Circadian rhythm sleep disorders (CRSD), (also known as circadian rhythm sleep–wake disorders (CRSWD)) are a family of sleep disorders that affect the timing of sleep.
CRSDs cause sleep/wake disturbances that arise either by dysfunction in one’s biological clock system, or by misalignment between endogenous oscillator and externally imposed cues.
Circadian misalignment causes sleep disorders: falling asleep at unconventional time points in the day, or experiencing excessive daytime sleepiness if they resist.
Circadian misalignment occurrences often lead to recurring instances of disrupted rest and wakefulness, where individuals affected by the disorder are unable to go to sleep and awaken at normal times for work, school, and other social obligations.
Delayed sleep phase disorder, advanced sleep phase disorder, non-24-hour sleep–wake disorder and irregular sleep–wake rhythm disorder represent
The four main types of sleep disorder; Delayed sleep phase disorder, advanced sleep phase disorder, non-24-hour sleep–wake disorder and irregular sleep–wake rhythm disorder
Humans, have various biological rhythms and these biologic clocks control processes that fluctuate daily: body temperature, alertness, and hormone secretion.
The sleep–wake propensity can also be considered one of the daily rhythms regulated by the biological clock system.
Sleeping cycles are tightly regulated by a series of circadian processes working in tandem.
Sleeping circadian processes allow for the experience of moments of consolidated sleep during the night and a long wakeful moment during the day.
Photosensitive retinal ganglion Cells, are involved in modulating the circadian rhythm because of the expression of melanopsin, which absorbs light in the blue part (around 480 nm).
Disruptions to these processes and the communication pathways between them can lead to problems in sleeping patterns, which are collectively referred to as circadian rhythm sleep disorders.
A circadian rhythm is an entrainable, endogenous, biological activity that has a period of roughly twenty-four hours.
This internal time-keeping mechanism is centralized in the suprachiasmatic nucleus (SCN),and allows for the internal physiological mechanisms underlying sleep and alertness to become synchronized to external environmental cues, like the light-dark cycle.
The SCN also sends signals to peripheral clocks in other organs, like the liver, to control processes such as glucose metabolism.
Genes that help control light-induced changes include positive regulators BMAL1 and CLOCK and negative regulators PER1 and CRY.
A full circadian cycle is a twenty-four hour circadian day, where circadian time (CT) zero marks the beginning of a subjective day for an organism and CT 12 marks the start of subjective night.
Regular circadian function maintains regular sleep schedules, regulates daily rhythms in hormone secretion, and sustain oscillations in core body temperature.
A normal circadian function allows people to maintain balance rest and wakefulness that allows people to work and maintain alertness during the day’s activities, and rest at night.
With circadian rhythm sleep disorder (CRSD) Is a misalignment between the timing of the circadian oscillator and the surrounding environment, or failure in the clock entrainment pathway.
Among people with typical circadian clock function, there is variation in chronotypes, or preferred wake and sleep times, of individuals.
Chronotype varies from individual to individual, as determined by rhythmic expression of clock genes.
With typical circadian clock function will be able to entrain to environmental cues.
To shift the onset of a biological activity, like waking time, light exposure during the late subjective night or early subjective morning can help advance one’s circadian cycle earlier in the day, leading to an earlier wake time.
About 3% of the adult population has a circadian rhythm sleep disorder (CRSD), but many people are often misdiagnosed with insomnia instead.
Of adults diagnosed with sleep disorders, an estimated 10% have a CRSD and of adolescents with sleep disorders, an estimated 16% may have a CRSD.
Patients diagnosed with circadian rhythm sleep disorders typically express a pattern of disturbed sleep, whether that be excessive sleep that intrudes on working schedules and daily functions, or insomnia at desired times of sleep.
Having a preference for extreme early or late wake times is not related to a circadian rhythm sleep disorder diagnosis.
With CRSD there must be distinct impairment of biological rhythms that affects the person’s desired work and daily behavior.
For a CRSD diagnosis, a history of a patient’s sleep and wake habits, body temperature patterns, and dim-light melatonin onset.
Gathering this data gives insight into the patient’s current schedule, as well as the physiological phase markers of the patient’s biological clock.
A standard questionnaire records the sleep habits of the patient, including typical bedtime, sleep duration, sleep latency, and instances of waking up, and external factors that may impact sleep, daily habits like work schedule and timing of exercise, and uses sleep diaries to assess the patient’s problems with sleep latency, undesired early-morning wakefulness, and problems with falling or staying asleep.
