www.thelancet.com/neurology Vol 12 March 2013 285
Somnambulism: clinical aspects and pathophysiological
Antonio Zadra, Alex Desautels, Dominique Petit, Jacques Montplaisir
Somnambulism, or sleepwalking, can give rise to a wide range of adverse consequences and is one of the leading
causes of sleep-related injury. Accurate diagnosis is crucial for proper management and imperative in an ever-
increasing number of medicolegal cases implicating sleep-related violence. Unfortunately, several widely held views
of sleepwalking are characterised by key misconceptions, and some established diagnostic criteria are inconsistent
with research fi ndings. The traditional idea of somnambulism as a disorder of arousal might be too restrictive and a
comprehensive view should include the idea of simultaneous interplay between states of sleep and wakefulness.
Abnormal sleep physiology, state dissociation, and genetic factors might explain the pathophysiology of the disorder.
Despite almost fi ve decades of clinical and laboratory
investigations, the pathophysiology of somnambulism
(or sleepwalking) remains poorly understood. Further-
more, unlike most other sleep disorders, somnambulism
is still diagnosed mainly or exclusively on the basis of the
patient’s clinical history. The widespread belief that
sleepwalking is a benign disorder is erroneous because
somnambulism can result in various adverse con-
sequences. Although childhood somnambulism is often
transitory and harmless, sleepwalking in adulthood has
substantial harm potential, including the placing of
oneself in dangerous situations (eg, running into walls
and furniture, trying to escape imaginary threats, leaving
one’s house), destruction of property, and serious injuries
to the sleeper, bed partner, or others.1–3 Somnambulism is
a major cause of reported injurious or violent behaviours
after an arousal from sleep,4–7 and episodes resulting in
injury to the patient or others are more prevalent than is
generally recognised.3,8,9 A history of aggressive or
injurious behaviour during sleep is what leads most
adult sleepwalkers to consult a medical specialist.1–3,10 The
number of legal cases of sleep-related violence is
rising.4–7,11 Driving of motor vehicles,12 suspected suicide,13
and even homicide14 or attempted homicide can occur
during somnambulism, raising fundamental questions
about the medicoforensic implications of these acts and
the neurophysiological and cognitive states that charac-
terise patients during such episodes.
Role of somnambulism within sleep
On the basis of a range of physiological measures
including electroencephalogram (EEG) activity, eye
movement activity, and level of muscle tone, sleep is
divided into two very distinct states—rapid eye
movement (REM) sleep and non-rapid-eye-movement
(NREM) sleep. NREM sleep can be further subdivided
into three stages, which the American Academy of Sleep
Medicine’s revised nomenclature refers to as N1 (sleep
onset), N2 (light sleep), and N3 (deep or slow-wave
sleep). Table 1 lists the main characteristics of REM and
NREM sleep stages, and fi gure 1 shows the corresponding
EEG traces. These sleep states are organised into sleep
cycles that have a characteristic distribution across a
typical night (fi gure 2). The neural structures implicated
in these sleep states (ie, the brainstem, anterior and
posterior hypothalamus, basal forebrain, ventral
tegmental area, thalamus, and cortex), their pathways
and interconnections, and the neuro transmitters that
generate and regulate these diff erent states are many
and have complex interactions.15,16
NREM sleep and REM sleep alternate throughout the
night in cycles that last for a mean of around 90 min.
