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Non-REM Parasomnias
15. Daftary AS, Walker JM, Farney RJ.NREM sleep parasomnia associated with Chiari I malfor-
mation. J Clin Sleep Med. 2011;7(5):526–9.
16. Giuliano L, Fatuzzo D, Mainieri G, La Vignera S, Soa V, Zappia M.Adult-onset sleepwalking
secondary to hyperthyroidism: polygraphic evidence. J Clin Sleep Med. 2018;14(2):285–7.
17. Labelle M, Desautels A, Montplaisir J, Zadra A.Psychopathologic correlates of adult sleep-
walking. Sleep Med. 2013;14:1348–55.
18. Ohayon MM, Guilleminault C, Priest RG.Night terrors, sleepwalking, and confusional arous-
als in the general population: their frequency and relationship to other sleep and mental disorders. J Clin Psychiatry. 1999;60:268–76.
19. Howell MJ.Parasomnias: an updated review. Neurotherapeutics. 2012;9(4):753–75.
20. Goodwin JL, Kaemingk KL, Fregosi RF, et al. Parasomnias and sleep disordered breathing
in Caucasian and Hispanic children– the Tucson children’s assessment of sleep apnea study.
BMC Med. 2004;2:14.
21. Lundetræ RS, Saxvig IW, Pallesen S, Aurlien H, Lehmann S, Bjorvatn B.Prevalence of para-
somnias in patients with obstructive sleep apnea. A registry-based cross-sectional study. Front
Psychol. 2018;9:1140.
22. Stallman HM, Kohler M, White J.Medication induced sleepwalking: a systematic review. Sleep
Med Rev. 2018;37:105–13. PMID: 28363449. https://doi.org/10.1016/j.smrv.2017.01.005.
23. Fois C, Wright MA, Sechi GP, et al. The utility of polysomnography for the diagnosis of
NREM parasomnias: an observational study over 4 years of clinical practice. J Neurol.
2015;262(2):385–93.
24. Pilon M, Montplaisir J, Zadra A.Precipitating factors of somnambulism: impact of sleep depri-
vation and forced arousals. Neurology. 2008;70(24):2274–5.
25. Pressman MR.Factors that predispose, prime and precipitate NREM parasomnias in adults:
clinical and forensic implications. Sleep Med Rev. 2007;11(1):5–30.
26. Attarian H.Treatment options for parasomnias. Neurol Clin. 2010;28(4):1089–106.
27. Schenck CH, Mahowald MW. Long-term, nightly benzodiazepine treatment of injuri-
ous parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med.
1996;100(3):333–7.
28. Cooper AJ.Treatment of coexistent night-terrors and somnambulism in adults with imipra-
mine and diazepam. J Clin Psychiatry. 1987;48:209–10.
29. Balon R.Sleep terror disorder and insomnia treated with trazodone: a case report. Ann Clin
Psychiatry. 1994;6:161–3.
30. Wilson SJ, Lillywhite AR, Potokar JP, et al. Adult night terrors and paroxetine. Lancet.
1997;350:185.
31. Ekambaram V, Maski K.Non-rapid eye movement arousal parasomnias in children. Pediatr
Ann. 2017;46(9):e327–31. https://doi.org/10.3928/19382359- 20170814- 01.
32. Castelnovo A, Lopez R, Proserpio P, Nobili L, Dauvilliers Y. NREM sleep parasomnias
as disorders of sleep-state dissociation. Nat Rev Neurol. 2018;14(8):470–81. https://doi.
org/10.1038/s41582- 018- 0030- y.
33. Drakatos P, Leschziner G.Diagnosis and management of nonrapid eye movement-parasomnias.
Curr Opin Pulm Med. 2019;25(6):629–35. https://doi.org/10.1097/MCP.0000000000000619.
34. Bargiotas P, Arnet I, Frei M, Baumann CR, Schindler K, Bassetti CL.Demographic, clinical
and polysomnographic characteristics of childhood- and adult-onset sleepwalking in adults.
Eur Neurol. 2017;78(5–6):307–11.
35. Stallman HM, Kohler M.Prevalence of sleepwalking: a systematic review and meta-analysis.
PLoS One. 2016;11(11):e0164769. Published 2016 Nov 10. https://doi.org/10.1371/journal.
pone.0164769.
36. Baldini T, Loddo G, Sessagesimi E, etal. Clinical features and pathophysiology of disorders
of arousal in adults: a window into the sleeping brain. Front Neurol. 2019;10:526. Published
2019 May 17. https://doi.org/10.3389/fneur.2019.00526.
37. Ellington E.It's not a nightmare: understanding sleep terrors. J Psychosoc Nurs Ment Health
Serv. 2018;56(8):11–4. https://doi.org/10.3928/02793695- 20180723- 03.
https://doi.org/10.1159/000481685.
377

378
https://t.me/medicina_free
38. Auger RR.Sleep-related eating disorders. Psychiatry (Edgmont). 2006;3(11):64–70.
39. Komada Y, Takaesu Y, Matsui K, etal. Comparison of clinical features between primary and
drug-induced sleep-related eating disorder. Neuropsychiatr Dis Treat. 2016;12:1275–80.
Published 2016 May 26. https://doi.org/10.2147/NDT.S107462.
