Sleep Medicine Reviews (2009) 13, 157e168

www.elsevier.com/locate/smrv

CLINICAL REVIEW

Parasomnias in childhood
Suresh Kotagal*
Division of Child Neurology and the Center for Sleep Medicine, Mayo Clinic, 200 First Street SW,
Rochester, MN 55905, USA

KEYWORDS
Sleep;
Ontogeny;
Central pattern generators;
Arousal parasomnias;
Seizures;
Enuresis;
Nightmares

Summary Common childhood parasomnias, including those occurring at sleep

onset and during rapid eye movement sleep or non-rapid eye movement sleep
and their ontogeny are discussed. The events may be distressing to both the patient
and family members. Stereotypic movements characteristic of some parasomnias
most likely arise from disinhibition of subcortical central pattern generators.
Genetic predisposition, an inherent instability of non-rapid eye movement sleep
and underlying sleep disturbances such as obstructive sleep apnea may predispose
to the activation of confusional arousals, sleep walking or sleep terrors. Many parasomnias can be recognized by history alone, but some require nocturnal polysomnography for appropriate diagnosis and management. A scheme to distinguish
non-rapid eye movement sleep parasomnias from nocturnal seizures is provided.
Behavioral therapy has a role in the management of many childhood parasomnias,
but evidence based recommendations are as yet unavailable.
2008 Elsevier Ltd. All rights reserved.

Introduction
This article provides an overview of common
childhood parasomnias. An emphasis has been
placed
on
formulating
pathophysiological
concepts. In the interests of brevity, some minor
and inconsequential parasomnias have not been
discussed.

* Tel.: 1 507 266 0774; fax: 1 507 284 0727.

E-mail address: kotagal.suresh@mayo.edu

Phylogeny, ontogeny, and

pathophysiology
Parasomnias are the consequence of dissociation
between wakefulness, NREM or REM sleep, with
behaviors characteristic of one state becoming
superimposed on another.1 The dissociation
between behaviors and motor patterns from their
specific state occurs even amongst marine
mammals, where it might help thermoregulation
and in the maintenance of vigilance during
continuous living in the aquatic environment. This
is exemplified by the unihemispheric sleep of
bottle nosed dolphins, seals, beluga whales and

1087-0792/$ - see front matter 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.smrv.2008.09.005

158
killer whales.2,3 In the beluga whale and the
dolphin, the eye contralateral to the awake
hemisphere is kept open and out of the water for
monitoring the environment during swimming
while simultaneously, the eye contralateral to the
sleeping hemisphere is kept closed.4,5 The transition to bihemispheric sleep appears in terrestrial
species. Precocial animals like the elephant and
giraffe, in which the central nervous system is
mature at birth, routinely dissociate sleep from
wakefulness as manifested by their sleeping while
standing e a posture during which they maintain
balance and tonic extensor muscle activity in the
extremities.6
In humans, the maturation of EEG-determined
REM and NREM sleep emerges in utero from
a background of undifferentiated, spontaneous
fetal activity, which has also been termed
pre-sleep by Hamburger.7,8 With progressive
maturation of the prematurely born infant, independent oscillations of neuronal activity, autonomic function and overt behavior become
organized into distinct sleep states9 like REM and
NREM sleep (also termed active and quiet sleep in
newborns). An overlap between sleep states is the
norm in term babies, with about 20% of newborn
sleep at 29 weeks post-conceptional age being
categorized as transitional or indeterminate
sleep, that shows intermingling of elements of
active and quiet sleep.10 With progressive cortical
maturation over the next few weeks, indeterminate sleep seems to resolve. Another important
feature of newborn sleep is the presence of nonepileptic, stereotyped motor patterns such as nonnutritive sucking and bicycling movement during
sleep, which may represent the intrusion of
features of wakefulness onto sleep.11,12 These
behaviors are fragmentary and unsustained
however, simply because the immature cortical
neuronal network, incomplete myelination of the
descending motor projection systems (like the
corticospinal tracts), combined with an immature
cerebellar system preclude external expression of
sustained motor behaviors during sleep. Indeed
the period from birth to 18 months may be termed
a silent period for parasomnias because overt
expression of the results of sleep state dissociation
is minimal.
One of the features of sleep state dissociation is
the appearance of non-epileptic, stereotyped
movements. The generation of these movements
at subcortical levels is related to activation of
networks of interneurons that are also referred to
as central pattern generators (CPGs).13 The CPGs
in turn recruit motor neurons in the ventral
brainstem or spinal cord as the final, effector step