However, deep sleep occurs preferentially during the fi rst
third of the night, whereas periods of REM sleep are
longest during the last third of the night. Somnambulism
usually arises from the deepest sleep stage (ie, N3 or slow-
wave sleep). Thus, episodes typically take place during the
fi rst third of the night when slow-wave sleep is
predominant, although episodes can also occur in N2
sleep. Somnambulism is therefore classifi ed as an NREM
parasomnia, the category that also includes confusional
arousals and sleep terrors. These three parasomnias,
which can coexist, have been termed disorders of arousals
and might be diff erent phenotypes of the same underlying
Clinical characteristics and epidemiology
Somnambulism is defi ned as “a series of complex
behaviours that are usually initiated during arousals from
slow-wave sleep and culminate in walking around with an
altered state of consciousness and impaired judgment”.17
Some somnambulistic behaviours can be mundane and
stereotyped, such as gesturing, pointing at a wall, or
walking around a room, but others (especially in adults)
are surprisingly complex and might necessitate high-level
planning and motor control—eg, getting dressed, cooking,
playing a musical instrument, driving a car. Episodes can
last from a few seconds to more than 30 min. Most
behavioural episodes are characterised by misperception
and unresponsiveness to external stimuli, mental
confusion, perceived threat, and variable retrograde
amnesia. The American Academy of Sleep Medicine has
established diagnostic criteria for somnambulism in the
second International Classifi cation of Sleep Disorders
(panel).17 Sleep-related abnormal sexual behaviours
Lancet Neurol 2013; 12: 285–94
Center for Advanced Research
in Sleep Medicine
(Prof A Zadra PhD,
A Desautels MD, D Petit PhD,
Prof J Montplaisir MD) and
Service of Neurology
(A Desautels), Hôpital du
Sacré-Cœur de Montréal,
Montreal, QC, Canada; and
Department of Psychology
(Prof A Zadra), Department of
Medicine (A Desautels), and
Department of Psychiatry
(D Petit, Prof J Montplaisir),
Université de Montréal,
Montreal, QC, Canada
Prof Jacques Montplaisir, Center
for Advanced Research in Sleep
Medicine, Hôpital du Sacré-Cœur
de Montréal, 5400 boul. Gouin
Ouest, Montreal, QC,
Canada H4J 1C5
www.thelancet.com/neurology Vol 12 March 2013
(so-called sexsomnia18) and sleep-related eating disorder,19
which are distinct and specialised variants of NREM sleep
parasomnias, are not discussed in this Review because
they are not classifi ed as somnambulism per se.17
Somnambulism is more common in childhood than in
adulthood; most children will have, at least temporarily,
one or more of the NREM sleep parasomnias. However,
childhood somnambulism is typically benign (and non-
violent) and usually does not necessitate intervention. The
prevalence of somnambulism is around 3% in toddlers
(age 2·5–4 years),20 and steadily increases to about 11% at 7
and 8 years21 and 13·5% at 10 years, before falling to 12·7%
at 12 years (data unpublished for ages 10 and 12; fi gure 3).
The prevalence of somnambulism rapidly decreases
during adolescence23,24 to about 2–4% in adulthood.9,25,26
Thus, most children outgrow the disorder during
adolescence, but somnambulism can persist into
adulthood in as much as 25% of cases.25 Why
somnambulism persists into adulthood in some people
but not in others is unclear. Somnambulism can also arise
de novo in adults.
No evidence suggests that chronic somnambulism
during adulthood is associated with the subsequent
development of neuropathological disorders (however,
longitudinal studies have not been done). This fi nding
contrasts with those for REM sleep behaviour disorder, a
parasomnia characterised by loss of muscle atonia and
prominent behaviours during REM sleep that generally
occurs in patients older than 50 years and is associated
with the development of neurodegenerative processes
including Parkinson’s disease and dementia with Lewy
Epidemiological data suggest that roughly 25% of
adult sleepwalkers self-report concurrent anxiety or
mood disorders.9 In early childhood, the occurrence of
somnambulism might be associated with separation
anxiety,20 and anxiety or stress might increase the
occurrence of episodes in both children and adults.
However, most adults who sleepwalk do not present
with a psychiatric or personality disorder,3,8 and
successful treatment of axis 1 disorders (as defi ned in
the fourth edition of the Diagnostic and Statistical
Specifi c EEG features Other characteristicsStage-specifi c sleep disorders
Wakefulness (eyes closed)
N1 (sleep onset)
N2 (light sleep)
Alpha waves (8–12 Hz) Alpha rhythm prominent in occipital cortex··
Theta waves (4–8 Hz)
Sleep spindles (11–16 Hz),
K-complexes (>0·5 s)
Delta waves (0·5–2 Hz; amplitude
>75 μV), slow oscillations (<1 Hz)
Low amplitude, mixed frequencies,
saw-tooth theta waves
Slow, rolling eye movements
Background of theta rhythm with occasional
sleep spindles and K-complexes
Delta waves occupy more than 20% of the
Rapid eye movements, muscle atonia,
Hypnic jerks, hypnagogic hallucinations
Bruxism, nocturnal frontal lobe epilepsy
N3 (slow-wave or deep
REM sleep (paradoxical sleep)
Somnambulism, sleep terrors,
REM behaviour disorder, nightmares
EEG=electroencephalogram. NREM=non-rapid-eye-movement. REM=rapid eye momevent.
Table 1: Key characteristics of sleep stages
Saw-tooth theta waves
Figure 1: Electroencephalogram tracings corresponding to relaxed wakefulness and diff erent sleep stages in healthy individuals
REM=rapid eye movement.
www.thelancet.com/neurology Vol 12 March 2013 287
Manual of Mental Disorders28) usually does not aff ect
Roughly 80% of sleepwalkers have at least one aff ected
family member, and the prevalence of somnambulism is
higher in children whose parents have a history of
somnambulism than in those whose parents have no
such history.29 First-degree relatives of sleepwalkers have a
ten-fold increased likelihood of somnambulism compared
with the general population.29 A population-based Finnish
twin cohort25 showed a concordance rate 1·5 times higher
in monozygotic than in dizygotic pairs for childhood
somnambulism and 5 times higher in monozygotic than
in dizygotic pairs for adult somnambulism. These results
suggest that a substantial proportion of the reported
familial aggregation could be explained by genetic factors.
