shift work schedule, long sleep duration, night shift exposure, and low and moderate exposure to quick returns were not. DISCUSSION: Frequent insufficient time for rest between shifts as well as short sleep was associated with poorer everyday memory.

Metabolism and the circadian clock converge.

Circadian rhythms occur in almost all species and control vital aspects of our physiology, from sleeping and waking to neurotransmitter secretion and cellular metabolism. Epidemiological studies from recent decades have supported a unique role for circadian rhythm in metabolism. As evidenced by individuals working night or rotating shifts, but also by rodent models of circadian arrhythmia, disruption of the circadian cycle is strongly associated with metabolic imbalance. Some genetically engineered mouse models of circadian rhythmicity are obese and show hallmark signs of the metabolic syndrome. Whether these phenotypes are due to the loss of distinct circadian clock genes within a specific tissue versus the disruption of rhythmic physiological activities (such as eating and sleeping) remains a cynosure within the fields of chronobiology and metabolism. Becoming more apparent is that from metabolites to transcription factors, the circadian clock interfaces with metabolism in numerous ways that are essential for maintaining metabolic homeostasis.

Work by day and sleep by night, do not sleep too little or too much: Effects of sleep duration, time of day and circadian synchrony on flanker-task performance in internet brain-game users from teens to advanced age.

Research elucidating the effects of sleep and circadian rhythm on cognitive performance is advancing, yet many important questions remain. Using flanker-task performance scores from a large internet sample (N = 48,881) with repeated measures of cognitive performance and linked prior-night self-reported sleep duration, we analysed the relationship between sleep duration, time of day of task performance, and chronotype synchrony with performance in participants aged 15-80 years. Results indicate a performance peak at 7 hr habitual sleep duration, and point to a variable effect of deviation from habitual sleep duration depending on users' habitual sleep duration and age. Time-of-day effects were notable for a steady decline in performance up until 01:00 hours-02:00 hours for the group as a whole, which was accounted for by nighttime deterioration on trials requiring inhibitory executive functioning, particularly in older subjects. Analyses did not demonstrate an advantage for playing in synchrony with self-identified chronotype. Results strengthen findings indicating an inverted U-shaped relationship between sleep duration and cognitive performance across a broad spectrum of age groups. These findings underscore the importance of daytime task performance for tasks requiring inhibitory function, especially in elderly people. Findings highlight the utility of large-scale internet data in contributing to sleep and circadian science.

Social jetlag, eating behaviours and BMI among adolescents in the USA.

There is a lack of research on associations of social jetlag with eating behaviours and obesity among adolescents. We examined the associations of social jetlag with eating behaviours and BMI in adolescents before and after adjustment for potential confounders. Self-report data were collected from 3060 adolescents (48·1 % female, mean age 15·59 (sd 0·77) years) from the Fragile Families and Child Wellbeing Study. In regression models, social jetlag predicted odds of consumption of breakfast, fruits/vegetables, fast food and sweetened drinks and BMI percentile. Primary models adjusted for school night sleep duration, sex, age, household income and youth living arrangements; secondary models further adjusted for race/ethnicity. In fully adjusted models, greater social jetlag was associated with lower odds of consumption of breakfast (OR = 0·92, P = 0·003) and fruits/vegetables (OR = 0·92, P = 0·009) and higher odds of consumption of fast food (OR = 1·18, P < 0·001) and sweetened drinks (OR = 1·18, P < 0·001). Social jetlag was positively associated with BMI percentile after additional adjustment for eating behaviours (b = 0·84, P = 0·037), but this relationship was attenuated after adjustment for race/ethnicity (b = 0·72, P = 0·072). Ethnoracial differences in social jetlag may attenuate the association of social jetlag with BMI and should be considered in future studies of circadian misalignment, eating behaviours and obesity markers.

Carotid intimal medial thickness in rotating night shift is related to IL1ß/IL6 axis.

