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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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16 Non-REM Parasomnias
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to cause REM sleep without atonia (RSWA) and are associated with RBD. Up to
15% of patients taking SSRIs have been shown to have RSWA [18]. In younger
patients with the onset of RBD, narcolepsy may be a key driver. As with other partial induction of the REM sleep state in narcolepsy, RBD can occur with the same
violent behaviors [48].
Diagnosis
The diagnosis of RBD requires two major features, the presence of dream enactment and the loss of REM sleep-related atonia. The ICSD-3 requires the following
features to make the diagnosis of RBD:
A. A. Repeated episodes of sleep-related complex motor behaviors and/or
vocalization.
B. The behaviors are documented on polysomnography to arise during REM sleep
or, based on the description of the events including dream enactment, they are
presumed to occur during REM sleep.
C. Polysomnographic recording demonstrates the loss of REM sleep atonia.
D. The disturbance is not better explained by another sleep or mental disorder,
medication, or substance.
Thus unlike the NREM-related parasomnias, the diagnosis of RBD requires a polysomnogram to document the loss of atonia in REM sleep (Fig.16.2). The loss of atonia is best demonstrated with recording EMG activity from all four extremities. Events
do not need to be captured during the recording; however, the diagnosis can be made
either with a clinical history consistent with RBD and the ndings of REM sleep without atonia on polysomnogram. If there is no history of dream enactment, the diagnosis
can be made by capturing an episode of complex behavior or vocalizations during
REM on the study. RBD should be distinguished from other diseases that have vivid
dreams with dream enactment, such as PTSD and obstructive sleep apnea [46].
Clinical Approach
For patients suspected of having RBD, historical features of dream enactment
with clear description of the events are key. These events should vary in their
content but may center around the theme of defending. For patients over 55years,
clinicians should ask about the other non-motor signs of alpha-synucleinopathies
such as constipation, loss of smell, or orthostatic hypotension. These features
may co-exist with the RBD events and precede other manifestations by years.
Similarly, a detailed neurological exam is essential to evaluate for other neurological features. Since RBD can be related to other processes impairing the atonia
pathways, patients should also be evaluated for possible underlying structural
causes of RBD such as stroke, demyelinating lesions, or tumors and undergo
brain imaging.
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a
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b
Fig. 16.2 This polysomnogram is a representative sample of loss of atonia during REM sleep.
Note that the submental EMG does not have a high amount of AMG activity but the extremities are
noted to demonstrate signicant muscle activity. (a) This tracing is from a 76-year-old man with
multiple system atrophy and history of violent dream enactment. (b) It is from a 65-year-old
female who was not being evaluated for parasomnia and had incidental sudden movement of her
arm and leg during REM sleep and noted dreaming she was shooing a cat off the bed. The patient
later admitted to multiple events of dream enactment
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Treatment
Patients should be counseled on bedroom safety to prevent injury. This includes
removal of furniture near the bed, placing the mattress on the oor, and removal of
weapons from the bedroom. The patient or the bed partner should be advised to
sleep in another bed or another room to prevent injury to others. Any OSA, if present, should be treated as this may reduce incidence of events [45, 46]. The mainstay
of pharmacologic treatment is melatonin and clonazepam. Melatonin of 3–15mg
dosed at bedtime has been shown in trials to reduce the incidence and severity of
events. In addition, clonazepam 0.25–2.0 mg at bedtime can be used as well.
However, the cautious use of clonazepam is advised in patients with dementia, gait
difculties, and OSA as the medication can worsen these conditions [44–47].
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Recurrent Isolated Sleep Paralysis
Recurrent isolated sleep paralysis is the phenomenon of the inability to move any
part of the body during the sleep-wake transition or vice versa. These events leave a
lasting impression upon the subject that can be remembered for decades. The events
typically occur upon awakening but may be related to going to sleep. Although
events are fairly uncommon, the events are noted to be described across a variety of
cultures and given sacred explanations.
Clinical Presentation
Sleep paralysis is the phenomenon of the inability to move the limbs, head, or trunk
at the onset of sleep or upon awakening. The episodes only last a few seconds to
minutes and resolve abruptly. Respiratory muscles are not affected, and the patient
is usually fully conscious of their environment. The episodes are frequently accompanied by an overwhelming sense of impending doom or hallucinations of someone
or thing in the room, a sense of pressure as if someone sitting on their chest, and a
sense of fear or distress [3, 49–51]. Patients remember these events for decades with
unusual clarity.
