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Narcolepsy andIdiopathic Hypersomnia
52. Faull KF, Thiemann S, King RJ, etal. Monoamine interactions in narcolepsy and hypersomnia: a preliminary report. Sleep. 1986;9:246–9.
53. Bassetti CL, Khatami R, Poryazova R, etal. Idiopathic hypersomnia: a dopaminergic disorder. Sleep. 2009;32:A248–9.
54. Arnulf I, Leu-Semenescu S, Dodet P.Precision medicine for idiopathic hypersomnia. Sleep
Med Clin. 2019;14(3):333–50.
55. Nishino S, Sakurai E, Nevsimalova S, etal. Decreased CSF histamine in narcolepsy with and
without low CSF hypocretin-1in comparison to healthy controls. Sleep. 2009;32:175–80.
56. Kanbayashi T, Kodama T, Kondo H, etal. CSF histamine contents in narcolepsy, idiopathic
hypersomnia and obstructive sleep apnea syndrome. Sleep. 2009;32:181–7.
57. Dauvilliers Y, Delallee N, Jaussent I, etal. Normal cerebrospinal uid histamine and telemethylhistamine levels in hypersomnia conditions. Sleep. 2012;35:1359–66.
58. Rack M, Davis J, Roffwarg HP, etal. The multiple sleep latency test in the diagnosis of narcolepsy. Am J Psychiatry. 2005;162(11):2198–9.
59. Ferri R, Franceschini C, Zucconi M, etal. Sleep polygraphic study of children and adolescents with narcolepsy/cataplexy. Dev Neuropsychol. 2009;34(5):523–38.
60. Carskadon MA.The second decade. In: Guilleminault C, editor. Sleeping and waking disorders: indications and techniques. Menlo Park: Addison-Wesley; 1982. p.99–125.
61. Pizza F, Barateau L, Jaussent I, etal. Validation of multiple sleep latency test for the diagnosis
of pediatric narcolepsy type 1. Neurology. 2019;93(11):e1034–44.
62. Mayer G, Lammers GJ.The MSLT: more objections than benets as a diagnostic gold standard? Sleep. 2014;37:1027–8.
63. Baumann CR. Bassetti CI Hypocretin (orexins) and sleep-wakedisorders. Lancet Neurol.
2005;10:673–82.
64. Sakai N, Matsumura M, Lin L, et al. HLPC analysis of CSF hypocretin-1in type 1 and 2
narcolepsy. Sci Rep. 2019;9:477.
65. Basseti CL, Adamantidis A, Burdakov D, etal. Narcolepsy- clinical spectrum, aetiopathophysiology, diagnosis and treatment. Nat Rev Neurol. 2019;15(9):519–39.
66. Stephansen JB, Olesen AN, Olsen M, etal. Neural network analysis of sleep stages enables
efcient diagnosis of narcolepsy. Nat Commun. 2018;9(1):5229.
67. Bin-Hasan S, Videnovic A, Maski K.Nocturnal REM sleep without atonia is a diagnostic
biomarker of pediatric narcolepsy. J Clin Sleep Med. 2018;14(2):245–52.
68. Murer T, Imbach LL, Hackius M, etal. OptimizingMSLT specicity in narcolepsy with cataplexy. Sleep. 2017;1:40(12).
69. Chritensen JAE, Kempfner L, Leonthin HL, etal. Novel method for evaluation ofeye movements in patients with narcolepsy. Sleep Med. 2017;33:171–80.
70. Aslan S, Erbil N, Tezer FI.Heart rate variability during nocturnal sleep and daytime naps in
patients with narcolepsy type 1 and type 2. J Clin Neurophysiol. 2019;36(2):104–11.
71. Sieminski M, Chwojnicki K, Sarkanen T, etal. The relationship between orexin levels and
blood pressure changes in patients with narcolepsy. PLoS One. 2017;12(10):e0185975.
72. Hong SB. Neuroimaging of narcolepsy and Kleine-Levin syndrome. Sleep Med Clin.
2017;12(3):359–68.
73. Black J, Reaven NL, Funk SE.Medical comorbidity in narcolepsy: ndings from the burden
of narcolepsy disease (BOND) study. Sleep Med. 2017;33:13–8.
74. Ruoff CM, Reaven NL, Funk SE.High rates of psychiatric comorbidity in narcolepsy: ndings from the burden of narcolepsy Dise ofase (BOND) study of 9312 patients in the United
States. J Clin Psychiatry. 2017;78(2):171–6.