S. Kotagal
in the elicitation of stereotypic movements.13
Rhythmic suckling in newborn animals can be
generated by activation of rhombomeres containing the VII and XII cranial nerve nuclei.14 The CPG
for fictive mastication, which may be relevant to
bruxism, is located in the pons and medulla, with
projections to the motor nucleus of the cranial
nerve V, and cranial nerves VII and XII.15 Stereotyped patterns of movement such as walking can
be generated in mammalian sacral spinal cord
segments even after it has been deafferented16;
this generator might be relevant to the phenomenon of sleep walking. Bruxism and rhythmic
movements may be physiological in early childhood. Additional, yet to be identified and more
rostral CPGs may also play a role in activation of
stereotyped walking movements. CPGs can be
activated by both glutaminergic and serotonergic
inputs.17,18 The application of NMDA receptor
antagonists leads to suppression of the activity of
spinal CPGs.19 Descending serotonergic projections
from the raphe nucleus to the spinal cord also play
a complex role in modulating spontaneous and
synchronous rhythmic activities generated at the
spinal level.20,21 A major advance in the understanding of the pathogenesis of parasomnias has
been provided by an extensive body of work of
Parrino et al.22 They clarify that arousals are
adaptive responses of the sleep regulatory system.
Arousal responses are not limited to a single EEG
pattern, but may range from K-complexes and
delta bursts to low amplitude, fast rhythms. They
are also reflected in the phase A subtypes of cyclic
alternating patterns (CAPs). The CAPs represent an
ultra-slow oscillation of the EEG and play a role in
the dynamic organization of sleep. They recur in
NREM sleep with a periodicity of 20e40 s. CAPs can
trigger a variety of stereotypic events in sleep that
can range from epileptic seizures to nocturnal
myoclonus, bruxism and sleep walking. Genetic
factors and underlying sleep disorders such as
sleep disordered breathing may activate spinal or
brainstem CPGs. Based upon the nature of the CPG
that has been activated, one may observe sleep
walking, rhythmic movement disorder, head
banging, bruxism, or other stereotyped behaviors
in sleep.
What Provokes Parasomnias in Childhood?
Starting around 8 months in the visual cortex and
by 24 months in the frontal cortex, a process of
synaptic pruning commences, with removal of
excess of excitatory and inhibitory synapses.
Approximately 40% of synapses in the cerebral
cortex are eliminated through this process, which
is generally completed by age 11 years.23e25
The elimination of unwanted synapses is an

Parasomnias in childhood
important manifestation of plasticity of the
developing brain. This pruning process also occurs
in the cerebellum and brainstem. At least in the
cerebellum, the activation of the NMDA type of
glutamate receptors is involved in the synapse
elimination.24 Concurrently, a process of programmed cell death is also initiated in the central
nervous system. Both programmed cell death and
synaptic pruning are physiologic and adaptive
processes that serve to limit competition for
trophic factors and eliminate aberrantly developed connections. Down-regulation of descending
GABAergic projections from the cerebral cortex to
the brainstem or diminished serotonergic inhibition of the spinal cord may play a key role in the
pathogenesis of sleepewake transition parasomnias and the arousal parasomnias. These
changes may also impact the regulation of CAPs,
which have been described by the group of Terzano and Tassinari.22
This author proposes that starting around 2
years of age, a combination of a genetic predisposition to sleep state dissociation, completion of
myelination of the pyramidal tracts and maturation of the cerebellar system, combined with
reflex activation of subcortical central pattern
generators (as might happen during sleep disordered breathing, gastroesophageal reflux or periodic limb movement activity) triggers certain
stereotypic patterns of behavior.22 At sleep onset,
these patterns may manifest as hypnic starts,
sleep paralysis or rhythmic movements, while
during sleep they manifest as confusional arousals,
sleep terrors or sleep walking. This hypothesis is
further supported by the prompt resolution of
most parasomnias upon treatment with GABAergic
agents like the benzodiazepines. Over the first
decade and a half, concurrent with progressive
maturation of these subcortical inhibitory projection systems, parasomnias gradually subside. In
adults with neurodegenerative processes involving
the brainstem, there may be reappearance of
disinhibition of the brainstem during sleep that
manifests in the form of parasomnias like REM
sleep behavior disorder.
A unifying theory for the pathogenesis of parasomnias must be able to explain why they are
relatively uncommon during the first 18e24
months of life, why they then become overtly
manifest in pre-school age children and resolve by
the latter half of the first decade, only to then
reappear in some adults. The above theory
reconciles
phylogeny,
ontogeny,
neurodevelopmental processes and the clinically
observed phenomena by applying the current
literature.

159

Epidemiology
In a longitudinal, population-based survey, Klackenberg found that up to 45% of children aged 4e16
years had experienced sleep walking; only 2e3%
however reported a frequency of at least one
episode per month.26 Frightened awakenings from
sleep were seen in about 40 of subjects, and 3.5%
of this group met criteria for sleep terrors. Petit
and Montplaisir have recently published their
findings from the only known prospective study of
childhood parasomnias.27 The study was from the
province of Quebec, Canada. Approximately 1000
subjects were followed prospectively between the
ages of 2.5 years and 6 years; 88% of the population was Caucasian. The overall prevalence rate
for sleep walking was 14.5%, for sleep terrors it
was 39.8%, and for sleep enuresis it was 25%. The
prevalence rates for bruxism and rhythmic movements were 45.6% and 9.2% respectively. The
authors point out that parasomnias are highly
prevalent in this age group and that 88% of the
cohort manifested at least one parasomnia during
the study period. The occurrence of parasomnias
in pre-school age children is quite ubiquitous.
Children frequently experience minor episodes of
partial awakening from sleep which might not even
come to parental attention, particularly if the
child does not cry for a long period or leave the
bedroom.