Epidemiology
Sleep paralysis is fairly uncommon in the full-blown events; however partial events
may have a lifetime prevalence as high as 7.6% in the general population. Events
appear to be more prevalent in students with history of sleep deprivation and circadian rhythm phase shifts ranging up to 28% in selected series, and almost 32% of
patients with psychiatric illness [49]. Women are slightly more likely to experience
sleep paralysis than men.
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Etiology/Pathophysiology
Sleep paralysis is thought to be a mixture of states with elements of REM invading
the waking state. Risk factors for experiencing sleep paralysis include sleep deprivation, sleep disruption, or shifts in circadian rhythm. Shift workers are noted to
experience sleep paralysis more commonly. Sleep paralysis is also more likely to
occur when sleeping in the supine position. Psychiatric illness has also been reported
to be a risk factor for sleep paralysis [3, 49–51].
Diagnosis
Recurrent isolated sleep paralysis is diagnosed by the clinical history and requires
that the episodes cause signicant distress including fear of sleep and/or the bedtime/bedroom. The ICSD-3 requires the following criteria to establish the diagnosis:
1. Recurrent episodes of inability to move the trunk and all of the limbs at sleep
onset or upon awakening from sleep.
2. Each of the individual episodes should last seconds to a few minutes.
3. The episodes cause signicant distress which can include bedtime anxiety or fear.
4. The disturbance is not better explained by another sleep disorder (especially
narcolepsy), mental or medical disorder, or medication, or substance use.
N. A. Walker and B. V. Vaughn
As noted in the criteria, recurrent isolated sleep paralysis should not be diagnosed in a patient with symptoms consistent with narcolepsy. The patient with sleep
paralysis will not have daytime sleepiness nor cataplexy [1, 51]. VPSG does not
need to be performed unless an underlying sleep disorder is suspected; however
rarely an event can be captured during a recording (Fig.16.3).
Treatment
For the most part, patients do not need to be treated for recurrent isolated sleep
paralysis as the majority do not have signicant distress associated with the events.
The pharmacologic treatment is based on treatment for narcolepsy. SSRIs and tricyclic antidepressants have been used to effectively treat sleep paralysis, presumably
for their REM suppressant effects [51].
Nightmare Disorder
Nightmare disorder involves recurrent frightening dreams that cause the patient
anxiety or daytime distress. There is a high association with psychiatric illness,
particularly PTSD.Nightmares are common and affect both children and adults.
They are often associated with awakening and, unlike night terrors, are associated
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Non-REM Parasomnias
Fig. 16.3 This is the tracing of a 27-year-old male with recurrent episodes of sleep paralysis, who
woke after this epoch, that he was having one of his events of paralysis. He noted a visual hallucination of a small older man sitting on his chest. The epoch shows typical features of REM sleep.
(Reprinted with permission from Bradley Vaughn)
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with complete recall and quick orientation to full consciousness. Nightmare disorder, however, results in daytime sequelae, which is what distinguishes it from the
general occurrence of nightmares.
Clinical Presentation
Nightmare disorder consists of repeated episodes of nightmares that cause clinically
signicant impairment in social, occupational, or other important areas of functioning. When the patient wakes from the nightmare, they are immediately oriented and
alert, and there is recall of the dream imagery. Nightmares are dened as dysphoric
dreams and usually involve threat of harm to the person [1]. The nightmares are
associated with negative emotions, most commonly fear. The nightmares can be
idiopathic or post-traumatic. Idiopathic nightmares are more imaginative and do not
have a traumatic content. Post-traumatic nightmares usually involve the direct replication of the traumatic event or contain material that is symbolically related to the
trauma [52, 53].
Epidemiology
Occasional nightmares are relatively common in the general population, and
approximately 3–8% of adults report recurrent nightmares. Although more common
in childhood roughly 7–11%, the rate increases to 15 to as high as 67% of adult
patients with psychiatric illness. Men and women appear to be equally affected, but
the overall prevalence of nightmare disorder is unclear.