Several widely held views in the medical and
neuroscientifi c communities about somnambulism,
including diagnostic considerations, run counter to
developments in the specialty. We present three key
examples: that sleepwalking has no daytime con-
sequences, that it is characterised by amnesia for the
episode, and that it is an automatic behaviour arising in
the absence of dream-like mental activity.
Somnambulism has no daytime consequences
Daytime somnolence or impairment of daytime
functioning has never been part of the clinical portrayal of
somnambulism. Despite the well documented increase in
slow-wave sleep fragmentation, little information is
available about subjective or objective daytime levels of
vigilance. A study30 of ten adult sleepwalkers showed that
they had daytime somnolence even after episode-free
nights. Not with standing a similar proportion of slow-wave
sleep, sleep walkers had signifi cantly lower mean sleep
onset latencies (ie, the time needed to transition from
wakefulness to sleep) on the multiple sleep latency test
(the gold standard in objective assessment of excessive
daytime sleepiness) than did matched controls. Seven of
these sleepwalkers (and none of the controls) had a mean
latency of less than 8 min,30 which is the accepted
threshold for clinical somnolence. Similarly, in a
retrospective study, Oudiette and colleagues31 used the
Epworth sleepiness scale to show that 47% of 43 patients
with NREM sleep parasomnia had a score greater than 10
(the cutoff for pathological somnolence). These fi ndings
are further supported by our results from 71 adult
sleepwalkers, which showed that 32 patients (45%) had an
Epworth sleepiness score greater than 10, compared with
only eight patients (11%) in a group of 71 healthy controls
(unpublished). In this cohort, reported somnolence did
not seem to correlate with the number of nocturnal
awakenings, periodic leg movements in sleep, or higher
Taken together, these results suggest that excessive
daytime somnolence might be an important characteristic
of somnambulism. Transcranial magnetic stimulation
and brain imaging have been used to show daytime
functioning anomalies in
supporting the idea that clinical considerations should
not be limited to patients’ sleep.32,33
Somnambulism is characterised by episodic amnesia
Because somnambulism is usually diagnosed exclusively
on the basis of clinical history, the validity and reliability
of the diagnostic criteria are of prime importance. A
study33 of the reliability of the diagnosis of various
parasomnias based on criteria from the second
International Classifi cation of Sleep Disorders showed
that sleepwalking only had a “fair” interobserver reliability
because of disagreement about the “amnesia for the
episode” criterion—which was also included in the fourth
edition of the Diagnostic and Statistical Manual of Mental
Disorders.28 However, work based on 94 patients referred
to our sleep clinic for chronic sleepwalking (unpublished
data presented at the fourth Meeting of the World
Association of Sleep Medicine) suggests that a substantial
proportion of adult sleepwalkers recall specifi c elements
of their episodes, at least occasionally. Upon awakening,
80% of patients remembered sleep mentation during
somnambulistic episodes. Additionally, 61% reported
remembering specifi c behaviours that they displayed
during episodes. Similarly, perceptual elements from the
0 12060 180300 240420 360
Figure 2: Distribution of diff erent sleep stages across a typical night in healthy individuals
REM=rapid eye movement. REMP=rapid eye movement sleep periods.