Sleepewake transition parasomnias

Hypnic starts
Also termed sleep starts, these are isolated,
quick jerks of the upper or lower extremities
that occur at sleep onset. They may be accompanied by a sensation of falling, a dream-like
feeling or a flashing sensation.28 Hypnic starts do
not portend a significant underlying neurological
disorder. They are benign, occur in approximately 70% of people of all ages,29 and most
likely represent a release phenomenon that has
been generated at the level of the brainstem or
spinal cord due to transient loss of suprasegmental, descending inhibitory influences.

Benign neonatal sleep myoclonus

This condition is characterized by symmetric or
asymmetric, repetitive jerks of extremities during
sleep in the first month of life. The movements
cease upon awakening. They can be mistaken for
seizures, but the movements do not temporally

160
coincide with epileptiform discharges on a simultaneously obtained video-electroencephalogram
(EEG). The movements are entirely benign and
resolve spontaneously over weeks to months.29,30

Isolated sleep paralysis (ISP)

The term refers to isolated or recurrent episodes
of transient inability to move the body as one is
drifting off to sleep, or immediately upon awakening from sleep. This phenomenon is not accompanied by features of narcolepsy such as daytime
sleepiness or cataplexy. ISP has been described in
a variety of ethnic populations. In Japan, the
condition has been termed Kanashibari, while
terms like Old Hag and Kokma have been
used to describe the condition in Newfoundland
and the West Indies, respectively.31 This parasomnia results from intrusion of elements of REM
sleep like muscle atonia onto wakefulness. The
disorder is common in adolescents and young
adults. In a survey of 8085 German and Italian
subjects aged > 15 years drawn from the general
population, Ohayon et al. found that 6.2% had
experienced at least one episode of sleep paralysis
in their lifetime.32 Further, 12.4% had experienced
onset of symptoms during childhood. Consciousness remains intact during these episodes. The
individual is aware of the surroundings. Hallucinations such as a feeling the presence of others
nearby, pressure on the chest, or hearing footsteps
is common. Approximately 20% of young adults
with anxiety disorder can manifest ISP.33 Sleep
deprivation in otherwise healthy teenagers may
also be a trigger. The differential diagnosis
includes partial seizures and periodic paralysis.
Isolated events do not require treatment. On an
empiric basis, recurrent episodes may be treated
with REM suppressing agents such as low doses of
tricyclic agents, clonidine or clonazepam.

Rhythmic movement disorder

Rhythmic movements in infants and toddlers at the
time of drifting off from wakefulness to sleep
are physiologic, and generally resolve by the age of
3e4 years. Rhythmic movements generally occur
at the transition from wakefulness to N1 sleep,
during NREM sleep and in REM sleep.34 Infrequently, the movements occur in the middle of the
night after the child has awakened and is then
trying to fall back to sleep. The three common
types of rhythmic movements are: side-to-side
head rolling, head banging and body rocking.
Rhythmic movement disorder is identified when
the movements lead to significant consequences

S. Kotagal
such as self-injury. The movement frequency can
vary, but it is generally 0.5e2 per s. There is a 4:1
male predominance.35 Children are generally
amnestic for the event upon awakening. The
rhythmic movements around sleepewake transition should be distinguished from those seen in
autism and pervasive developmental disorders,
which tend to persist also during wakefulness.
From the pathophysiologic standpoint, rhythmic
movements most likely represent a release
phenomenon, with activation of a subcortical
central pattern generator as a result of a transient
diminution of descending suprasegmental inhibitory input.
There is no satisfactory treatment for rhythmic
movement disorder. Anecdotal therapies suggested have included creating intentional and
extraneous rhythmic movements before bedtime,
rhythmic sounds in the sleeping environment, and
the use of antihistamines or carbamazepine. Shortterm benzodiazepine therapy has been tried on an
empiric basis.34 Padding the sides of the crib might
be necessary to prevent injury.

Arousal parasomnias
This group is composed of confusional arousals,
sleep terrors, and sleep walking. More than one
type may coexist within the same patient, and it is
reasonable to discuss them here as a group. Typically, arousal parasomnias occur at the time of
transition from slow wave sleep (N3) into lighter
stages of sleep, and appear time-locked to appear
during the first third of night sleep.34,35 Table 1
summarizes the characteristics of these three
arousal parasomnias. Sleep deprivation and fever
can trigger all three forms of arousal parasomnia.
The earlier discussion in this chapter about
pathophysiology applies especially to confusional
arousals, sleep walking and sleep terrors. With
regard to predisposing factors, it is appropriate to
discuss cyclic alternating patterns, which are periodic EEG events of NREM sleep that are characterized by repeated and spontaneous sequences of
transient events that recur at intervals of up to
2 min in duration.36 They are a reliable marker of
unstable sleep and such, are increased during the
slow wave sleep of children with sleep terrors.37 As
in most parasomnias, a familial pattern can be
demonstrated, without any clear genetic pattern of
transmission.34 The combination in varying degrees
of familial predisposition, acquired disturbances
that trigger an increase in shifts from slow wave
sleep to lighter stages of sleep (such as sleep
disordered breathing, periodic limb movement,
gastroesophageal reflux), and vulnerable age seems