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Etiology/Pathophysiology
Nightmares by themselves usually occur in relationship to either an experience of
the day, such as a horror movie, or related to a substance consumed– such as alcohol. Nightmare disorder, however, is associated with psychopathologies, particularly PTSD, and personality characteristics. Some medications that affect serotonin,
norepinephrine, GABA, histamine, acetylcholine, and dopamine are associated
with nightmares. The withdrawal of REM suppressant medication is also associated
with nightmares [1, 52]. Dream generation is thought to be a process of brain regions
and mechanisms independent of REM generation. Nightmare disorder has been
proposed to be due to a two-factor process of hyperarousal and impaired fear extinction. Hyperarousal is a hallmark of not only insomnia but PTSD in which 80% of
patients report nightmares [53, 54].
Diagnosis
Diagnosis is usually established by clinical history. Nightmares should be distinguished from night terrors as discussed above. The ICSD-3 requires the following
for the diagnosis:
1. Recurrent extremely dysphoric, distressing well-remembered dreams that usu-
ally involve threats to survival, security, or physical integrity.
2. Upon awakening from the nightmare, the person quickly becomes oriented
and alert.
3. When awakening from the nightmare, the person has clinically signicant dis-
tress or impairment in social, occupational, or other important areas of functioning as indicated by the report of at least one of the following:
• Mood disturbance (e.g., persistence of nightmare affect, anxiety, dysphoria)
• Sleep resistance (e.g., bedtime anxiety, fear of sleep/subsequent nightmares)
• Cognitive impairments (e.g., intrusive nightmare imagery, impaired concentration, or memory)
• Negative impact on caregiver or family functioning (e.g., nighttime disruption)
• Behavioral problems (e.g., bedtime avoidance, fear of the dark)
• Daytime sleepiness
• Fatigue or low energy
• Impaired occupational or educational function
• Impaired Interpersonal/Social Function
When considering this diagnosis, the key is to have a clear description of the
nightmare events, and also the key features of the sequelae during wake. The later
part is what distinguishes nightmare disorder, from the occasional disturbing
dream. Many times patients may not spontaneously disclose the impairment in
social, occupational, or other important areas as they have not drawn the connection. Thus further questioning may be needed.
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Treatment
Non-pharmacologic treatment consists of image rehearsal therapy (IRT), cognitive
behavioral therapy (CBT), lucid dreaming therapy, and hypnosis, among others
[52]. IRT is part of the recommended guidelines and appears to be successful in
patients with history of trauma. IRT consists of changing dream content by recreating the dream with positive images and rehearsing the dream for 10–20minutes
daily while awake. Several RCTs have shown efcacy of IRT in the treatment of
nightmare disorder with reduction in nightmare frequency [52, 53]. Pharmacologic
treatment of nightmare disorder is based on studies of their efcacy in treating
PTSD-associated nightmares. Prazosin was initially thought to reduce the recurrence of nightmares but has mixed results in larger trials [55]. Other commonly
used medications in this instance include the atypical antipsychotics, clonidine,
cyproheptadine, trazodone, tricyclic antidepressants, and clonazepam with mixed
results [52].
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Other Parasomnias
Other parasomnias include a collection of disorders that are either related to
sleep- wake transitions, or have no clear tie to a particular sleep stage. Some of
these are very specific phenomena, while others are more general catch-all
disorders. Each has specific criteria to help the clinician distinguish the
syndromes.
Exploding Head Syndrome
Exploding head syndrome is named due to the phenomenon of the sudden sensation
of an explosion or loud noise going off in the head. This usually occurs at sleep
onset, but can occur upon awakening. The person usually has an abrupt arousal
immediately after the event, which is brief, and is accompanied by a sense of fright,
but is not accompanied or associated with any signicant pain [1, 56]. The prevalence is not well known due to the transient nature of the phenomenon and due to
underreporting and under recognition. However, prevalence has been reported to be
roughly 11% in the general population. Individuals may only have one episode in a
lifetime or may have clusters of events over a night or more. The most common
concern for a patient is bleeding or a tumor. Treatment is focused on reassurance as
the condition is benign and usually self-limiting. In the instances that exploding
head syndrome is recurrent or results in distress for the patient, medications may be
tried. Several medications, such as clonazepam, clomipramine, and topiramate,
have had varying success [57, 58].