Panel: Somnambulism diagnostic criteria of the American
Academy of Sleep Medicine—second International
Classifi cation of Sleep Disorders
A Ambulation occurs during sleep
B Persistence of sleep, a changed state of consciousness, or
impaired judgment during ambulation shown by at least
one of the following:
• Diffi culty in arousal of the person
• Mental confusion when awakened from an episode
• Amnesia (complete or partial) for the episode
• Routine behaviours that occur at inappropriate times
• Inappropriate or nonsensical behaviours
• Dangerous or potentially dangerous behaviours
C The disturbance is not better explained by another sleep,
medical, neurological, or mental disorder; drug use; or
substance use disorder
Adapted from the second International Classifi cation of Sleep Disorders.17
www.thelancet.com/neurology Vol 12 March 2013
sleeper’s actual environment during somnambulistic
episodes were recalled upon awakening by 75% of
patients. 75% of sleepwalkers reported that emotions
including fear, anger, frustration, and helplessness were
often or always experienced during their episodes.35 These
data add to descriptive reports36–38 showing that many
patients can and do recall at least portions of episodes
upon awakening, and thus suggest that complete amnesia
of the event is not standard for adult sleepwalkers. In
children, somnambulism might be more likely to consist
of automatic behaviours and complete amnesia might be
more common, possibly because of higher arousal
Somnambulism is an automatic behaviour arising in the
absence of dreamlike mental activity
That dreamlike mentation is not confi ned to REM sleep
only,40,41 but occurs in NREM sleep (including slow-wave
sleep) also, is now well established. Previously, complex
mental contents were thought not to be implicated in
behaviour during somnambulistic episodes, but a growing
body of evidence shows the contrary. In addition to well
documented cases,36–38 empirical evidence suggests that
sleep mentation is not only frequently part of the main
experience of somnambulism, but also can modulate
motor behaviour during an episode. Oudiette and
colleagues31 showed that 27 of 38 patients (71%) recalled
short, unpleasant, dreamlike mentations associated with
sleepwalking episodes. Furthermore, the mentation
reported by patients was congruent with recorded
nocturnal behaviour, suggesting that sleepwalking might
be the acting out of dreamlike mentations. Sleep
laboratory investigations of adult sleepwalkers suggest
that, when available, patients’
experiences are broadly consistent with behaviours
recorded during episodes.42
sleepwalkers are aware of their immediate physical
environment during an episode and can interact with
other people nearby, such fi ndings are not reported in
normal dreaming or in dream-enactment behaviours in
patients with REM-sleep behaviour disorder.43 Additionally,
sleepwalkers’ eyes are usually open throughout episodes,
thereby allowing navigation, whereas REM and NREM
dreaming occur in a virtual, offl ine environment with very
restricted awareness of the actual physical environment.
Various fi ndings show that somnambulistic behaviours
are construed by many patients as being motivated by an
intrinsic sense of urgency or underlying logic (although
judgment is often impaired) that accounts for actions
during actual episodes. This evidence raises important
questions about the role that sleep-related mentations
have in how somnambulistic episodes are experienced
Diagnosis and clinical management
Both nocturnal frontal lobe epilepsy and REM-sleep
behaviour disorder can cause complex and sometimes
violent behaviours during sleep that can be confused with
somnambulism (table 2). Guidelines22 and the frontal lobe
epilepsy and parasomnias scale44 have been suggested to
help with diff erential diagnosis. Challenging cases might
warrant thorough poly somno graphic assessments with an
extended EEG montage and continuous audiovisual
recording. Dis orders that are known to increase pressure
for deep sleep or arousals during sleep, or to induce
confusional states should be considered in clinical
management of somnambulism. Factors that increase
pressure for deep sleep include intense exercising in the
evening, fever, and lack of sleep; disorders that produce
repeated arousals during sleep include sleep apnoea and
periodic leg movements during sleep (fi gure 4)
Situations that intensify pressure for slow-wave sleep
(eg, sleep deprivation) might precipitate disorders of
arousal in predisposed individuals. Thus, clinicians
should emphasise the importance of getting suffi cient
sleep and avoidance of irregular sleep schedules to
patients with somnambulism. Similarly, most causes of
increased arousals from sleep (eg, environmental
disturbances, stress) and the presence of concomitant
sleep disorders capable
microarousals are pre cipitating factors. Thus, clinicians
should ensure that breathing problems and movement
disorders during sleep, if present, are treated, which
should alleviate and control the parasomnia.
Disorders that ease dissociation or induce confusional
states can trigger somnambulism. Sleepwalking has
been noted in patients with psychiatric disorders45 and
those given various psychotropics, including sedatives,
stimulants, and antihistamines.5,45,46 Possibly, these dis-
orders and drugs ease regional dissociation and lead to
somnambulism through modulation of states of sleep
of causing recurrent
Proportion with somnabulism (%)
Figure 3: Prevalence of somnambulism in children aged 2·5–12 years in a
prospective cohort of 1400 children
Adapted from data from the Quebec Longitudinal Study of Child Development
(Quebec Institute of Statistics). Only data for children aged 2·5–8 years have
www.thelancet.com/neurology Vol 12 March 2013 289
Irrespective of underlying disorders, precautions
should be taken to ensure a safe sleep environment.
When the parasomnia continues to cause distress or
poses a threat, three main treatment options are available:
hypnosis, scheduled awakenings, and drugs. However, as
emphasised in a 2009 review,47 no adequately powered,
controlled, clinical trials for the treatment of
somnambulism have been done. Hypnosis (including
self-hypnosis) is eff ective in both children and adults
with chronic somnambulism.48,49 In children, the
preferred treatment is anticipatory or scheduled
awakening50—a behavioural technique whereby parents
awaken their child nightly about 15 min before the typical
time of occurrence of an episode for about a month.