75. Maestri M, Monzani F, Bonanni E, etal. Insulinoma presenting as idiopathic hypersomnia.
Neurol Sci. 2010;31(3):349–52.
76. Shinno H, Inami Y, Inagaki T, et al. Successful treatment with levothyroxine for idiopathic hypersomnia patients with subclinical hypothyroidism. Gen Hosp Psychiatry.
2009;31(2):190–3.
347
348
https://t.me/medicina_free
77. Masel BE, Scheibel RS, Kimbark T, etal. Excessive daytime sleepiness in adults with brain
injuries. Arch Phys Med Rehabil. 2001;82(11):1526–32.
78. Dl P, Ponsford JL, Rajaratnam SM, etal. Self reported changes to nighttime sleep after traumatic brain injury. Arch Phys Med Rehabil. 2006;87(2):278–85.
79. Baumann CR, Werth E, Stocker R, etal. Sleep-wake disturbances 6 months after traumatic
brain injury: a prospective study. Brain. 2007;130(Pt 7):1873–83.
80. Baumann CR, Bassetti CL, Valko PO, etal. Loss of hypocretin (orexin) neurons with traumatic brain injury. Ann Neurol. 2009;66(4):555–9.
81. Black J, Guilleminault C.Medications for the treatment of narcolepsy. Expert Opin Emerg
Drugs. 2001;6(2):239–47.
82. Didato G, Nobili L.Treatment of narcolepsy. Expert Rev Neurother. 2009;9(6):897–910.
83. Mitler MM, Hayduk R.Benets and risks of pharmacotherapy for narcolepsy. Drug Saf.
2002;25:791–809.
84. Harsh JR, Hayduk R, Rosenberg R, etal. The efcacy and safety of armodanil as treatment for adults with excessive sleepiness associated with narcolepsy. Curr Med Res Opin.
2006;22(4):761–74.
85. Dinges DF, Arora S, Darwish M, etal. Pharmacodynamic effects on alertness of single doses
of armodanil in healthy subjects during a nocturnal period of acute sleep loss. Curr Med Res
Opin. 2006;22(1):159–67.
86. U.S.Xyrem® International Study Group. A double blind placebo controlled study demonstrates sodium oxybate is effective for the treatment of excessive sleepiness in narcolepsy. J
Clin Sleep Med. 2005;1(4):391–7.
87. U.S. Xyrem® Multicenter Study Group. Sodium oxybate demonstrates long-term efcacy
for the treatment of cataplexy in patients with narcolepsy. Sleep Med. 2004;5:119–23.
88. Xyrem® Product Information, Orphan Medical, Inc.
89. Li S, Yang J.Pitolisant for treating patients with narcolepsy. Expert Rev Clin Pharmacol.
2020;13(2):79–84.
90. Dauvilliers Y, Arnulf I, Szakacs Z, etal. Long-term Use of Pitolisant to Treat Patients with
Narcolepsy: Harmony III Study. Sleep. 2019;42(11):zsz174.
91. Thorpy MJ, Shapiro C, Mayer G, etal. A randomized study of solriamfetol for excessive
daytime sleepiness in narcolepsy. Ann Neurol. 2019;85(3):359–70.
92. Abad VC. Guilleminault. New developments in the management of narcolepsy. Nat Sci
Sleep. 2017;9:39–57.
93. Morgenthaler TI, Kapur VK, Brown T, etal. Practice parameters for the treatment of narcolepsy and other hypersomnias of central origin. Sleep. 2007;30(12):1705–11.
94. Guilleminault C, Raynal D, Takahashi S, etal. Evaluation of short-term and long-term treatment of the narcolepsy syndrome with clomipramine hydrochloride. Acta Neurol Scand.
1976;54:71–87.
95. Houghton WC, Scammell TE, Thorpy M.Pharmacotherapy for cataplexy. Sleep Med Rev.
2004;8:355–66.
96. Martinez-Rodriguez J, Iranzo A, Santamaria J, etal. Status cataplecticus induced by abrupt
withdrawal of clomipramine. Neurologia. 2002;17:113–6.
97. Frey J, Darbonne C. Fluoxetine suppresses human cataplexy: a pilot study. Neurology.
1994;44:707–9.
