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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_41_библиотеки_им_акад_М_И_Перельмана
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Confusional Arousals
Confusional arousals are the events of disorder of arousal in which the patient neither shows a prominent fear reaction nor ambulates. This diagnosis can include a
wide variety of behaviors that range from mild sitting with a confused look to complex actions appearing to meet a variety of basic needs. Patients may engage in a
range of emotions from amorous to aggressive outbursts, and behaviors can include
a variety of common everyday activities to more intrusive events including eating
and sexual behaviors.
Clinical Presentation
Confusional arousals are one of the disorders of arousal from NREM sleep [1].
Patients appear to be both asleep and awake. As the name implies, the patient
appears very confused. The patient is typically in bed, and the event commonly
involves the patient sitting upright with their eyes open and looking around. The
patient is often unresponsive or poorly responsive to questions or commands, and
some sleep talking may occur. The events are associated with partial or total amnesia and typically last only a few minutes with the person returning to sleep.
Confusional arousals occur in the rst third of the night, predominantly from N3 or
slow wave sleep (SWS), when SWS is most likely to occur.
Epidemiology
Confusional arousals are more common in children than adults. Although these
events are nearly ubiquitous in children under the age of 3years, the events are
noted to occur in 20–50% of preschool to school aged children [2]. These events are
present in up to 1–4% of young adults and as possibly as high as 7% in older adults
[26, 31]. The true incidence in all age groups is likely higher due to lack of reporting
and/or observation of events.
Pathophysiology
It is thought that confusional arousals and the other disorders of arousal (sleepwalking and night terrors) are due to a dissociation between the wake state and NREM
sleep. There is an incomplete arousal from NREM sleep that tends to occur in the
rst third of the night when SWS predominates. However, 20% of cases may occur
from N2 or Stage 2 sleep [31, 32]. The preponderance of NREM parasomnias in
children may be due to the increased amounts of SWS as compared to adults.
Arousal thresholds are also at their highest during SWS.Substances or scenarios
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that increase the arousal threshold can increase the likelihood of disorders of arousal,
such as sleep aides and sleep deprivation, respectively [31]. Conversely, agents that
increase arousals, such as a noisy sleeping environment or sleep apnea, can increase
the occurrence of NREM-related parasomnias [32]. There is a strong genetic component to confusional arousals and the other disorders of arousals as there is usually
a strong family history [31, 33].
Diagnosis
Currently, the diagnosis of confusional arousals is based on the clinical history. The
ICSD-3 sets the specic characteristics for the diagnosis of confusional arousals as
disorders of arousal:
1. The disorder meets the general criteria for NREM disorder of arousal.
2. The episodes are characterized by mental confusion or confused behavior that
occurs while in bed.
3. An absence of terror or ambulation out of the bed.
The criteria specic for confusional arousal help differentiate these events from
sleepwalking and sleep terrors. Video polysomnography (VPSG) is used for the
diagnosis of confusional arousals when there is concern for the patient harming
themselves or others or the other disorder of arousals except to differentiate from
other disorders, i.e., seizures, in complex cases or to diagnose concomitant disorders, such as sleep apnea [1, 2, 33].
Treatment
Confusional arousals are usually self-resolving and usually resolve by adolescence.
In children with little risk of harm, parents should be offered reassurance. Parents and
bed partners should be counseled not to attempt to wake the patient during these
events as it can result in worsening the confusion, increased agitation or aggressiveness, and prolonging the event. Treatment should focus on the priming and precipitating factors of the three P model (predisposing, priming and precipitating) of NREM
parasomnias. Priming factors such as avoidance of actions such as sleep deprivation
that increase the amount of slow wave sleep, and avoidance of substances that may
increase arousals, such as caffeine or alcohol. Precipitating factors also need evaluation; thus the patient should be asked about things that cause arousals such as environmental noise and light as well as other symptoms suggestive of other sleep disorders.
Therefore, targeting good sleep hygiene, avoidance of priming substances/situations,
and precipitating factors are useful tactics to reduce events [2, 25, 33]. In the event
that episodes are persistent despite the above or that the severity of the events is placing the patient or others at risk of harm, pharmacologic treatment may be necessary.
Clonazepam is the medication with the most evidence for use, but melatonin, antidepressants, and even the hypnotic z-drugs have been used with reported effect [33].