Currently, the International Classification of Sleep Disorders (ICSD-3) lists 6 disorders under the category of circadian rhythm sleep disorders.
CRSDs are categorized into two groups based on their underlying mechanisms:
The first category:disorders where the endogenous oscillator has been altered, known as intrinsic type disorders.
The second category: extrinsic disorders in which the external environment and the endogenous circadian clock are misaligned.
Intrinsic disorders:
Delayed sleep phase disorder (DSPD): Individuals have sleep–wake times that are delayed when compared to normal functioning individuals.
DSPD patients typically have very long periods of sleep latency when they attempt to go to sleep during conventional sleeping times.
Similarly, they also have trouble waking up at conventional times.
Advanced sleep phase disorder (ASPD) people exhibit characteristics opposite to those with delayed sleep phase disorder: they tend to go to bed and wake up much earlier as compared to normal individuals.
ASPD is less common than DSPD, and is most prevalent within older populations.
Familial Advanced Sleep Phase Syndrome (FASPS) is linked to an autosomal dominant mode of inheritance.
Familial Advanced Sleep Phase Syndrome (FASPS) is associated with a missense mutation in human PER2 that replaces serine for glycine at position 662 (S662G).
Irregular sleep–wake rhythm disorder (ISWRD) is characterized by a normal 24 h sleeping period, but this disorder experience fragmented and highly disorganized sleep that can manifest in the form of waking frequently during the night and taking naps during the day, yet still maintaining sufficient total time asleep.
Patients with irregular sleep–wake rhythm disorder (ISWRD) often experience a range of symptoms from insomnia to excessive daytime sleepiness.
Non-24-hour sleep–wake disorder (N24SWD) is most common in individuals that are blind and unable to detect light, is characterized by chronic patterns of sleep/wake cycles that are not related to the 24 h light–dark environmental cycle.
With the Non-24-hour sleep–wake disorder patients will usually experience a gradual yet predictable delay of sleep onset and waking times.
Shift work sleep disorder (SWSD): Approximately 9% of Americans who work night or irregular work shifts are believed to experience shift work sleep disorder.
Night shift work directly opposes the environmental cues that affects our biological clock, and this disorder arises when an individual’s clock is unable to adjust to the socially imposed work schedule.
Shift work sleep disorder can lead to severe insomnia as well as excessive daytime sleepiness.
Jet lag: difficulty falling asleep or staying asleep as a result of misalignment between one’s internal circadian system and external, or environmental cues, and is typically associated with rapid travel across multiple time zones.
CRSD has been frequently associated with excessive daytime sleepiness and nighttime insomnia in patients diagnosed with Alzheimer’s disease (AD), representing a common characteristic among AD patients as well as a risk factor of progressive functional impairments.
Treatments for circadian rhythm sleep disorders include:
Chronotherapy to treat delayed sleep phase disorder; it acts by systematically delaying an individual’s bedtime until their sleep–wake times coincide with the conventional 24 h day.
Light therapy utilizes bright light exposure to induce phase advances and delays in sleep and wake times: 30–60 minutes of exposure to a bright (5000–10000 lux) white, blue, or natural light at a set time until the circadian clock is aligned with the desired schedule.
Treatment is initially administered either upon awakening or before sleeping, and if successful may be continued indefinitely or performed less frequently.
Light therapy proven very effective in the treatment of individuals with DSPD and ASPD.
Hypnotics have also been used clinically alongside bright light exposure therapy and pharmacotherapy for the treatment of CRSDs.
In conjunction with cognitive behavioral therapy, short-acting hypnotics also present an avenue for treating co-morbid insomnia in patients with circadian sleep disorders.
Melatonin, a naturally occurring biological hormone with circadian rhythmicity, has been shown to promote sleep and entrainment to external cues when administered in drug form with 0.5–5.0 mg.
Melatonin administered in the evening causes phase advances in sleep–wake times while maintaining duration and quality of sleep.
Similarly, when administered in the early morning, melatonin can cause phase delays.
It is most effective in cases of shift work sleep disorder and delayed phase sleep disorder.
It has not been proven particularly useful in cases of jet lag.
Dark therapy, the use of blue-blocking goggles, is used to block blue and blue-green wavelength light from reaching the eye during evening hours so as not to hinder melatonin production.