Drugs should be prescribed only when behaviours are
potentially hazardous or extremely disruptive to bed
partners or other household members. Benzodiazepines,
particularly clonazepam and diazepam, have been
used.51,52 These drugs decrease arousals and anxiety and
suppress slow-wave sleep, but do not always adequately
control sleepwalking.8 Even when pharmacotherapy is
chosen, treatment should always include instructions
about regular sleep routine and good sleeping habits,
avoidance of sleep deprivation, and stress management.
Theoretical frameworks for understanding
Somnambulism is usually classifi ed as a disorder of
arousal;17 however, several clinical and experimental
fi ndings suggest that somnambulism could be due to a
dysfunction in slow-wave sleep regulation (fi gure 4).
We review these complementary views and the
neurophysiological fi ndings
that support each
Somnambulism as a disorder of slow-wave sleep
Two lines of evidence favour the notion of a dysfunction
in slow-wave sleep as the primary underlying cause for
somnambulism—namely, the presence of intrinsic
abnormalities in slow-wave sleep and the atypical
response that sleepwalkers have to sleep deprivation.
A robust feature of the otherwise preserved sleep
architecture in sleepwalkers relative to healthy controls is
the absence of NREM sleep continuity, which is shown
Somnambulism Nocturnal frontal lobe epilepsyREM-sleep behaviour disorder
Age at onset
Time of night
Events per week *
69–90% of patients
First third of the night
Simple to complex movements
(ambulation), might be goal directed,
eyes are open
Less than 40% of patients
A few seconds to 3 min
Highly stereotyped (eg, abnormal
posturing) and purposeless, eyes
can be open or closed
No (patient remains prone or
Last half of the night
Typically gross motor movements
(eg, fl ailing of limbs), related to
dream content, eyes are closed
Yes Can get out of bed
Can leave bedroomYes Rarely
Interaction with immediate environment Might respond to external
stimulation or verbal questions, and
navigate in familiar environments
NoPoor or incidental
Spontaneous full awakening after the
Recall of the events
Mental state after the event when
Confused and disoriented
Usually fully awake
Vivid dream recall
Fully awake and functional
Sleep deprivation, noise, stress,
obstructive sleep apnoea, periodic leg
movements during sleep
Low to moderate
Frequent awakenings and
microarousals in slow-wave sleep,
hypersynchronous delta waves
Alcohol withdrawal, selective
serotonin reuptake inhibitors,
Absence of muscle atonia or
excessive phasic electromyographic
activity in REM sleep
Polysomnographic fi ndings
Often normal, epileptiform in
about 10% of patients
Potential for injury or violence Yes
REM=rapid eye movement. *These values are estimates based on means reported in published work and should be interpreted with caution because frequency and duration
of episodes vary greatly between and within patients.
Table 2: Key clinical features of somnambulism, nocturnal frontal lobe epilepsy, and REM-sleep behaviour disorder
www.thelancet.com/neurology Vol 12 March 2013
by increased spontaneous awakenings and EEG recorded
arousals outside slow-wave sleep, even on nights without
episodes.53–55 This fi nding is especially noteworthy
because the number of awakenings in the other sleep
stages does not increase.53
Sleepwalkers also have disturbances in sleep intensity as
measured quantitatively by slow-wave activity (spectral
power in the delta band frequency). Specifi cally, their sleep
is characterised by an overall decrease in slow-wave activity
during the fi rst sleep cycles53,56 and a diff erent timecourse
of slow-wave activity decay throughout the night.54 These
results suggest that sleepwalkers’ frequent awakenings
from deep sleep interfere with the normal build-up of
slow-wave activity, especially during the fi rst two sleep
cycles when most awakenings from deep sleep occur in
sleepwalkers. Consistent with fi ndings suggesting a
disturbance in consolidation of slow-wave sleep, recurring
electrocortical events marked by abrupt changes in EEG
frequency or amplitude are noted in sleepwalkers during
NREM sleep. These periodic sequences of transient EEG
activity have been formally investigated as part of the cyclic
alternating pattern rate,57–59 an endogenous rhythm thought
to be a physiological marker of NREM sleep instability. An
increased cyclic alternating pattern rate has been recorded
both in adult and in child sleepwalkers58,59 even on nights
without episodes. That this abnormal transient EEG
activity might lead to recurrent fragmentation of slow-
wave sleep and contribute to the occurrence of NREM
sleep parasomnia has been suggested.57,60
Hypersynchronous delta waves, which are usually
defi ned as several continuous high-voltage (≥150 μV)
delta waves occurring during deep sleep, were probably
the fi rst EEG marker described in relation to
somnambulism.61 Irrespective of behavioural episodes,
sleepwalkers have signifi cantly more hypersynchronous
delta waves during NREM sleep than do controls.62
Episode onset, however, does not seem to be preceded by
a gradual accumulation
delta waves,62 but rather by an abrupt change in high-
amplitude slow oscillations (<1 Hz) in the 20 s
immediately preceding the episodes.63 These processes
may show cortical reactions to brain activation.