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Sleepwalking (Also Known asSomnambulism)
Sleepwalking or somnambulism is another disorder or arousal from NREM sleep. It
is characterized by an incomplete arousal from NREM sleep with complex behavior
and ambulation out of the bed. These events may go unnoticed as the sleepwalker
may return to bed unnoticed and therefore not be reported. The main adverse outcome from sleepwalking is injury to the patient or others. Patients have limited
ability to respond to the environment and thus are at risk for injury. As with other
disorders of arousal, they occur mostly in children and usually improve with age;
however onset in adulthood likely points to prior sleepwalking history or another
underlying sleep disorder.
Clinical Presentation
Sleepwalking usually starts like a confusional arousal with the patient sitting up
confused; however, unlike confusional arousal the patient gets out of bed. The
events can be more complex than simple wandering about and involve opening
locked doors or windows, dressing, and even urinating in inappropriate places. The
episodes can end with the patient back in bed without reaching conscious awareness, or it may end suddenly in an inappropriate place, such as outdoors in inclement weather. Patients may have limited or no memory or vague dream like mentation
of the event. Most events are relatively brief, but some patients have events that last
several minutes [1, 2].
Epidemiology
Like the other disorders of arousal, sleepwalking is more common in children. The
peak incidence is in the pre-teen to early teen years, 10–13, and resolves by adolescence in 75% of people. The lifetime prevalence is estimated to be between 22 and
29% [2, 34]. In roughly 13% of adults sleepwalking develops de novo, and the
overall prevalence in adults is 4% [34]. Most adults with sleepwalking have a history of sleepwalking as children, and the de novo cases are most often associated
with medications and neurodegenerative disorders [35].
Pathophysiology/Etiology
The basic pathophysiology of sleepwalking like other disorders of arousal is related
to incomplete arousal from SWS.The patient has both features of being asleep and
awake that evoke motor central pattern generators for complex motor behaviors.
Several studies have shown that different brain regions have dissociative activity,
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that is, certain regions showing activity consistent with the waking state and others
with activity consistent with the sleep state [10, 36]. Like the other disorders of
arousal, there is a strong family history pointing to a genetic underpinning. There
has been identication of chromosome 20q12-q13 as a possible locus as well as high
frequency in patients with the HLA-DQB1 05:01 allele [2, 32]. Sleepwalking can be
precipitated by increased arousals from SWS such as in the case of OSA, or it can
be primed in the case of sleep deprivation. There are numerous reports of medications associated with somnambulism, particularly the z-drugs (zolpidem, zaleplon),
but also for antidepressants of all classes, antipsychotics, and beta- blockers [22].
Diagnosis
The ICSD-3 criteria for sleepwalking include that the disorder meets the general
criteria for a disorder of arousal and that the patient has events that are associated
with ambulation or other complex behaviors out of bed. The ICDS-3 requires the
following to establish the diagnosis:
1. The disorder meets the general criteria for NREM disorder of arousal.
2. The arousals are associated with ambulation and other complex behaviors
out of bed.
The diagnosis of sleepwalking can usually be diagnosed based on clinical history, but since the patient is at inherent risk of harm by virtue of leaving the bed,
video PSG is an important component of the evaluation. Patients need evaluation to
determine if the events appear to be occurring from NREM sleep as well as other
possible provoking factors such as sleep apnea.
Treatment
For most patients, therapy can focus on non-pharmacologic avenues unless the
patient is at signicant risk for harm. Reassurances should be given to parents that
sleepwalking is not a sign of developmental disability nor other mental issues. The
sleep environment should be made safe for the sleepwalker by removing sharp
objects and sharp-edged furniture, locking doors and windows, and bed alarms.
Parents and bed partners should be advised not to attempt to wake the patient as this
can result in prolongation of the event, aggressive or violent behavior, or running
away potentially causing harm to self and others. Additionally, efforts should be
directed at avoiding or targeting priming and precipitating factors, such as sleep
deprivation, sedative hypnotics, other sleep disorders, anxiety, etc. In the majority
of childhood cases, sleepwalking is self-resolving, but adults may frequently need
further intervention. Melatonin and clonazepam may be options [2, 6, 25, 33].