98. Ruppert E, Zagalaa H, Chambe J, et al. Intravenous immunoglobulin therapy administered
early after narcolepsy type 1 onset in three patients evaluated by clinical and polysomnographic follow-up. Behav Neurol. 2018;2018:1671–2.
99. Thorpy MJ, Snyder M, Aloe FS, etal. Short-term triazolam use improves nocturnal sleep of
narcoleptics. Sleep. 1992;15(3):212–6.
100. Morse AM, Kelly-Pieper K, Kothare SV.Management of excessive daytime sleepiness in
narcolepsy with baclofen. Pediatr Neurol. 2019;93:39–42.
I. Ahmed and M. Thorpy
Chapter 16
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Non-REM Parasomnias
NathanA.Walker andBradleyV.Vaughn
Keywords Parasomnia · Disorders of arousal · Sleepwalking · Sleep terror
Confusional arousal REM sleep behavior disorder · Sleep-related eating disorder
Exploding head syndrome
Introduction
Parasomnias are dened as “undesirable physical events or experiences that occur
during entry into sleep, within sleep, or during arousal from sleep” [1]. As part of a
larger collection of nocturnal events, parasomnias are included in the pathologies
that produce behaviors and occurrences at night. Many envision these events as
entertaining stories from family or roommates, or may be thought of as strange
inexplicable incidents. The clinical symptoms of parasomnias include complex purposeful movements, unusual behaviors, perceptions, or emotional experiences.
Many of the parasomnias are very common in the general population, especially in
children. Although the majority of parasomnias are not harmful, injuries, sleep disruption, and psychosocial impairment can result from the events, and these events
provide the opportunity to diagnose underlying sleep disorders or medical issues
that may provoke the events. Therefore, it is useful to know the symptoms, clinical
associations, and treatment options to guide patients.
In early nomenclature, parasomnias were categorized based upon the most prominent behavior. Some remnants of this convention still exist in terms such as sleepwalking and sleep-related eating. However, as we have furthered our understanding
of the neuronal circuits determining the states of sleep and wake, we have grouped
events toward the originating sleep-wake state while acknowledging pathologies
N. A. Walker · B. V. Vaughn (*)
Department of Neurology, University of North Carolina, Chapel Hill, NC, USA
e-mail: vaughnb@neurology.unc.edu
M. S. Badr, J. L. Martin (eds.), Essentials of Sleep Medicine,
Respiratory Medicine, https://doi.org/10.1007/978-3-030-93739-3_16
349© Springer Nature Switzerland AG 2022
350
N. A. Walker and B. V. Vaughn
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that are held in common [1]. The brain’s three distinct states of wake and NREM
and REM sleep allow us to understand the starting physiological state that provides
the substrate for some of these parasomnias. Thus parasomnias may be associated
with NREM sleep, REM sleep, or the transitions between wake and sleep as a platform which demonstrates the underlying pathology. The current categorization in
the International Classication of Sleep Disorders third edition (ICSD 3) divides the
parasomnias into four main categories: NREM-related parasomnias, REM-related
parasomnias, other parasomnias, and normal variants (Table 16.1). This context
includes consideration of the drivers for the parasomnias as well as how to separate
mimics that may present with similar behaviors.