Parasomnias in childhood
Table 1

161

A comparison of the arousal parasomnias

Clinical
feature

Confusional
arousal

Sleep
terror

Sleep
walking

Age of onset
Frequency

2e10 years
3e4/week
to 1e2/month
First third
of night sleep
Whimpering,
some articulation,
sitting up in bed,
inconsolable
Slow wave sleep
with rhythmic theta
or delta activity
10e30 min

2e10 years
3e4/week to 1e2/month

5e10 years
3e4/week to 1e2/month

First third of
night sleep
Screaming, agitation,
flushed face,
sweating, inconsolable

First third of night sleep

Peak time of occurrence

Ictal behavior

Ictal polysomnogram

Duration

Slow wave sleep

with rhythmic theta
or delta activity
10e20 min

Walking about the

room or house, may
be quiet or agitated,
unresponsive to verbal commands
Slow wave sleep with
rhythmic theta or delta activity
10e20 min

Adapted from Kotagal S. Parasomnias of childhood. Current Opinion in Pediatrics, 2008;20:659e65.

to precipitate arousal parasomnias. Separation

anxiety may be a predisposing factor for both sleep
terrors and sleep walking.27 In this regard Mehlenbeck et al. have found that as compared to age
matched community control subjects, children
with parasomnias showed higher rates of bedtime
resistance, sleep onset delay, night awakenings,
and reduced sleep duration.38 There is activation of
primitive motor and behavioral patterns while
patient is still asleep. The EEG may show rhythmic
activity in the theta or delta range.

these events due to worry about the child! The

frequency of these events varies from two to three/
month to nightly. There are generally no daytime
neurobehavioral consequences in patients with
a primary, genetic predisposition to confusional
arousals. In patients where sleep disordered
breathing or periodic limb movements play a role in
triggering the arousals from slow wave sleep, there
may be associated daytime behavioral manifestations such as hyperactivity and mood swings related
primarily to the underlying, triggering disorder.

Confusional arousals

Sleep terrors

This NREM parasomnia is most common in infants and

toddlers.35,39 The prevalence of occasional or
frequent confusional arousals in children of 3e13
years in a study conducted by Laberge et al. was
17%.40 The onset of symptoms is typically within
2e3 h of sleep onset, at the time of transition from
slow wave sleep (N3) to a lighter state of sleep. The
child will typically sit up in bed, whimper, cry or
moan, may utter words like no or go away,
appear distressed, and to the utter exasperation of
the parents, remain inconsolable regardless of all
parental efforts. Sometimes the parental efforts at
comforting the child may lead to a paradoxical
increase in the level of agitation. There is generally
no sweating, flushing of the face or stereotypic motor
behavior. The child remains sitting in the bed. The
duration of these events can be 10e30 min. A
simultaneously obtained electroencephalogram may
show generalized, high amplitude rhythmic delta or
theta activity. The following morning, the patient
awakens feeling alert and refreshed, and shows no
recollection of the event. Paradoxically, the sleep of
parents and other family members is disrupted from

The age of occurrence is between 3 and 10 years.

The events generally occur in the first third of night
sleep. Their frequency varies from two to three
times/week to two to three/month. The child
awakens abruptly from sleep with a blood curdling
scream, appears agitated, flushed over the face,
with sweating, and tachycardia. The patient may
jump out of bed as if running away from an unseen
threat,39 and remain unresponsive to parental
efforts at calming down. A simultaneously obtained
EEG may show high amplitude, rhythmic delta or
theta activity. There is a strong genetic predisposition. Most patients show gradual, spontaneous
resolution over months to years.

Sleep walking
The age of onset, time of occurrence at night and
the frequency of spells are identical to confusional
arousals and sleep terrors. Mild episodes in which
a toddler sits up and crawls around the crib, or
a child walking quietly in sleep to come and stand
by the bed of the parents may sometimes go

162

S. Kotagal

unnoticed.35,39 Others may become agitated and

run around the house. Some patients have at times
injured themselves by unconsciously carrying out
dangerous behaviors like jumping out of a second
storey bedroom window. Others may unknowingly
risk injury with behaviors like walking out of the
house on a cold winter night and exposure to
accidental hypothermia. Autonomic dysfunction
may occur in the form of sweating and flushing of
the face. Some children exhibit a combination of
sleep terrors and sleep walking, though one
manifestation or another predominates.