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Sleep Terrors (Also Known asNight Terrors or
Pavor Nocturnum)
Sleep terrors are the most dramatic of the disorders of arousal from NREM sleep.
They often start with a piercing scream followed by consolable fear. These events
are very impressive to the observer, but have little impact on the patient. Like the
other disorders of arousal, they usually occur in the rst part of the night and are
more common in children. Sleep terrors resolve with age and rarely occur
after age 7.
Clinical Presentation
Sleep terrors start abruptly, usually with an intense terried scream, associated
with intense fear and signicant sympathetic outlay of the autonomic system. The
patient can be found profusely diaphoretic with tachycardia, mydriasis, and tachypnea. The patient will be inconsolable and attempts to calm the patient can prolong the event. The patient is poorly responsive to observers and the environment
but may look around or reach around. The episodes usually only last a few minutes, and then the patient will spontaneously return back to sleep. There is no
memory for the event, and if the patient does wake at the end of the event, there is
usually only a vague remembrance of fear, but no accompanying dream imagery
[2, 31–33].
Epidemiology
Sleep terrors are more common in preschool children with 20–40% of children
younger than 3years experiencing an event and reduces to less than 14% of school
aged children [37]. It is rare for adults, but prevalence has been reported to be
around 2.7% [2].
Etiology/Pathophysiology
Sleep terrors occur from an incomplete arousal from SWS as with the other
disorders of arousals above. The exact cause is unknown, but a strong genetic
component is suspected based on strong family histories in patients and concordance twin studies. Patients have been shown to have more fragmented N3
sleep [2].
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Diagnosis
The diagnosis can be made by clinical history. The key is related to the piercing
scream at the beginning of the event. The ICSD-3 requires the following items to
establish the diagnosis [1]:
1. The disorder must meet the general criteria for NREM disorders of arousal.
2. The events are characterized by episodes of abrupt terror, typically beginning
with an alarming vocalization such as a frightening scream.
3. The events also have accompanying features of intense fear and signs of auto-
nomic arousal, including mydriasis, tachycardia, tachypnea, and diaphoresis
during an episode.
Sleep terrors can be distinguished from nightmares as night terrors tend occur in
the rst third of the night, when N3 is most prevalent, and there is lack of memory
for the event and the patient is difcult to arouse. By contrast, nightmares occur
from REM sleep, and the patient is not confused and is easily arousable. There is
also story-like recall in the case of nightmares, whereas night terrors are only associated with vague, fragmented memory if any [2, 37].
Treatment
N. A. Walker and B. V. Vaughn
Sleep terrors are very dramatic and patients must rst be protected from harming
themselves or others. Typically the patients are trying to escape and may even ing
themselves out of windows. The environment must be made safe from potential
hazards, and windows need to be blocked. Other means are locks on doors or notication alarms to avoid the patient leaving the house. Treatment should be focused
on addressing predisposing factors as mentioned above and examination for other
sleep and medical disorders such as sleep apnea that need treatment. Some have
recommended that anticipatory awakening therapy can be helpful in this population.
For this therapy the patient is awakened roughly 10–30minutes prior to the usual
event time each night for 2weeks, then allowed to sleep to see if the events resume.
The process can be repeated; however this should only be performed once other
disorders such as sleep apnea have been ruled out. In cases that are refractory to the
nonpharmacologic interventions or there is risk of harm to self or others, clonazepam or tricyclic antidepressants have been used [2, 25, 33].
Sleep-Related Eating Disorder
Sleep-related eating disorder is characterized by patients having repeated bouts of
eating while in a partial sleep state. Unlike the other NREM parasomnias, sleeprelated eating disorder is not considered one of the disorders of arousal as discussed
above. However, SRED has similar characteristics including occurring from NREM
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sleep and is also associated with incomplete arousal. The eating occurs after sleep
onset has occurred and needs to be distinguished from nocturnal eating syndrome
(NES) as discussed below.