In healthy sleepers, sleep deprivation produces a
rebound of slow-wave sleep and generates a consolidated
(ie, fewer awakenings) NREM sleep as a result of
heightened sleep homoeostasis
physiological need for sleep to restore the body’s
equilibrium between sleep and wakefulness).64 This
physiological response is not noted in sleepwalkers, and
sleep deprivation actually results in more awakenings
from slow-wave sleep during recovery sleep (ie, sleep
occurring immediately after sleep deprivation) than are
noted during baseline sleep (ie, normal nocturnal sleep
without deprivation). This uncharacteristic response to
sleep deprivation seems to be restricted to slow-wave
sleep; awakenings from N2 and REM sleep are reduced.65
More importantly, 25–38 h of sleep deprivation
increases the number of somnambulistic events recorded
in the laboratory by a factor of 2·5 to 5 compared with
deprivation diff er so greatly from those of healthy
sleepers that they are highly sensitive and specifi c for the
diagnosis of adult somnambulism.42,65,66 That none of the
healthy controls in these studies had nocturnal
behavioural manifestations shows that sleep deprivation
does not lead to sleepwalking, but rather that sleep
deprivation increases the probability of somnambulistic
behaviours in predisposed individuals.
Sleep deprivation also substantially increases the
complexity of somnambulistic events recorded during
recovery sleep.65,66 Somnambulistic episodes are not only
more complex but also often more agitated, with forced
arousals out of recovery slow-wave sleep.42 A possible
explanation for these fi ndings is that other subcortical
regions might be recruited after sleep deprivation. Two
functional MRI studies67,68 showed that sleep deprivation
increased activation of the amygdala resulting from the
presentation of negative visual stimuli and signifi cantly
strengthened amygdala connectivity with autonomic
activating centres of the brainstem. This activation was
accompanied by a decrease in connectivity with the
prefrontal cortex—a top-down cognitive regulator of
pressure (ie, a
responses to sleep
Somnambulism as a disorder of arousal
Somnambulism was originally described as a disorder of
arousal69 because of the autonomic and motor arousals
that propel patients towards incomplete wakefulness.
Three postarousal EEG patterns have been described that
Disorder of slow-wave sleep
Abnormalities of slow-wave sleep
• Increased spontaneous arousals
• Decreased slow-wave activity
• Increased cyclic alternating pattern rate
• Hypersynchronous delta waves or very slow
oscillations just before somnambulistic episodes
Abnormal response to sleep deprivation
• Absence of normal rebound of slow-wave sleep
• Increased number and complexity of
Disorder of arousal
Incomplete awakening from sleep
• Postarousal EEG patterns
• Abnormal arousal reactions
Genetic predisposition to somnambulism
Disorders that increase slow-wave-sleep pressure
Disorders that increase arousals in slow-wave sleep
• Get sufficient sleep
• Avoid irregular sleep schedules
• Avoid noisy environments
• Adopt good stress management
• Treat sleep-disordered breathing and sleep-related
• Consider discontinuation of psychotropic drugs
• Treat with hypnosis or benzodiazepines
Figure 4: Somnambulism as a disorder of arousal or slow-wave sleep
www.thelancet.com/neurology Vol 12 March 2013 291
characterise most slow-wave-sleep arousals70 and
somnambulistic events71 in adults with somnambulism
or sleep terrors. The same EEG patterns are present in
somnambulistic events during N2 sleep.71 Delta activity
(indicative of sleep-related processes) is recorded in
almost half of all episodes during slow-wave sleep and
about 20% of those during N2 sleep.71 Taken together,
these fi ndings suggest that sleepwalkers are caught
between NREM sleep and full EEG arousal and are thus
neither fully awake (as translated clinically by the
seeming absence of conscious awareness or insight) nor
fully asleep (as shown behaviourally by the capacity to
interact with others and navigate the immediate
environment) during episodes.
Other fi ndings support the notion of somnambulism
as a disorder of arousal. Arousals from slow-wave sleep,
whether occurring spontaneously, triggered by external
stimuli, or produced by other sleep disorders, can induce
sleepwalking episodes in predisposed individuals.