Differential diagnosis of arousal parasomnias

Nocturnal seizures can mimic the arousal parasomnias e disorganized bodily movements,
staring, unresponsiveness, vocalizations and
confused behavior are common to both groups of
disturbances. Hypermotor behavior such as
thrashing of the limbs that lasts 10e20 s is common
in nocturnal frontal lobe seizures. Table 2
summarizes the distinction between arousal parasomnias and seizures. Nocturnal frontal lobe
epilepsy is generally autosomal dominant with
reduced penetrance, although sporadic cases have
also been reported. It is due to mutations in the
genes CHRNA2, CHRNA4 or CHRNB2 that regulate
the expression of nicotinic acetyl choline receptors.41e43 A 16-channel EEG montage should be
incorporated into the polysomnogram for the
investigation of any nocturnal events that might be
suspected as seizures. Some useful clinical clues to
Table 2

nocturnal seizures are that these events occur

randomly through the night, and unlike the arousal
parasomnias, the occurrence is not linked to any
specific time of the night.44,45 Also, seizures can
happen multiple times on one night; with parasomnias, this occurs less often. Epileptiform
discharges like spikes and sharp waves associated
with nocturnal seizures are most prevalent during
stages N1 and N2 of NREM sleep whereas arousal
parasomnias occur during N3 sleep and are associated with diffuse, rhythmic delta or theta
activity. The epileptiform features of nocturnal
seizures may be unifocal, multifocal, or generalized in distribution. Unfortunately the interictal EEG is not always informative from the
standpoint of presence of epileptiform abnormalities. Mild daytime sleepiness is common in
patients with nocturnal seizures, but generally not
observed in arousal parasomnias. Home video of
spells provided by the parents can sometimes be
very helpful in establishing an accurate diagnosis.
Management
Infrequently occurring (1e2 times/month) confusional arousals, sleep terrors and sleep walking do
not need to be treated. Parents should be
informed about the benign and self-limiting nature
of the disturbance, with likely spontaneous resolution over 1e2 years. Toddlers should receive
adequate napping time during the day as sleep
deprivation can be a trigger. In the case of sleep
walking, environmental safety issues should be
discussed with the parents.31 This may include

Distinction between arousal parasomnias and nocturnal seizures

Feature

Arousal
parasomnias

Nocturnal
seizures

Age of onset

Pre-school age and childhood

Family history of
similar events
Time of occurrence
Most common sleep
stage at occurrence
Duration of event
Multiple events on a
single night
Polysomnogram (EEG)

May be positive

Infancy, pre-school age,

childhood, and adolescence
May or may not be positive

First third of night sleep (usually)

Slow wave sleep

Randomly through the night

Stages N1 or N2 of NREM sleep

10e30 min
Less likely

0.5e5 min
More likely

Rhythmic theta or delta activity

Normal/spikes or sharp waves

over a focal or generalized distribution
Usual daytime behavior Normal (unless complicated by sleep
May be irritable and sleepy;
related breathing disturbance or restless seizures may also occur during the day
legs/periodic limb movement disorder)
Pharmacological therapy Benzodiazepine at bedtime
Daytime and bedtime administration
of oxcarbazepine/lamotrigine/levetiracetam
/carbamazepine/phenytoin
Adapted from Kotagal S. Parasomnias of childhood. Current Opinion in Pediatrics, 2008;20:659e65.

Parasomnias in childhood
installation of motion sensors within the house and
dead bolts on the doors. When arousal parasomnias
become associated with daytime mood or behavioral disturbance suggesting an underlying trigger
like obstructive sleep apnea or restless legs
syndrome/periodic limb movement disorder, when
the safety of the child starts becoming a concern
or when the sleep of other family members starts
becoming disrupted, nocturnal polysomnography
and specific pharmacologic measures should be
considered. A low threshold is maintained for
adding a 16-channel EEG montage to the polysomnogram (for excluding seizures). If sleep
disordered breathing, periodic limb movement
disorder or gastroesophageal reflux are identified
as triggers, treatment efforts should be directed at
these underlying disorders. If no specific underlying triggers are found and the parasomnias are
problematic, low dose benzodiazepines at bedtime
is recommended, e.g., clonazepam in a dose of
0.125e0.5 mg. Potential side effects like drooling
and paradoxical hyperactivity may occur in children
with
neurodevelopmental
disabilities
(authors observation).
Anticipatory awakening or scheduled awakening
is a behavioral technique that can be utilized to
prevent arousal parasomnias. As the occurrence of
these events is generally time-locked to the first
third of the night, momentary awakening of the
child by the parents, 15e20 min prior to the usual
time of occurrence may alter the sleep state and
thereby abort the event. During the scheduled
awakening, the parent comforts the child and
generally behaves as he/she would when awakened
by the child.46 The effectiveness of anticipatory
awakening in preventing arousal parasomnias has
been described only in case reports.47,48 Nevertheless, the technique may be worth trying, particularly if the family is reluctant to administer
a benzodiazepine to the child and inclined towards
non-pharmacologic management. The potential
drawback of actually triggering a parasomnia by the
awakening procedure should also be considered.

