NREM Parasomnias: Sleepwalking, Sleep Terrors, and Confusional Arousals
Sleepwalking and sleep terrors arise from incomplete arousal during N3 slow-wave sleep; prevalence 3–4% in adults; 60% monozygotic twin concordance indicates strong genetic basis; typically resolve in adulthood.
| Measure | Value | Unit | Notes |
|---|---|---|---|
| Sleepwalking prevalence (adults) | 3–4 | % of adults | AASM estimates; up to 15–30% of children experience it; prevalence falls with age |
| Monozygotic twin concordance | ~60 | % | Hublin 2001; vs ~15% for dizygotic twins; strong genetic basis |
| Sleep terror onset | Within first 1–3h of sleep | sleep timing | During first SWS episode; most intense SWS — rarely from light sleep |
| SWS proportion in sleepwalkers | Higher | vs non-sleepwalkers | Also have more frequent and prolonged slow oscillations; more fragmented SWS |
| Risk with family history | 10× | higher relative risk | First-degree relative with sleepwalking; autosomal dominant in some families |
What Are NREM Parasomnias?
NREM parasomnias — sleepwalking (somnambulism), sleep terrors (pavor nocturnus), and confusional arousals — are “disorders of arousal”: states in which motor and/or autonomic systems activate during slow-wave sleep (N3) while full cortical awakening does not occur. The result is a dissociated brain state where the individual can move, vocalize, and appear awake, but lacks full consciousness, judgment, and will not form memories.
All NREM parasomnias share:
- Occurrence during the first third of the night (when SWS is most abundant)
- Amnesia for the episode
- Difficulty arousing fully during the episode
- Resume sleep without distress (in sleepwalking/confusional arousal)
Sleepwalking (Somnambulism)
Sleepwalking ranges from simple sitting up in bed to complex behaviors including walking through the house, eating, driving short distances, and in rare cases aggressive behavior. Episodes typically last 1–15 minutes. The eyes are open but with a glassy, non-focused gaze; the person can navigate around furniture but has no responsive awareness.
Predisposing factors:
- Genetic: 60% MZ twin concordance; first-degree relative raises risk 10-fold
- Sleep deprivation: deepens subsequent SWS → more incomplete arousals
- Fever: disrupts sleep architecture
- Medications: sedative-hypnotics (especially z-drugs like zolpidem) increase risk
- Alcohol: promotes deeper initial SWS followed by fragmentation
Sleep Terrors
Sleep terrors are more dramatic: the individual suddenly bolts upright, emits a blood-curdling scream, has tachycardia and dilated pupils, and appears profoundly terrified. Unlike nightmares (which occur in REM and are followed by full awakening and detailed recall), sleep terrors are not recalled. The terror reflects activation of the autonomic fear response without cortical narrative.
Sleep terrors in children typically resolve without treatment as sleep architecture matures. In adults, evaluation for triggering factors (sleep deprivation, OSA, stress, medications) is appropriate before considering pharmacotherapy.
EEG During Parasomnias
High-density EEG studies by Zadra et al. and others have shown that during parasomnias, there is a dissociation within the brain itself: posterior and motor cortices show activation patterns while prefrontal regions remain in slow-wave sleep. This “local sleep” model — where different brain regions are simultaneously in different sleep/wake states — provides the physiological explanation for complex, goal-directed behavior without consciousness.
Related Pages
Sources
- Mahowald MW & Schenck CH — Non-rapid eye movement sleep parasomnias. Neurol Clin (2005)
- Hublin C et al. — Sleepwalking and sleep terrors: epidemiology and genetics. Sleep (2001)
- AASM — International Classification of Sleep Disorders, 3rd Edition (2014)
- Zadra A et al. — Somnambulism: clinical aspects and pathophysiological hypotheses. Lancet Neurol (2013)
Frequently Asked Questions
Why do NREM parasomnias happen during deep sleep?
NREM parasomnias are 'disorders of arousal' — the brain partially arouses from slow-wave sleep but doesn't complete the transition to full wakefulness. The motor cortex and brainstem become activated enough to generate behavior (walking, screaming), but the prefrontal cortex (governing judgment, memory formation, full consciousness) remains in a sleep-like state. This dissociation explains complex behaviors with no memory.
Is it dangerous to wake a sleepwalker?
The myth that waking a sleepwalker is dangerous is false. Waking a sleepwalker will not cause harm and may prevent dangerous behavior. Sleepwalkers may be briefly confused and disoriented upon waking — this is normal. The priority when encountering a sleepwalker is to gently guide them back to bed to prevent physical injury (falls, leaving the house).