Several studies,72–74 including a population-based cohort
study of preadolescent children,73 have shown an
association between somnambulism and both obstructive
sleep apnoea and upper airway resistance syndrome.
Treatment of sleep-disordered breathing might result in
the disappearance of somnambulism through restoration
of, or an increase in, sleep consolidation.
stimulation during slow-wave sleep induce episodes in
sleepwalkers during normal sleep and even more
frequently during recovery sleep. In a study by Pilon and
coworkers,42 the combined eff ects of sleep deprivation
and auditory stimulation induced somnambulistic
episodes in all ten sleepwalkers tested but in none of the
control population. Furthermore, the mean intensity of
stimuli that induced somnambulistic episodes during
slow-wave sleep (roughly 50 dB) was similar to the mean
intensity that produced full awakenings both in
sleepwalkers and in controls. In another more extensive
study,75 auditory arousal thresholds in sleepwalkers did
not diff er signifi cantly from those in controls for either
slow-wave sleep or N2 sleep. However, the mean
proportion of auditory stimulations that induced arousal
responses during slow-wave sleep was signifi cantly
higher in sleepwalkers than in controls.
These fi ndings show that sleepwalkers are neither
more easy nor more diffi cult to awaken from deep sleep
than are controls, but rather that sleepwalkers have
abnormal arousal reactions. A study71 corroborated that
50% of postarousal EEG signals in sleepwalkers
contained clear evidence of delta activity, which could
explain the mental confusion after awakenings from
slow-wave sleep and point to changes in cortical reactivity.
arousals by auditory
Somnambulism as a phenotypical expression of
simultaneous states of sleep and wakefulness
Irrespective of the two notional frameworks discussed
already, somnambulism needs to be considered in view of
new models and fi ndings about the interplay between the
states of wakefulness, REM sleep, and NREM sleep.76,77
Although human sleep has traditionally been thought of
as a global process occurring uniformly in the whole
brain, increasing evidence shows that sleep—or functional
correlates of sleep—might be controlled by local events.
Surface EEG studies78,79 showed that sleep depth does not
occur simultaneously throughout the brain and that the
frequency-specifi c topographical
distributed along the anteroposterior axis. Data obtained
via intracerebral electrodes showed that EEG patterns
related to sleep and
simultaneously in diff erent brain regions. During an
episode of sleepwalking in an epileptic patient, Terzaghi
and colleagues80 recorded an EEG pattern of wakefulness
in the motor and central cingulate cortices and
concomitant increased delta bursts (indicative of sleep) in
the frontal and parietal dorsolateral associative cortices,
suggesting that awakening of the motor and cingulate
cortices is in apparent confl ict with the simultaneously
persistent sleep state of the associative cortical regions.
The cingulate and motor cortices could cause the complex
motor behaviours, and the degree of activation of
frontoparietal associative cortices could explain the
various degrees of awareness of the environment and
mentation that accompany the awakening.
Nobili and colleagues81 used a similar depth EEG
electrode strategy and noted frequent, short-lasting, local
activations of the motor cortex, which were characterised
by an abrupt interruption of the slow-wave pattern and a
high-frequency EEG pattern, suggesting the coexistence
of sleep and wakefulness. These activations in the motor
cortex were paralleled by a concomitant increase in slow
waves in the dorsolateral prefrontal cortex. Brain imaging
by SPECT during a sleepwalking episode82 showed, on
one hand, a deactivation of frontoparietal associative
cortices (typical of sleep), and, on the other hand, an
activation of the posterior cingulate and anterior
cerebellum networks and no deactivation of the
thalamus—characteristic of the emotionally driven
behaviour of wakefulness.