Parasomnias linked to rapid eye movement sleep

Nightmares
These events are bad dreams that awaken the
dreamer. The International Classification of Sleep
Disorders II defines nightmares as recurrent
episodes of awakening from sleep with recall of
intensely disturbing dream mentation, usually
involving fear or anxiety, but also anger, sadness,

163
disgust, and other dysphoric emotions. There is
generally full alertness upon awakening immediately after a nightmare, and intact recall of the
dream experience. Additionally, there may be
delayed return to sleep after the episodes.49 Since
REM sleep is preponderant during the second half of
the night, nightmares tend to be generally experienced in the early hours of the morning. The
historical origin of the suffix mare is from the protoGermanic maron, which refers to demons, more
specifically incubi, who were believed to sit on the
chest of sleepers and cause a feeling of pressure or
weight,50 representing combined sleep paralysis and
hypnagogic hallucinations. This depiction is also
nicely portrayed in a 1781 painting.51
Close to a third of adults with recurrent nightmares have onset of the symptom during childhood.52 Partinen and Hublin have indicated that
nightmares occur always or often in 2e11% of
children, and now and then in 15e31%.53 Unlike
adults, who show increased prevalence in females,
children do not show any gender predilection. Preverbal children of 6e24 months may awaken from
sleep with agitation, but it is difficult to determine if
they actually experience bad dreams.
In older children with post-traumatic stress
disorder, the dream content may be distressing,
with themes of inflicted violence, death or separation from close family members. The description of
dreams in pre-school age children is usually short
and simple, while older children may embellish the
dream content by adding fantasy. As muscle tone
and mobility are actively inhibited during REM
sleep, bodily movement is rare. Autonomic manifestations like sweating and flushing of the face are
minimal. There may be mild tachycardia. The
duration of the event is generally brief, though
there may be a prolonged post-ictal period in which
it becomes hard to fall back to sleep. In children who
are verbal, the recall of dream content is good.
Polysomnography is not routinely indicated for
the investigation of nightmares, but during an
infrequently recorded event in the sleep laboratory with video monitoring, one may observe an
abrupt awakening from out REM sleep with
minimal associated motor activity.
Management
It is emphasized that recommendations for the
management of nightmares in children are based
on observations from small, non-randomized case
series.54 Some nightmares may subside simply with
reassurance. Avoiding television viewing within
2e3 h of bedtime is reasonable as children can
incorporate these images into their dreams
(authors opinion). Rescripting techniques in which

164
children are taught to create a new, more pleasant
ending to the nightmare may minimize the
distress. Desensitization techniques have also
been documented to help alleviate the fear of
nightmares.55 Some therapists have found it useful
to encourage the child to write down the content
of the nightmare, or draw pictures of the object/s
which may help make the experience less scary.55
Hauri et al. have reported that one or two sessions
of hypnotherapy will help adults and children with
nightmares, with 5/7 (71%) remaining spell free or
much improved at 18 months and 4/6 (67%)
remaining spell free after 5 years.56

REM sleep behavior disorder (RBD)

Aggressive motor behavior during dream enactment is seen in adults, in whom it is predictive of
degenerative neurological disorders, especially
synucleinopathies like Parkinson disease and idiopathic Lewy Body disease.57 RBD is rare in childhood. To some extent the rarity in childhood is
a self-fulfilling prophecy-sleep specialists may be
less attuned to inspect the polysomnograms of
children for features characteristic of this parasomnia. Nevsimalova et al. have however reported
two girls aged 7 and 9 years with combined RBD
and narcolepsy-cataplexy.58 Sheldon and Jacobsen
have described the clinical and polygraphic
features of five children who met criteria for
RBD.59 Over a 4.5-year period, Schenck and
Mahowald documented 17 narcolepsy patients
with REM sleep motor dyscontrol. The age at
diagnosis ranged from 8 to 74, but in 4/17
subjects, it was between 8 and 17 years.60 Selective serotonin reuptake inhibitors and selective
norepinephrine reuptake inhibitors commonly
provoke REM sleep without atonia, with or without
clinical RBD episodes. This parasomnia may be
more common in children with congenital or
degenerative disturbances of the brainstem. This
author has encountered four patients with the
disorder over a 4-year period of clinical practice at
his sleep center (unpublished observation). Two of
the subjects had Moebius syndrome (a congenital
disorder affecting the development of brainstem
motor cranial nuclei), one had Niemann Pick
disease type C (a degenerative disorder affecting
the brainstem) and one had non-specific developmental delay. The locus ceruleus contains cells
which have receptors for hypocretin-1. These very
same cells also serve a REM off function, and
actively inhibit muscle tone and movement during
REM sleep.61 It is conceivable that decreased
activity of these REM off neurons in childhood
neurological disorders underlies REM sleep

S. Kotagal
behavior disorder. The polygraphic features are
loss of the physiologic submental electromyographic REM atonia and excessive phasic twitching
of the limbs during REM sleep. Events captured on
videotape may show yelling, agitation, or flailing
of the limbs. As in adults, the disorder responds
promptly to treatment with benzodiazepines like
clonazepam. The long-term outcome of childhood
RBD is unknown.