BACKGROUND AND AIMS: Sleep disturbances may promote glucose abnormalities and inflammatory burden among shift workers. Therefore, precocious subclinical atherosclerotic process might develop in healthy shift workers even without known metabolic and cardiovascular risk factors. METHODS AND RESULTS: We measured anthropometric parameters, glucose, lipids, inflammation and common carotid Intimal Medial Thickness (cIMT) in rotating-night shift workers (r-NSW, n = 88, age = 40.3 ± 7.8 y) in comparison with former-night shift workers (f-NSW, n = 35, age = 44.2 ± 6.4 y) and with day-only workers (DW, n = 64, age = 44.1 ± 8.9 y). R-NSW and f-NSW showed significantly higher cIMT and high sensitivity C-Reactive Protein (hs-CRP) respect to DW (p = 0.043 and p = 0.025, respectively). IL-1ß levels were higher in r-NSW than in DW and f-NSW (p = 0.043) and significantly correlated with IL6 (r = 0.365, p < 0.001). In addition, r-NSW and f-NSW had higher HbA1c levels in comparison with DW (p = 0.047). Carotid-IMT was significantly related to night shift work (p = 0.023), with age (p < 0.001), with HOMA IR (p = 0.009), with insulin (p = 0.006) with HbA1c (p = 0.002), with LDL cholesterol (p < 0.001), with diastolic BP (p < 0.001), with WBC (p = 0.002) and with IL6 (p = 0.004). After performing a multivariate analysis night shift work remained statistically related to cIMT (B = 2.633, 95%CI = 0.489-4.776, p = 0.016). CONCLUSIONS: Our result described a possible link bridging night shift work, inflammation and carotid Intimal Medial Thickness. Future studies are warranted to understand if carotid atherosclerosis process should be mainly driven by the IL1ß/IL6 citokine axis connected to sleep disturbances.

Observing Ramadan and sleep-wake patterns in athletes: a systematic review, meta-analysis and meta-regression.

OBJECTIVE: To evaluate the effect of observing Ramadan on athletes' sleep patterns. DESIGN: Systematic review and meta-analysis. DATA SOURCES: The entire content of PubMed/MEDLINE and Web of Science. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Single-group, prepost and cross-over design studies conducted in athletes aged ≥18 years, training at least twice a week and published in English before 12 July 2018 were included. Studies assessing sleep quantity, quality, daytime sleepiness and/or daily naps based on objective or subjective methods were deemed eligible. STUDY APPRAISAL: The methodological quality was assessed using 'QualSyst'. RESULTS: Of 13 selected articles, 7 were of strong quality, 3 were moderate and 3 were weak. 11 studies evaluated total sleep time (TST); this decreased during Ramadan in 4 studies, increased in 1 and remained unchanged in 6. Pooled TST findings indicated a moderate effect size (- 0.97, SE=0.37, 95% CI -1.69 to -0.25, t=-2.64, p=0.01) with significant heterogeneity but no publication bias. Meta-regressions showed no effects of study year, age, sample size, type of sport or competition level, but there were effects of country (with France and Tunisia being the most affected countries and Turkey the least affected, Q=32.14, p<0.0001) and study design (Q=7.74, p=0.02). Four studies measured self-reported sleep quality and it decreased in three studies. One study of sleep architecture reported more frequent waking and more light sleep during Ramadan. Daily nap duration was increased in two studies, but daytime sleepiness remained unchanged in four studies. CONCLUSION: When athletes continue to train at least two times/week while observing Ramadan, TST is decreased compared with athletes' baseline levels.

Disruption of Circadian Rhythms: A Crucial Factor in the Etiology of Infertility.