The two sets of brain regions that are incongruent
during somnambulism—ie, the motor and cingulate
cortices, and the medial prefrontal and lateral parietal
cortices—have been associated with the so-called task-
positive (brain regions activated during cognitively
demanding tasks) and default mode (cortical regions
activated during the brain’s resting state) networks,83
respectively. A dysfunctional interplay between these two
networks is implicated in other pathological disorders
including schizophrenia,84 Alzheimer’s disease,85 and
Collectively, these fi ndings support the idea that sleep
and wakefulness are not mutually exclusive—an
increasingly accepted view termed local sleep.87 They also
suggest that somnambulism and other parasomnias
might result from an imbalance between the two
diff erences are
wakefulness can coexist
www.thelancet.com/neurology Vol 12 March 2013
behavioural states.77 Thus, disorder of arousal might be
too notionally restrictive to fully account for the
pathophysiology of somnambulism. A broad and
unifying view might implicate the simultaneous
activation of localised cortical and subcortical networks
that have roles in sleep and wakefulness.88
Three promising research directions could help to
elucidate the pathophysiology of somnambulism. First,
PET neuroimaging can detect subtle changes in cerebral
blood fl ow and metabolism throughout the human
sleep–wake cycle89 and specifi c measures—eg, neural
correlates of delta activity during NREM sleep.90,91
However, few neuro imaging studies have been done in
sleep-disordered patients, and the only neuroimaging
study of somnambulism is the single case report by
Bassetti and colleagues.82 Variations in regional cerebral
blood fl ow during NREM sleep in sleepwalkers are
unexplored, but could further understanding of NREM
Second, the general
sleepwalkers should be investigated to record the nature
and extent of impairments. In addition to fi ndings
suggesting excessive daytime somnolence in some
patients, two studies32,33 support the view that adult
sleepwalkers evince functional abnormalities during
wakefulness. A transcranial magnetic stimulation study32
of sleepwalkers showed hypoexcitability of some cortical
GABAergic and cholinergic inhibitory circuits during
wakefulness, and a high-resolution SPECT study33 done
during wakefulness in sleepwalkers showed hypo-
perfusions in the frontopolar cortex, superior and middle
frontal gyri, superior and inferior temporal gyri, and
angular gyrus, and additional hypoperfusions of limbic
structures (hippocampus). Changes in limbic structures
might be associated with disturbances in emotional
regulation in sleepwalking patients when submitted to
Finally, despite several reports of familial aggregation,
very few molecular studies to identify genes that
predispose to somnambulism have been done. Licis and
coworkers92 did a genome-wide study in a single family of
22 members. They assumed an autosomal dominant
daytime functioning of
model with reduced penetrance, and established
signifi cant linkage at chromosome 20q12–q13.12. The
candidate interval included the adenosine deaminase
gene, which has been associated with slow-wave sleep.93
Unfortunately, sequencing revealed no coding mutation
within the gene. Lecendreux and colleagues94 described
an association between familial sleepwalkers and the
HLA DQB1*05 and DQB1*04 alleles. However, the
functional importance of this fi nding is unclear. None of
these fi ndings has been replicated so far.
An alternative approach for the identifi cation of genes
that aff ect complex traits is association analysis of
candidate genes.95 Genes94,96,97 implicated in sleep
homoeostasis, sleep depth, or slow-wave generation
could be attractive candidates. To that eff ect, a twin
study98 showed substantial genetic overlap between
parasomnias and dyssomnias, supporting the notion of
somnambulism as a disorder of regulation of slow-wave
sleep and the association between sleepwalking and
Although a comprehensive understanding of the clinical,
neurobiological, and genetic factors associated with
chronic somnambulism remains elusive, much progress
has been made in clarifi cation of the key relations
between waking and sleep-related processes in this
disorder. However, some
somnambulism have hindered refi nements in clinical
assessment and defi nition. The validation and use of a
polysomnographically based diagnosis for somnam-
bulism, such as a sleep-deprivation protocol, would be
useful in uncertain diagnoses. But in the context of
medicolegal cases of sleep-related violence,5,6 whether
even a polysomnographically diagnosed sleepwalker was
having a somnambulistic episode during a remote
forensic event cannot be ascertained. Similarly, because
neurophysiological markers of sleepwalking can also be
detected in controls, they cannot be used to provide
direct evidence in the courtroom. Well designed clinical
trials for the treatment of chronic somnambulism are
virtually non-existent.47 Greater eff orts are needed to
establish treatment effi cacy for somnambulism, which
should be thought of, at least in most adults, as a
disorder with a high potential for serious injury and
both night-time and daytime sequelae.
All authors contributed equally to the search of medical literature,
structuring and writing of the review, and critically reviewing all versions
of the paper.
Confl icts of interest
JM has received grants from the Canadian Institute of Health Research
and the Government of Canada Senior Research Chair in Sleep
Medicine (PI), research grants or support, or both, from Merck and
GlaxoSmithKline, and honoraria for speaking engagements from
Valeant and Otsuka, and has served as an advisor for Sanofi -Aventis,
Servier, Merck, Jazz, Valeant, and Impax. All other authors declare that
they have no confl icts of interest.
Search strategy and selection criteria
We searched PubMed with the search terms “sleepwalking”
and “somnambulism” for papers published between Jan 1,
1979, and Sept 30, 2012. Additional references (abstracts)
and book chapters that were cited in relevant reports were
also used. We included some papers about topics other than
somnambulism to strengthen hypotheses about underlying
mechanisms. Most papers included were published in English,
but non-English articles with English abstracts were included
For more on medicolegal cases
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