Catathrenia
Nocturnal groaning or catathrenia is a parasomnia
of REM and NREM sleep that was recently
described.62 The patient is generally unaware of
the predominantly expiratory groaning sound,
which however causes significant concern in the
parent or bed partner. The condition is observed
more often during the second half of the night. It is
not accompanied by respiratory distress, anguish
or emotional facial expression. There is no daytime
sleepewake complaint. Patients and families seem
to seek sleep consultation more often for social
reasons than for symptoms of sleep disordered
breathing. Guilleminault et al. recently reported
on a series of seven, non-obese young women with
catathrenia, all of whom experienced onset of
symptoms during childhood.63 Flow limitation on
nasal pressure transducers and increased disordered breathing indices was documented in all
subjects, who also exhibited abnormally high
Mallampati scores and small mandibles. On polysomnography, the patients showed a mild increase
in their sleep disordered breathing index. Though
the groaning subsided with continuous positive
pressure breathing (CPAP), patients preferred
surgical options for augmentation of their upper
airway. In some instances the groaning persists
despite effective CPAP. Owing to the association of
catathrenia with sleep disordered breathing and
resolution with treatment of the latter, Guilleminault et al.63 have raised a valid question of
whether catathrenia should even be categorized as
a parasomnia under ICSD-2. The true relationship
between catathrenia and sleep disordered
breathing still remains to be clarified.

Miscellaneous parasomnias
Sleep related enuresis
Recurrent bedwetting affects approximately 4e15%
of school children.64,65 In pre-pubertal subjects,
boys are affected twice as often as girls, but after
puberty, the incidence is similar in both sexes.

Parasomnias in childhood
The majority of sleep enuresis occurs only at
night, but about 15% of children have both daytime
and night-time symptoms.66 From the developmental standpoint, complete control of the bladder
at night is usually achieved by the age of 5 years,
thus bedwetting in toddlers is physiologic.67 The
spontaneous remission rate for bedwetting in
childhood is 14e19% per year67 e this natural history
should be kept in mind when counseling parents and
children about the prognosis and while considering
the effectiveness of various treatments.
A distinction is made between primary and
secondary enuresis. In the primary form, the child
has not had a consistent dry period of six or more
months. There seems to be a strong genetic
predisposition for primary enuresis e when both
parents give a history of enuresis in childhood,
close to three fourths of their children are also
affected.68 Studies of twins with enuresis show
a higher concordance rate for monozygotic twins
than dizogotic twins.68 In the study of Abe et al.,69
the concordance rate for monozygotic twins was
0.9 while in dizygotic twins it was 0.5. On the basis
of segregation analyses, multiple modes of inheritance such as autosomal dominant with high
penetrance, autosomal dominant with low penetrance, and autosomal recessive modes of inheritance have been postulated.68 Linkage analysis has
shown association with chromosome 4 (in autosomal dominant families), and also with chromosomes 8q, 12q, 13q, and 22q. Individual genes and
mutations have not yet been identified.68
In secondary enuresis, there is usually a period of
six or more months during which the child has
remained completely dry at night, only to then reexperience bedwetting. Secondary enuresis may be
from acquired factors such as urinary tract infection, obstructive sleep apnea, diabetes mellitus,
diabetes insipidus and psychological disturbances.
In pre-pubertal age group, urinary tract infections
(UTI) are ten times more common in enuretic girls as
compared to age and gender matched, non-enuretic
controls.67 The pathogenesis of both primary and
secondary enuresis is also influenced by additional
factors such as small bladder functional capacity,
decreased capacity to inhibit spontaneous bladder
contractions, and decreased nocturnal secretion of
vasopressin. Deficits in central arousal and in
control of the micturition reflex due to brainstem
dysfunction have also been causally implicated.70
Negative emotional feedback about the enuresis,
whether overt or self-perceived, may further
undermine the childs self-image and hinder resolution of the disturbance.
The assessment of a child with enuresis includes
asking about familial predisposition and acquired

