Delayed sleep phase disorder
| Delayed sleep phase disorder | |
|---|---|
| Other names | Delayed sleep–wake phase disorder, delayed sleep phase syndrome, delayed sleep phase type, social jet lag |
| Comparison of standard (green) and DSPD (blue) circadian rhythms | |
| Specialty | Sleep medicine, neurology, psychiatry |
| Symptoms | Delayed sleeping times (usually after midnight), resistant to conscious attempts to change, potential occasional bouts of insomnia, extreme jet lag-like effects. |
| Complications | Severe cases can be disabling from a social and occupational perspective. DSPD can aggravate other medical issues that often worsen from sleep issues and/or stress, such as psychiatric disorders, which themselves can have complications. |
| Duration | Usually chronic if symptoms occur/persist past adolescence. |
| Causes | Genetics, traumatic brain injury (secondary) |
| Risk factors | Major depressive disorder (disputed), attention deficit hyperactivity disorder, obsessive–compulsive disorder, long COVID, traumatic brain injury (secondary). |
| Diagnostic method | Debated, a consistent inability to change the late sleep cycle for a certain period of time needs to be demonstrated during a clinical interview and or a sleep diary, polysomnography, and actigraphy can also be used. The ICSD criteria are often used. |
| Differential diagnosis | Other parasomnias. DSPD should also be distinguished from symptoms that are part of much greater psychiatric/neurological issues until ruled out as the primary cause. |
| Prevention | Secondary causes from brain injuries can be mitigated by PPE |
| Treatment | Light therapy, darkness therapy, moving important tasks to earlier times, gradually shifting to earlier bedtime and waking times, medication for augmentation or monotherapy. |
| Medication | Aripiprazole (in low doses), Agomelatine, melatonin (most evidence-based and on-label), ramelteon, modafinil (for eugeroic effects, known to work for other disorders like SWSD), other stimulants may be used for the same purpose. |
| Prognosis | Milder cases (those with earlier sleeping times) have a higher rate of remission and a longer time until relapses start after treatment is discontinued. Prognosis is generally poorer in severe cases and those who do not or cannot seek treatment. 90% will relapse after medication therapy is discontinued. |
| Frequency | Exact estimates are unreliable due to varying definitions of DSPD, though it is generally accepted that it is more common in adolescents (see Epidemiology |
Delayed sleep phase disorder (DSPD), more often known as delayed sleep phase syndrome and also as delayed sleep–wake phase disorder, is the delaying of a person's circadian rhythm (biological clock) compared to those of social norms. The disorder affects the timing of biological rhythms including sleep, peak period of alertness, core body temperature, and hormonal cycles. People with this disorder are often called “night owls”.
The diagnosis of this disorder is currently a point of contention among specialists of sleep disorders. Many insomnia-related disorders can present significantly differently between patients, and circadian rhythm disorders and melatonin-related disorders are not well understood by modern medical science. The orexin system was only identified in 1998,[1] yet it appears intimately implicated in human sleep-wake systems.
Evidence for the plasticity of human circadian rhythm cycles has been provided by multiple studies. In one example, 15 volunteers spent 40 days and nights underground in a French cave while researchers monitored their periods of waking and sleeping. Their results found significant divergence between individuals, with most participants settling upon a rhythm of 30 ± 4 hours.[2] Researchers have speculated that the lack of exposure to natural sunrise/sunset cycles relates many of the symptoms of these circadian disorders to modern habits of humans spending extended periods indoors, without sunlight exposure and with artificial light.
Symptom management may be possible with therapeutic drugs such as orexin antagonists or melatonin receptor agonists, as well as regular outdoor exercise. There may be a genetic component to the syndrome.[3]
- ^ Siegel, J. M.; Moore, R.; Thannickal, T.; Nienhuis, R. (November 2001). "A Brief History of Hypocretin/Orexin and Narcolepsy". Neuropsychopharmacology. 25 (1): S14 – S20. doi:10.1016/S0893-133X(01)00317-7. ISSN 1740-634X. PMC 8788648. PMID 11682268.
- ^ "Out of the cave: French isolation study ends after 40 days". AP News. 24 April 2021. Retrieved 3 December 2023.
- ^ Patke A, Murphy PJ, Onat OE, Krieger AC, Özçelik T, Campbell SS, Young MW (April 2017). "Mutation of the Human Circadian Clock Gene CRY1 in Familial Delayed Sleep Phase Disorder". Cell. 169 (2): 203–215.e13. doi:10.1016/j.cell.2017.03.027. PMC 5479574. PMID 28388406.