This classication scheme also allows us to ultimately move toward a classication structure more aligned with physiology and subsequently underlying pathology. Several parasomnias represent a mixture of states [2]. This model is best
demonstrated when considering the non-REM sleep-related parasomnias, disorders
of arousals. The disorders of arousals (sleep terrors, sleepwalking, and confusional
arousals) are associated with a mixture of features of NREM sleep with some wakelike behaviors. These disorders represent a continuum of complex behaviors that
share features of NREM sleep, such as minimal cognitive functioning and amnesia
for the events, with features of the awake state such as complex motor patterns and
eyes open (Table16.2) [1]. Commonly these events are triggered by stimuli during
deeper NREM sleep and involve a variety of nonstereotyped behaviors. One REMrelated parasomnia, recurrent isolated sleep paralysis, also represents a mixture of
wake and REM sleep. Although many times associated with narcolepsy, these
Table 16.1 Outline of parasomnias
1. Non-REM parasomnias
(a) Disorders of arousal
(i) Confusional arousals
(ii) Sleepwalking
(iii) Sleep terrors
(b) Sleep-related eating disorder
2. REM-related parasomnias
(a) REM sleep behavior disorder
(b) Recurrent isolated sleep paralysis
(c) Nightmare disorder
3. Other parasomnias
(a) Exploding head syndrome
(b) Sleep-related hallucinations
(c) Sleep enuresis
(d) Parasomnia due to a medical disorder
(e) Parasomnia due to a medication or substance
(f) Parasomnia, unspecied
4. Isolated symptoms and normal variants
(a) Sleep talking
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Nocturnal
seizures
portion of brain
involved
Psychogenic
events
Variable Dependent on the
Exploding head
syndrome
Painless sensation
of explosion inside
the head
Recurrent
isolated sleep
paralysis
Episodes of
inability to
move
Variable
to adulthood
Anytime Anytime
Usually near sleep
onset but can be
awakening
variable
Rare Variable Frontal
seizures—
multiple per
night
Usually under
Seconds Variable
than weekly
3minutes
minutes or
longer
minutes
Variable Variable
immediately open
following the event
351
Potentially
epileptiform
activity
Occur from
awake state
Usually occurs in
light sleep
Arousal from
REM sleep
REM sleep behavior
disorder
Sometimes combative
with eyes closed
Sleep-related
eating disorder
Eating
typically
high-calorie
foods; eyes
semipurposeful
movement with eyes
open
Feature Disorders of arousal
Table 16.2 Distinguishing features of nocturnal events. Reprinted with permission from Bradley Vaughn
Behavior Confused;
open
Variable Older adult Variable Adult Adolescence
adolescence
Age of onset Childhood and
During REM Typically on
night
Variable Multiple per night Variable less
First third of night First half of
Time of
Less than one per
occurrence
Frequency of
night
events
Dream recall Ye s Yes None Usually none
Duration Minutes Minutes Seconds to minute Seconds to
Memory of event Usually none Usually none
or limited
Eyes open Eyes open Eyes closed Eyes closed Eyes closed but
Eyes open or
closed
Excessive
electromyogram tone
Arousal from
NREM sleep
No No No No Similar sensation No Ye s
Arousals from slow
wave sleep
Stereotypical
movements
Polysomnogram
ndings
during REM sleep
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events in isolation are related to the intrusion of REM sleep-related paralysis into
wakefulness [3, 4]. Other REM sleep parasomnias such as nightmare disorder and
REM sleep behavior disorder are conned to the state. The latter is an example of
neurological impairment of the circuitry that produces the REM sleep associated
paralysis [5]. This disorder represents an example of how sleep dedicated neural
circuitry may be uniquely more vulnerable to specic types of degeneration
or injury.
Many of the “other parasomnias” represent events that occur during the transition between wake and sleep (Table16.1). Some sensory events such as exploding
head syndrome and sleep-related hallucinations are events that may occur as the
patient enters light sleep, but may also occur upon awakening. Additionally, in this
group are parasomnias that occur across the spectrum of sleep states or represent a
loss of sleep-wake state distinction.
The goal of this chapter is to review the variety of disorders classied as parasomnias. This chapter provides a framework for parasomnias and outlines an overarching approach to patients with nocturnal events. The text reviews the known
pathology and the possible drivers for the parasomnias as well as describes mimics
that may present with similar behaviors. The challenge for the ardent clinician is to
utilize historical and physical examination clues with the appropriate investigative
tools to discern the underlying causes and propose appropriate therapy to improve
the patient’s condition.
N. A. Walker and B. V. Vaughn
Non-REM Related Parasomnias
As the name implicates, non-rapid eye movement (NREM) sleep-related parasomnias are parasomnia events that arise from NREM sleep. This group includes the
disorders of arousal and sleep-related eating disorder. As a whole, the episodes may
include a variety of complex movements that range a variety of basic behaviors.
These parasomnias are classically thought of as partial triggered awakenings with
retention of some features of sleep. Each of these disorders has their own criteria for
diagnosis and unique features.
Disorders ofArousal
The International Classication of Sleep Disorders, 3rd edition (ICSD-3) denes
disorders of arousal by specic universal features and then specic ndings for the
subdivisions of confusional arousals, and sleepwalking and sleep terrors. The disorders of arousal (DOA), as a group, have several common manifestations that dene
the cluster, while each also has unique features in behavior that allow their distinction. For the group of DOA, the ICSD-3 requires several features to be present to
qualify as a DOA (Table16.3).