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Sleep-Related Hallucinations
Hypnic hallucinations are dreamlike imagery that occur during the wake-sleep
transition or vice versa. Hypnopompic hallucinations occur on the transition from
sleep to wake, and hypnogogic hallucinations occur at the onset of sleep and are
thought to be the intrusion of REM into the wake state [59–61]. The hallucinations
are most often visual, but can be auditory or tactile. Though hypnic hallucinations
occur commonly in narcolepsy, they can occur independent of any other disorder
and are common in the general population. Hypnogogic hallucinations are more
common than hypnopompic, with a reported prevalence of 37% and 12.5%,
respectively [62]. Sleep-related hallucinations are associated with sleep problems,
such as insomnia or poor sleep/wake schedules. Treatment is not usually necessary
as the episodes are short-lived and benign. Most individuals are aware that the
images are not real, but they can be distressing [59–61]. Treatment with benzodiazepines and tricyclics has been unsuccessful, but there are reports of success with
melatonin [59].
Sleep Enuresis or Nocturnal Enuresis
Sleep enuresis is the phenomenon of involuntary voiding during sleep in a patient
that is older than 5, occurring at least 2 nights a week, for at least 3months.
Sleep enuresis or nocturnal bedwetting is delineated into primary and secondary
nocturnal enuresis, wherein primary there has never been dry periods of at least
6months and in secondary forms the patient had previously been dry. Though
there is a common symptomatology of wetting the bed a night, the two have
distinct etiologies [1]. The prevalence is between 6 and 10% by age 7, which
then decreases to 2% and less than 2% in teenagers and adults, respectively. The
pathophysiology of nocturnal enuresis is thought to involve nocturnal polyuria,
decreased bladder storage ability, and poor arousal [63]. Primary nocturnal
enuresis is usually considered a disorder of acquired developmental skills, and
therefore there is a range of ages when these skills are acquired. However, in
secondary nocturnal enuresis it can be caused by a number of problems, including diabetes, urinary tract infections, urinary tract malformations, and psychosocial factors [1, 64]. In addition, there is a high rate of sleep disordered breathing
associated with nocturnal enuresis, being reported in 8–47% of cases. Diagnosis
involves a careful history, and it is important to distinguish between primary and
secondary enuresis as further workup is warranted in the latter. The mainstay of
treatment in primary enuresis is bed alarms. In secondary enuresis the underlying cause should be investigated and treatment targeted based on the underlying
pathology. In suspected cases of sleep apnea, a PSG may need to be performed
[63–65].
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Approach toDistinguishing Nocturnal Events
The goal of any evaluation of a patient with nocturnal events is to prevent harm to
the patient or others. For this the clinician should focus the initial consultation upon
answering the following questions: (1) Is the patient at risk potential for harm or
causing harming to someone else? (2) What may be driving the appearance of these
events? (3) Are these events indicating another underlying disorder?
In general, an astute clinician can differentiate parasomnias by looking for key
distinguishing features (Table16.2). The key for any evaluation of nocturnal events
is a thorough history and excellent physical exam. Although these are foundational,
the underpinning of the evaluation is based on a clear description of the events from
witnesses who can give an accurate testimony of the behaviors. Key historical features such as time of night, duration, frequency of occurrence, behavioral characteristics with each event, eyes open or closed, memory recall, age of onset, and family
history of nocturnal events may help differentiate these disorders [66]. The physician should also search for factors that precipitate parasomnias such as poor sleep
environment, improper sleep hygiene, sleep deprivation, circadian rhythm abnormalities, other sleep disorders, medical issues, fever or other illnesses, emotional
stress, medication use, and ingestion of alcohol or sedatives before sleep onset [22,
67–69]. Additional search for other neurological symptoms such as decrease sense
of smell, constipation, or other autonomic issues may give clues to REM sleep
behavior disorder [46]. Similarly, features suggesting cognitive decline in adult may
provide the opening for further investigation of encephalopathic processes or
dementia [69].