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Clinical Presentation
This condition is characterized by recurrent eating episodes that occur after an arousal
from sleep. During these events patients may consume unusual to bizarre foods
including raw meats, cake batter, and frozen foods to inedible non-foodstuffs like
buttered cigarettes to toxins such as cleaning liquids. In addition to ingesting harmful
foods or substances, there is risk of harm from improperly attempting to prepare
foods [38–41]. The person with sleep-related eating disorder (SRED) has partial or
total amnesia for the event. The events occur almost nightly. Occurring during NREM
sleep they tend to occur in the rst half of the night. SRED is, not surprisingly, associated with weight gain and morning anorexia, but also injury from eating toxic substances or inedible items. These types of events also raise several issues beyond being
unusual stories, and a complete evaluation is vital for the patients’ well being.
Epidemiology
The prevalence of SRED is estimated at 1–4.6% in the general population [38–40].
However Winkelman found up to 17% in patients with other eating disorders and
that these symptoms are more common in those patients who have been hospitalized
for eating disorders than the general population [42]. Sleep-related eating disorder
appears to have a peak incidence in young adulthood and is more common in
females than males. Santin, who examined a Chilean population, described a peak
age of diagnosis around 39years, but symptoms starting on average 8years prior to
diagnosis [43]. Concomitant sleep disorders are present in up to 80% of patients
with SRED [38].
Etiology/Pathophysiology
A familial relationship has been shown in 5–26% of patients [38]. This may be in
part related to the possible relationship to the DOA for some of these patients; however, other contributors such as eating disorders also appear to run in families. Thus
the pathophysiology is not known, but it is surmised that arousals from NREM sleep
may result in varying levels of consciousness resulting in SRED in susceptible individuals. The strongest association is with other eating disorders, and this may have
a relationship to the underlying focus on food and eating. There is also an association with restless leg syndrome, suggesting a possible dopaminergic pathway
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involving the reward system of the mesolimbic region. Some medications such as
zolpidem are associated with episodes of sleep-related eating, and there is also an
association with many psychoactive drugs. Sedative hypnotics, antidepressants, and
antipsychotics have all been associated with SRED [38, 40, 41].
There is a high rate of psychiatric comorbidity and SRED as well. In the original
description of SRED over 40% of the patients had a coexisting mood disorder [41].
The rate of depression has been reported at 37% and 18% for anxiety disorder. The rate
of substance abuse is also high at 24% [38]. Daytime eating disorders, i.e., anorexia
and bulimia, also have a high association with SRED.The frequent co- occurrence of
SRED and psychiatric illness suggests a similar underlying pathology [41].
N. A. Walker and B. V. Vaughn
Diagnosis
The diagnosis of SRED is typically based upon the clinical features presented at the
initial history and physical examination. The key element is to have a reliable witness of the events describe the features of several events. The ICSD-3 sets four criteria for diagnosing SRED.These include:
1. Recurrent episodes of dysfunctional eating occurring after an arousal from sleep
2. The presence of one of the following: ingestion of odd or peculiar foodstuffs or
combinations or inedible or toxic substances, injuries sustained by or potentially
injurious behavior when getting food or in the preparation of food that is sleep
related, and adverse health consequences, e.g., weight gain or diabetes
3. Partial or complete amnesia for the event
4. And nally that the above is not better explained by some other disorder, sub-
stance, or medication
Although the presence of SRED can usually be diagnosed based on the clinical
history, the clinician needs to have a high suspicion for other sleep, neurological, or
psychiatric disorders. If the episodes are stereotypic or other sleep disorders are
considered in the differential, then the VPSG should be performed. During this
study, the usual foods that the patient tends to eat during SRED should be available
in the room during the overnight study [38].
Differential Diagnosis
– SRED needs to be distinguished from another form of abnormal nighttime eating
disorder. Nocturnal eating syndrome (NES) is dened differently depending on
the literature, but key distinctions are the level of consciousness, timing of eat-
ing, and frequency of comorbid sleep disorders [41]. Nocturnal eating syndrome
has similar features of eating during the night, but, as opposed to SRED, these
patients are fully conscious during the nocturnal eating. In addition, nighttime
eating very often occurs prior to sleep onset as NES is actually a circadian phase
delay in the eating schedule. Finally, SRED is more associated with other sleep
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disorders, e.g., sleep apnea, than patients with NES [38, 41]. There is, however,
considerable overlap in other features of NES and SRED. NES can also be
accompanied by an eating episode after arousal from sleep. In addition, affective
disorders are also highly associated with NES as with SRED [38]. The astute
clinician may be able to delineate the two disorders by careful history; however
the diagnosis of NES should be on the differential with any sleep disturbance
accompanied by eating. On PSG studies of NES eating was accompanied by full
consciousness and no other sleep disorders were described, save for decreased
total sleep time and sleep efciency [38].
