Aetiology
The most common explanation for parasomnias is that sleep and wakefulness are not mutually exclusive states but frequently overlap, and intrusion of these states into one another may cause parasomnias.[1] Intrusion of wakefulness into non-rapid eye movement (NREM) sleep may produce arousal disorders, and intrusion of wakefulness into rapid eye movement (REM sleep) may produce REM sleep parasomnias.[1]
The onset of disorders of arousal tends to occur during slow-wave sleep (SWS). Given that SWS predominates during the first third of the sleep period, these disorders are more prevalent at the beginning of the night. However, they may still occur in the second half of the night. They are common in childhood, usually decreasing in frequency with increasing age.[7][8]
Genetic predisposition may give rise to an inherent instability of NREM sleep.[18] In particular, HLA gene DQB1*05 and *04 alleles are associated with a risk of NREM parasomnias.[19][20]
Arousal disorders may be triggered by a variety of conditions, including fever, acute sleep deprivation, emotional stress, and drugs.[6] Frequently, medical sleep disorders such as restless legs syndrome and obstructive sleep apnoea cause NREM parasomnias due to the frequent arousals they cause.[21][22] These precipitators should be viewed as triggering events in susceptible individuals rather than as causal factors.
An underlying psychopathology may play a role in patients with nightmares.[10][23]
Pathophysiology
NREM sleep parasomnias.
The pathophysiology of NREM parasomnias is thought to stem from impaired arousal mechanisms, and specifically an impaired ability to arouse fully from deep slow-wave sleep.[18][24][25][26][27] This leads to a dissociation between sleep and wakefulness, wherein certain brain regions exhibit wake-like activity while others remain in a sleep-like state, giving rise to the characteristic behaviours of NREM parasomnia episodes.[28][29][30][31]
The interplay of genetic predisposing factors, priming factors such as sleep deprivation or stress, and precipitating factors such as noise or physical contact are involved in the generation of NREM parasomnias.[32] In children, developmental factors such as a higher proportion of slow-wave sleep, along with immature GABAergic activity and cholinergic inhibitory networks, may also play a role.[33]
Increasing evidence suggests that dreamlike mentation and complex cognitive activity often accompany NREM parasomnia episodes, contributing to the behaviours observed during these events. This mentation may modulate motor actions during episodes, suggesting that parasomnias are not purely automatic phenomena but involve elements of conscious processing.[34][35]
REM sleep parasomnias
Rapid eye movement sleep behaviour disorder often results from serious neuropathology, which affects the area of the brain responsible for inhibiting muscle tone during REM sleep.[1] In children, this dysfunction may be influenced by developmental factors or comorbid conditions.[36]
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