Increased prevalence in adolescence may be a consequence of both physiological and be- havioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is as- sociated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be differentiated from the common delay in the tinting of circadian rhythms in this age group. In the familial form, the course is persistent and may not improve significantly with age.
Genetic and physiological. Predisposing factors may include a longer than average cir- cadian period, changes in light sensitivity, and impaired homeostatic sleep drive. Some in- dividuals with delayed sleep phase type may be hypersensitive to evening light, which can serve as a delay signal to the circadian clock, or they may be hyposensitive to morning light such that its phase-advancing effects are reduced. Genetic factors may play a role in the pathogenesis of familial and sporadic forms of delayed sleep phase type, including mutations in circadian genes (e.g., PER3, CKIe).
Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigra— phy (i.e., a wrist-worn motion detector that monitors motor activity for prolonged periods and can be used as a proxy for sleep-wake patterns for at least 7 days). The period covered should include weekends, when social and occupational obligations are less strict, to ensure that the individual exhibits a consistently delayed sleep-wake pattern. Biomarkers such as salivary dim light melatonin onset should be obtained only when the diagnosis is unclear.
Functional Consequences of Delayed Sleep Phase Type
Excessive early day sleepiness is prominent. Extreme and prolonged difficulty awakening with morning confusion (i.e., sleep inertia) is also common. The severity of insomnia and pends on the occupational and social demands on the individual.
Normative variations in sleep. Delayed sleep phase type must be distinguished from personal, social, or occupational distress (most commonly seen in adolescents and young adults).
Other sleep disorders. Insomnia disorder and other circadian rhythm sleep-wake dis- orders should be included in the differential. Excessive sleepiness may also be caused by other sleep disturbances, such as breathing-related sleep disorders, insomnias, sleep- related movement disorders, and medical, neurological, and mental disorders. Overnight polysomnography may help in evaluating for other comorbid sleep disorders, such as sleep apnea. The circadian nature of delayed sleep phase type, however, should differen- tiate it from other disorders with similar complaints.
Delayed sleep phase type is strongly associated with depression, personality disorder, and somatic symptom disorder or illness anxiety disorder. In addition, comorbid sleep disor- ders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depres- sive and bipolar disorders and anxiety disorders, can exacerbate symptoms of insomnia and excessive sleepiness. Delayed sleep phase type may overlap with another circadian rhythm sleep-wake disorder, non-24—hour sleep-wake type. Sighted individuals with non- 24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep phase.
Advanced sleep phase type may be documented with the specified ”familial." Although the prevalence of familial advanced sleep phase type has not been established, a family history of advanced sleep phase is present in individuals with advanced sleep phase type.
In this type, specific mutations demonstrate an autosomal dominant mode of inheritance.
In the familial form, onset of symptoms may occur earlier (during childhood and early adulthood), the course is persistent, and the severity of symptoms may increase with age.