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Treatment
In general most treatments of SRED are anecdotal reports. If a patient started the
sleep-related eating events with the initiation of a medication such as a short-acting
hypnotic, then the hypnotic should be discontinued. Similarly good sleep hygiene
and avoidance of initiating or provoking factors are a foundation point for therapy.
Pharmacologic treatment includes pramipexole which showed some modest effectiveness in a small placebo controlled trial [40]. Another trial has shown the antiepileptic medication topiramate to be effective as well. Case reports have shown the
SSRIs uvoxamine, paroxetine, and uoxetine to be successful [38, 40]. Treatment
should also be aimed at any sleep disruptors, including other sleep disorders that
may arouse the patient from NREM.
REM-Related Parasomnias
REM sleep is characterized by relative atonia of the voluntary muscles, rapid eye movements, and vivid dream mentation. Portions of these characteristics are key in the
description of REM-related parasomnias as a group of parasomnias that, obviously,
arise out of REM sleep. These disorders share many of the characteristics of REM but
represent a variety of underlying pathologies. The disorders can be an intrusion of
REM sleep into wake, such as sleep paralysis, demonstrate a vulnerable neurocircuitry
as in REM sleep behavior disorder, or an over expression of emotion into the state such
as in nightmare disorder. Arising from REM sleep these parasomnias tend to occur in
the second half of the night. They affect both children and adults, and in the case of
REM behavior disorder can be a sign of or precursor to a neurodegenerative disorder.
REM Sleep Behavior Disorder
REM sleep behavior disorder (RBD) is characterized by the loss of the usual paralysis during REM sleep resulting in the patient acting out their dreams. These events
are often violent resulting in injury of the patient as well as the bed partner. RBD
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has a high association with a group of neurodegenerative disorders and can precede
the hallmark clinical characteristics by years.
Clinical Presentation
RBD is a parasomnia that is characterized by abnormal behaviors occurring during
REM sleep. Due to the loss of the muscle atonia that normally accompanies REM
sleep, the affected sleeper has motor responses correlating to dream imagery. In
general RBD manifests as dream enactment, resulting in thrashing, slapping, or
kicking of the extremities and even yelling [44–47]. Self-injury is a common occurrence and a little over 60% of patients injuring a bed partner [44]. The usual dream
semiology involves predominantly defensive types of events in which the patient is
being attacked or threatened by animals or intruders or has to defend in a sport. The
resulting behaviors are the result of attempts at self-defense or the defense of others.
The patient usually wakes at the end of the dream and can recall the dream content
that parallels the observed behavior while asleep.
Epidemiology
The prevalence of RBD in the general population has been reported to be from 0.38
to roughly 2% [47]. However, the prevalence has been suggested to be as high as
5–13% of adults aged 60–99 [46]. The disorder is thought to be more common in
men than women, yet some of this may be related to reporting bias. In younger onset
patients, those under 50years old, men and women are equal [46].
Etiology/Pathophysiology
The exact mechanisms underlying RBD appear to be related to impairment of the
pathway that induces atonia during REM sleep. This syndrome can be created in
animal models by lesions involving the REM atonia pathways, suggesting involvement of the REM sleep control centers located in the pons and medulla. The resulting dysfunction results in loss of the normal atonia associated with REM sleep [45].
Although several reports show that lesions in the pons, midbrain, and medulla can
elicit RBD, in older adults there is a high association with RBD, and a group of
neurodegenerative disorders called alpha-synucleinopathies. This group is named
for the protein that can be found intracellularly in these disorders. The alphasynucleinopathies include Parkinson’s disease (PD), multiple system atrophy
(MSA), and dementia with Lewy bodies (DLB). RBD is considered a predictor for
future conversion to one of the above disorders. Indeed RBD may precede phenoconversion to one of the alpha-synucleinopathies by decades. The risk of conversion
over 2–5years is roughly 15–35% and after 25years is over 90% [45]. Many medications have been associated with RBD as well. SSRIs and SNRIs are well known
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