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Non-REM Parasomnias
Table 16.3 Features of disorders of arousal (adapted from ICSD-3)
1. Recurrent episodes of incomplete awakening from sleep
2. Inappropriate or absent responsiveness to intervention from observers or from others
attempting to redirect the person during the episode
3. Limited or no associated cognition or dream imagery
4. Partial or complete amnesia for the episode
5. The disturbance is not better explained by other medical, psychiatric or sleep conditions or
medications, or substance use
353
Furthermore, these three diagnoses share clinical features that help clinicians
identify these as NREM sleep events. The majority of events occur in the rst third
of sleep and are relatively brief. Most of the events in disorders of arousal last for
30 seconds to a few minutes, but some may last up to 30minutes. Many times,
patients have their eyes open but have a glassy confused stare. They may be partially
reactive to the environment and even may appear disoriented for several minutes
following the events. During the events, patients lack higher cognitive processing
and appear to be functioning unconsciously. These patients are difcult to awaken
from the events, and stimulation may result in the patients becoming agitated.
Following the event patients may have partial or total amnesia, although adults are
more likely to remember portions of the episodes. These disorders are most common in children and typically improve with age. Males and females are equally
represented in disorders of arousal, and family history of events is in nearly two
thirds of carefully screened cases.
Pathology
The vast majority of patients with disorder of arousal are neurologically and psychologically normal. When examining the sleep physiology in these patients, the
studies show relatively normal sleep architecture. On sleep studies the onset of
NREM parasomnia is an abrupt arousal, usually from stage N3 sleep with the
patients having a dull confused look on video. Some studies have shown increased
spontaneous awakening or arousals from slow wave sleep, and some investigators
have found increased runs of hypersynchronous delta waves just prior to events [6,
7]. These studies have suggested increased slow wave activity and slow oscillations
in EEG patterns prior to sleepwalking events. These ndings suggest that the
pathology is related to incomplete switching of deeper NREM sleep to wake.
Examination of the gross structure of the brain shows little differences between
patients and control subjects. However, Heidbreder reported that subjects with
NREM parasomnias had smaller gray volume of the dorsal posterior cingulate
when compared to nonparasomnia controls using magnetic resonance imaging
(MRI) and diffusion tensor imaging (DTI) [8]. Further studies using depth EEG
electrode recordings showed that disorder of arousal events activated the motor and
central cingulate cortex while deactivating the hippocampal and association
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N. A. Walker and B. V. Vaughn
cortices [9, 10]. This activation pattern of cingulate motor area while deactivation
of other association cortices was seen using Single-Photon Emission Computed
Tomography (SPECT) when tracer was injected during a sleepwalking episode
[11]. Furthermore, studies of network function related to frontal inhibition elicited
by transcranial magnetic stimulation (TMS) showed that sleepwalkers have an
impaired efciency of inhibitory circuits [12]. Based on their results, the authors
postulated that sleepwalkers have a dysfunction of both GABA-A and cholinergic
pathways leading to an inability to maintain slow wave sleep and suppress partial
arousals in sleep. As part of testing this functional inhibition, another study of
sleepwalkers showed they had greater impairment of inhibitory control resulting in
increased errors on Stroop Color Word Test and errors of commission on Continuous
Performance Test following 25 hours of sleep deprivation [13]. These studies
appear to suggest that the typical processes that inhibit specic portions of the
subclinical arousals are not sufcient in suppressing these partial arousals. Thus
patients with disorders of arousal are more vulnerable to activity that produces
arousals from NREM sleep.
Associated Conditions
Disorders of arousal have been reported with a variety of medical disorders including endocrinological, vascular, neurological, and sleep disorders. Case reports of
new onset DOA have described right thalamic lesion, breathing disorder with Chiari
I malformation, hyperthyroidism, and diabetes [14–16]. Historically, disorders of
arousal were thought to be associated with depression and anxiety. However, more
recent studies show no relationship of these disorders to psychopathology [17, 18].
One caveat is that sleep terrors in children do not usually present with psychopathology, but it may play a larger role in adults with sleep terrors [19].
The most common sleep disorder associated with NREM parasomnias is obstructive sleep apnea. Several studies have suggested the link of breathing disorders
increasing the frequency of disorder of arousal events. Goodwin found that children
with even mild upper airways disturbance were signicantly more likely to have
parasomnia events than those without any disturbance [20]. Similarly in adults,
Lundetræ reported that sleepwalking has a higher prevalence in patients with severe
OSA than those with mild OSA [21]. These reports highlight that disorders of
arousal events may signal the presence of other sleep disorders and that patients
with NREM parasomnias may benet from investigation and treatment of these
disorders.