Further testing may be indicated for patients with parasomnia. Key features may
elucidate the need for further study in the sleep lab (Table16.4). Polysomnographic
recording can also provide important information in determining the etiology of the
nocturnal events, with the goal of capturing the physiology of each sleep state and
to evaluate the possibility of other contributing sleep disorders. Overnight polysomnography is necessary if the history is atypical, sleepiness is signicant, other sleep
disorders are suspected, or the patient is at risk for harming themselves or others
Table 16.4 Indications for polysomnography in patients with nocturnal events. Reprinted with
permission from Bradley Vaughn
Unusual or atypical presentation for a parasomnia (time of night, behavioral description)
Events injurious or with signicant risk for injury
Signicant disturbance to patient’s home life
Unusual age of onset
Events stereotyped or repetitive
High frequency of the events
Patient has excessive daytime sleepiness or complaints of insomnia
Complaints suggestive of sleep apnea, periodic limb movements, or other sleep disorders
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[70]. Studies should include complete respiratory monitoring, time-synchronized
video monitoring, additional electromyographic recording from all four limbs, a
complete set of cephalic electrodes, and ability to extensively review the electroencephalogram [5, 71, 72]. Incorporation of a full 10- to 20-electrode array and ability
to view the tracing at 10second windows is necessary in evaluating for seizures and
the differentiation of the epileptiform discharges from potential normal variants or
artifacts [73].
Parasomnias may be distinguished using key features. The challenge for the
ardent clinician is to utilize historical and physical examination clues and appropriate diagnostic tools to distinguish the underlying causes and propose directed therapy to improve the patient’s condition.
References
1. American Academy of Sleep Medicine. International classication of sleep disorders. 3rd ed.
Darien, IL: American Academy of Sleep Medicine, 2014.
2. Provini F, Tinuper P, Bisulli F, Lugaresi E. Arousal disorders. Sleep Med. 2011;12(Suppl
2):S22–6. https://doi.org/10.1016/j.sleep.2011.10.007.
3. Denis D, French CC, Gregory AM.A systematic review of variables associated with sleep
paralysis. Sleep Med Rev. 2018;38:141–57. PMID: 28735779. https://doi.org/10.1016/j.
smrv.2017.05.005.
4. Stefani A, Holzknecht E, Högl B.Clinical neurophysiology of REM parasomnias. Handb Clin
Neurol. 2019;161:381–96.
5. Gieselmann A, Ait Aoudia M, Carr M, Germain A, Gorzka R, Holzinger B, Kleim B, Krakow
B, Kunze AE, Lancee J, Nadorff MR, Nielsen T, Riemann D, Sandahl H, Schlarb AA, Schmid
C, Schredl M, Spoormaker VI, Steil R, van Schagen AM, Wittmann L, Zschoche M, Pietrowsky
R.Aetiology and treatment of nightmare disorder: state of the art and future perspectives. J
Sleep Res. 2019;28:e12820.
6. Gaudreau H, Joncas S, Zadra A, Montplaisir J.Dynamics of slow-wave activity during the
NREM sleep of sleepwalkers and control subjects. Sleep. 2000;23:755–60.
7. Desjardins M, Carrier J, Lina J, etal. EEG functional connectivity prior to sleepwalking: evi-
dence of interplay between sleep and wakefulness. Sleep. 2017;40:zsx024.
8. Heidbreder A, Stefani A, Brandauer E, etal. Gray matter abnormalities of the dorsal posterior
cingulate in sleep walking. Sleep Med. 2017;36:152–5.
9. Gibbs SA, Proserpio P, Terzaghi M, etal. Sleep-related epileptic behaviors and non-REM-
related parasomnias: insights from stereo-EEG.Sleep Med Rev. 2016;25:4–20.
10. Januszko P, Niemcewicz S, Gajda T, etal. Sleepwalking episodes are preceded by arousal-
related activation in the cingulate motor area: EEG current density imaging. Clin Neurophysiol.
2016;127(1):530–6.
11. Bassetti C, Vella S, Donati F, et al. SPECT during sleepwalking. Lancet.
2000;356(9228):484–5.
12. Oliviero A, Della Marca G, Tonali PA, etal. Functional involvement of cerebral cortex in adult
sleepwalking. J Neurol. 2007;254(8):1066–72.
13. Labelle MA, Dang-Vu TT, Petit D, Desautels A, Montplaisir J, Zadra A. Sleep depriva-
tion impairs inhibitory control during wakefulness in adult sleepwalkers. J Sleep Res.
2015;24:658–65.
14. Di Gennaro G, Autret A, Mascia A, et al. Night terrors associated with thalamic lesion. Clin
Neurophysiol. 2004;115(11):2489–92.
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