165
factors like sleep disordered breathing, diabetes
mellitus, diabetes insipidus, epilepsy and determining the impact of enuresis on the child from the
emotional standpoint. Urinalysis is routinely indicated in all. A low specific gravity in an early
morning sample of urine might indicate decreased
nocturnal vasopressin secretion. A urine culture is
recommended if the urinalysis is abnormal or if
there are symptoms suggestive of a UTI. Children
with symptoms of sleep-disordered breathing may
require nocturnal polysomnography.
No treatment is needed for bedwetting before
the age of 5 or 6 years as it might still be physiologic
in this age group. After 5 or 6 years, treatment may
be indicated, based upon the frequency and
severity of the disturbance. The parents should
maintain a positive and optimistic attitude and
remain emotionally supportive of the child.
Daytime bladder training exercises such as voluntarily suspending voiding midstream during micturition may help increase the tone of the bladder
neck sphincter. Postponing micturition by a few
minutes whenever the urge develops may increase
functional residual capacity of the bladder. A
recent prospective study has however found that
such exercises do not add to the overall cure rate.71
Alarm systems that work by operant conditioning
are effective in children who are motivated and
cooperative. They are applied over the perineal
skin, and upon sensing moisture, lead to activation
of a buzzer or bell. The child is awakened by the
stimulus and at this stage, is led to the restroom by
the parent and encouraged to evacuate the
bladder. Ultimately, the child becomes accustomed
to awakening to the stimulus and voiding independently in the restroom. The resolution rate for
enuresis with conditioning devices is excellent,
varying from 65 to 80%, with a relapse in 10e15%.67
Guided imagery techniques are also associated with
some success, and can be easily combined with
a conditioning alarm device. In refractory cases,
medications can be utilized. Imipramine (25e50 mg
at bedtime) and oxybutynin (5 mg at bedtime) may
control enuresis by decreasing the parasympathetic
tone of the bladder detrusor muscle. Desmopressin
in a dose of 0.1e0.2 mg at bedtime works by
promoting fluid retention. Combining medication
and operant conditioning may help in the shortterm, though this approach does not seem to
change the functional characteristics of the
bladder as a reservoir.72

Bruxism
Bruxism is the involuntary, non-functional and
forceful clenching, grinding or rubbing of teeth.

166
Under the revised, International Classification of
Sleep Disorders (ICSD-2), it is now classified as
a sleep related movement disorder. In a survey of
358 children of third to sixth grade who were
administered the Child Sleep Habits Questionnaire,
Canet-Santz and Oltra found a prevalence rate of
6.7%.73 Children with neurodevelopmental disorders like Rett syndrome and Down syndrome may
exhibit bruxism even during wakefulness. Patients
with bruxism may be more prone to develop
temporomandibular disorders and headache,
though evidence in this regard is insufficient.74 As
compared to controls, children with sleep related
bruxism show increased tendency for anxiety75 on
the Childrens Personality Questionnaire and the
Conners Parent Rating Scale. Sleep disordered
breathing may exacerbate an underlying tendency
for bruxism; in a prospective study,76 adenotonsillectomy seemed to significantly lessen the
incidence of bruxism from 25% to 7% (p 0.02).
There is not sufficient evidence to state that
occlusive splints are effective in treating bruxism,
but it may be that there is some benefit with
regard to tooth wear.77

Status dissociatus
Structural brainstem lesions involving the pontomesencephalic tegmentum such as cavernomas
have been associated with sleep talking, vigorous
movements accompanied by vivid dreams,
enuresis and daytime sleepiness.31,78 Nocturnal
polysomnography shows ambiguous sleep with
mixture of the polygraphic features of REM and
NREM sleep (possibly a regression to the transitional sleep of the newborn!). During REM sleep,
the 36-year-old patient described by Provini
et al.78 demonstrated persistence of tonic electromyographic tone (REM sleep without atonia)
and violent motor behaviors that were consistent
with REM sleep behavior disorder. Similar disturbances may occur in rapidly progressive childhood
neurodegenerative disorders also (authors
opinion).

Practice points
1. The range of parasomnias encountered in
children varies from those occurring at
sleep onset, to partial arousal events, REM
sleep parasomnias, sleep enuresis and
bruxism.

S. Kotagal
2. Home video recordings of suspected parasomnias provided by the family to the
sleep specialist at the time of the clinical
assessment may offer valuable diagnostic
clues.
3. Arousal parasomnias like confusional
arousals, sleep terrors and sleep walking
may be confused with sleep related
epileptic seizures. Arousal parasomnias
can be generally distinguished from
seizures on the basis of clinical and electroencephalographic features. A low
threshold should be kept for adding a full
16-channel EEG montage during the polysomnographic investigation of children
with nocturnal spells.
4. REM sleep behavior disorder is probably
under-diagnosed in childhood.
5. Sleep enuresis remains by far the most
inadequately understood and problematic
childhood parasomnia as treatment efforts
show limited and often transient success.
Pediatric sleep specialists will need to
work closely with pediatric urologists and
psychologists to better understand the
pathophysiology and design more effective
treatments.

Research agenda
1. We know that the tendency for problematic parasomnias is clustered in families.
Whole genome analyses may help determine specific DNA sequence variants associated with the common parasomnias.
Studies of sporadic cases, familial cases,
and twins may also help in discerning the
genes
responsible
for
common
parasomnias.
2. Advances in understanding of the control of
sodium, potassium and calcium ion channels at the cellular level may further the
appreciation of pathophysiologic concepts
and the design of specific therapies.
3. The role of central pattern generators in
the pathogenesis of various NREM parasomnias needs further study.
4. The role of behavioral techniques in the
management of childhood parasomnias in
general needs also to be explored using
large scale, prospective studies.

Parasomnias in childhood

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