Some disorder of arousal events appear to be elicited by specic medications.
Medications such as antidepressants, antipsychotic agents, beta blockers, and
GABA modulators have been reported as possible agents that can trigger events. Of
these, the most well recognized are the short-acting hypnotic agents, such as zolpidem or sodium oxybate. These medications are linked to increase frequency of
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355
sleepwalking and confusional arousal events. This association raises the possible
question that the mechanism is impairment of arousal circuitry caused by the medication [22].
Diagnosis
The gold standard for making the diagnosis of DOA is capturing an event arising
from NREM sleep on polysomnography (PSG). This nding helps elucidate the key
features of a mixture of wake and NREM sleep (Fig.16.1). This testing also can
shed some light if the patient is having other sleep issues, such as sleep apnea, that
may be provoking the nocturnal events. Fois showed, in a study of 124 subjects, that
PSG conrmed parasomnia diagnosis in up to 60% of their study group [23]. PSG
was also helpful in identifying other diagnoses that may mimic the parasomnia.
Video PSG can capture the events in detail, and these events may show a spectrum
of behaviors from appearing awake and confused to non-agitated motor activity to
events with extreme emotional distress. These events typically arise from stage N3
sleep but less commonly occur from N2 sleep. Although recording spontaneous
Fig. 16.1 This gure shows a standard polysomnogram during a confusional arousal in a 7-yearold boy. The patient is with eyes open during the event and has a confused look on his face.
(Reprinted with permission from Bradley Vaughn MD)
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N. A. Walker and B. V. Vaughn
parasomnia activity during PSG is uncommon, Pilon tested a technique that provoked events in nearly all of their subjects [24]. In their protocol, subjects with a
history of sleepwalking were kept awake through the night and then allowed to
sleep during the day. Once the subjects entered stage N3, an auditory stimulus was
introduced to cause an arousal. Nearly all of the patients had a subsequent event.
This study has yet to be repeated, but offers a possibility of a higher yield of events.
Management
Management of patients with disorders of arousal focuses on three major areas:
safety, decreasing the frequency of events, and determining the possibility of other
underlying provocative factors. The clinician initially needs to assess the possibility
of harm from the events to the patient or family members. Many patients may have
events without leaving the bed and have little chance of harm. For these patients
reassurance is an important component in the treatment plan. For all cases, the
patients and their families should be counselled on a safe sleeping environment and
how to safely interact with the patient when they are having an event. For those at
risk, placing the bed on the oor, securing windows and doors, and eliminating any
access to sharp or dangerous objects are key. For some patients having their bedroom on the rst oor to avoid falling or the use of door alarms is helpful.
Management may also focus on the predisposing, priming, and precipitating factors of what is called the three P model of NREM parasomnias [25]. The predisposing
factors such as genetics, thus understanding family history, may help families be
aware of the risks. Priming factors include medication that may increase the arousal
threshold, e.g., Z-drugs; sleep deprivation which can increase the amount of SWS and
increase arousal threshold; or substances that may increase arousals, caffeine or alcohol. Precipitating factors can include pain, a sleeping environment unconducive to
sleep, and a myriad of other sleep disorders. Therefore, targeting good sleep hygiene,
avoidance of priming substances/situations, and precipitating factors are useful tactics to reduce events. Tracking the frequency of events on a calendar may help identify patterns that lead to clues of provoking agents, as well as response to therapies.
Patients and their families may look for sources of arousals to reduce, such as
environmental noise or stimuli as well as keeping a regular sleep schedule and avoiding sleep deprivation. Anticipatory awakening therapy is one behavioral therapy that
is shown to be successful in children in reducing the frequency of events [26]. For this
therapy the patient is allowed to go to sleep but awoken anywhere from 10 to 30minutes prior to the typical time of the event. This is repeated for 2–3weeks, and then the
patient is assessed for further events. If the patient does resume having events, another
round of awakenings can be performed. For a small minority of patients, medication
is needed. Due to a lack of case control studies or randomized control trials, recommendations at times can be contradictory. Clinically, patients appear to respond to
agents such as clonazepam or longer-acting benzodiazepines. In one series of 69
patients treated with these agents, 86% showed improvement [27]. Several case
reports have suggested response to imipramine, trazadone, or paroxetine [28–30].
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