: Infertility represents a growing health problem in industrialized countries. Thus, a greater understanding of the molecular networks involved in this disease could be critical for the development of new therapies. A recent finding revealed that circadian rhythmicity disruption is one of the main causes of poor reproductive outcome. The circadian clock system beats circadian rhythms and modulates several physiological functions such as the sleep-wake cycle, body temperature, heart rate, and hormones secretion, all of which enable the body to function in response to a 24 h cycle. This intricated machinery is driven by specific genes, called "clock genes" that fine-tune body homeostasis. Stress of modern lifestyle can determine changes in hormone secretion, favoring the onset of infertility-related conditions that might reflect disfunctions within the hypothalamic-pituitary-gonadal axis. Consequently, the loss of rhythmicity in the suprachiasmatic nuclei might affect pulsatile sexual hormones release. Herein, we provide an overview of the recent findings, in both animal models and humans, about how fertility is influenced by circadian rhythm. In addition, we explore the complex interaction among hormones, fertility and the circadian clock. A deeper analysis of these interactions might lead to novel insights that could ameliorate the therapeutic management of infertility and related disorders.

Sleep quality among shift-work nurses: A systematic review and meta-analysis.

AIM: We systematically reviewed the quality of sleep measurement instruments applied to shift-work nurses and analyzed the effects of intervention research. BACKGROUND: There is a need to test the effects of experimental studies worldwide that conducted interventions to improve the sleep quality of nurses who work shiftwork. METHODS: In this systematic literature review and meta-analysis, we used PICO (Participant, Intervention, Comparison, and Outcome) and searched for papers in Korean and English published up until August 2018. We utilized Cochrane Review Manager Software 5.3. RESULTS: Thirteen articles from 1991 to 2018 were included in the systematic literature review, and 6 of those were used in a meta-analysis. The instrument used most often to asses subjective sleep quality was the Pittsburgh Sleep Quality Index. Additionally, an actigraph and sleep logs were used to collect physiological data about participants' sleep quality. Intervention types were categorized into aroma-inhalation therapy, shift-rotation interventions, physical-activity interventions, and cognitive-behavioral therapy. Ultimately, the effects of the aroma-inhalation therapy intervention significantly improved shift-work nurses' sleep quality. CONCLUSIONS: We established a basic understanding of a strategy to measure and improve participants' sleep quality. Consequently, sleep interventions that can positively promote nurses' health and foster effective job performance should be developed.

[Circadian rhythm sleep disorders: clinical picture, diagnosis and treatment]. / Troubles du rythme circadien veille-sommeil†: tableau clinique, diagnostic et prise en charge.

Circadian rhythm sleep disorders (CRSD) represent sleep-wake disturbances due to a disruption of endogenous circadian system or to a desynchronization between internal sleep-wake rhythms and the external environment. They comprise seven diagnostic entities grouped in two main categories: endogenous and exogenous. The patients typically describe chronic excessive daytime sleepiness and/or insomnia symptoms, impacting their daytime functioning. The exact prevalence of CRSD is probably underestimated. The diagnosis is based on sleep diary coupled with actigraphy. Several therapeutic options are validated to allow the realignment between endogenous circadian rhythm and the external environment. The correct diagnostic of CRSD is important to improve the patient's quality of life and to propose them appropriate treatment.

Les troubles du rythme circadien veille-sommeil (TRCVS) résultent d'un dysfonctionnement du rythme circadien endogène ou d'une désynchronisation entre ce dernier et l'environnement extérieur. Ce groupe de pathologies du sommeil comprend 7 sous-entités réparties en 2 catégories : des troubles exogènes et des troubles endogènes. La symptomatologie commune sont des plaintes chroniques de somnolence diurne et/ou d'insomnie, ayant des répercussions sur le fonctionnement quotidien. Leur prévalence exacte est inconnue et les TRCVS sont potentiellement sous-diagnostiqués. Le diagnostic repose sur l'utilisation de l'agenda de sommeil et de l'actigraphie. Diverses approches thérapeutiques existent pour permettre une resynchronisation entre le rythme circadien endogène et l'environnement extérieur.