40. Chiaro G, Caletti MT, Provini F.Treatment of sleep-related eating disorder. Curr Treat Options
Neurol. 2015;17(8):361.
41. Inoue Y.Sleep-related eating disorder and its associated conditions. Psychiatry Clin Neurosci.
2015;69(6):309–20.
42. Winkelman JW, Herzog DB, Fava M.The prevalence of sleep-related eating disorder in psy-
chiatric and non-psychiatric populations. Psychol Med. 1999;29:1461–6.
43. Santin J, Mery V, Elso MJ, Retamal E, Torres C, Ivelic J, Godoy J.Sleep-related eating disor-
der: a descriptive study in Chilean patients. Sleep Med. 2014;15(2):163–7.
44. McGrane IR, Leung JG, St Louis EK, Boeve BF.Melatonin therapy for REM sleep behavior
disorder: a critical review of evidence. Sleep Med. 2015;16(1):19–26. https://doi.org/10.1016/j.
sleep.2014.09.011.
45. Barone DA, Henchcliffe C. Rapid eye movement sleep behavior disorder and the link to
alpha-synucleinopathies. Clin Neurophysiol. 2018;129(8):1551–64. https://doi.org/10.1016/j.
clinph.2018.05.003.
46. St Louis EK, Boeve BF. REM sleep behavior disorder: diagnosis, clinical implications,
and future directions. Mayo Clin Proc. 2017;92(11):1723–36. https://doi.org/10.1016/j.
mayocp.2017.09.007
47. Porter VR, Avidan AY. Clinical overview of REM sleep behavior disorder. Semin Neurol.
2017;37(4):461–70. https://doi.org/10.1055/s- 0037- 1605595.
48. Zhou J, Zhang J, Du L, Li Z, Li Y, Lei F, Wing YK, Kushida CA, Zhou D, Tang X.Characteristics
of early- and late-onset rapid eye movement sleep behavior disorder in China: a case-control
study. Sleep Med. 2014;15(6):654–60.
49. Sharpless BA, Kliková M. Clinical features of isolated sleep paralysis. Sleep Med.
2019;58:102–6. https://doi.org/10.1016/j.sleep.2019.03.007.
50. Ramos DF, Magalhães J, Santos P, Vale J, Santos MI. Recurrent sleep paralysis – fear of
sleeping. Rev Paul Pediatr. 2019;38:e2018226. Published 2019 Nov 25. https://doi.
org/10.1590/1984- 0462/2020/38/2018226.
51. Sharpless BA.A clinician’s guide to recurrent isolated sleep paralysis. Neuropsychiatr Dis
Treat. 2016;12:1761–7. Published 2016 Jul 19. https://doi.org/10.2147/NDT.S100307.
52. Morgenthaler TI, Auerbach S, Casey KR, etal. Position paper for the treatment of nightmare
disorder in adults: an american academy of sleep medicine position paper. J Clin Sleep Med.
2018;14(6):1041–55. Published 2018 Jun 15.
53. Gieselmann A, Ait Aoudia M, Carr M, et al. Aetiology and treatment of nightmare dis-
order: state of the art and future perspectives. J Sleep Res. 2019;28(4):e12820.
org/10.1111/jsr.12820.
54. Simor P, Blaskovich B. The pathophysiology of nightmare disorder: signs of impaired
sleep regulation and hyperarousal. J Sleep Res. 2019;28(6):e12867. https://doi.org/10.1111/
jsr.12867.
55. Rubin ML, Copeland LA, Kroll-Desrosiers AR, Knittel AG.Demographic variation in the use
of prazosin for treatment of sleep disturbance in combat veterans with PTSD.Psychopharmacol
Bull. 2020;50:26–35.
56. Ceriani CEJ, Nahas SJ. Exploding head syndrome: a review. Curr Pain Headache Rep.
2018;22(10):63. Published 2018 Jul 30. https://doi.org/10.1007/s11916- 018- 0717- 1.
57. Sharpless BA.Exploding head syndrome. Sleep Med Rev. 2014;18(6):489–93. https://doi.
org/10.1016/j.smrv.2014.03.001.
58. Palikh GM, Vaughn BV.Topiramate responsive exploding head syndrome. J Clin Sleep Med.
2010;6:382–3.
59. Lysenko L, Bhat S. Melatonin-responsive complex nocturnal visual hallucinations. J Clin
Sleep Med. 2018;14(4):687–91. Published 2018 Apr 15. https://doi.org/10.5664/jcsm.7074.
https://doi.org/10.1007/s11940- 015- 0361- 6.
https://doi.org/10.1111/pcn.12263.
.
https://doi.org/10.5664/jcsm.7178.
N. A. Walker and B. V. Vaughn
https://doi.

Non-REM Parasomnias
https://t.me/medicina_free
16
379
60. Silber MH, Hansen MR, Girish M. Complex nocturnal visual hallucinations. Sleep Med.
2005;6(4):363–6.
61. Mishra BR, Sarkar S, Mishra S, Mishra A, Praharaj SK, Nizamie SH.Isolated nocturnal audi-
tory hallucinations: a case report. Gen Hosp Psychiatry. 2011;33(5)
genhosppsych.2011.04.008
62. Ohayon MM, Priest RG, Caulet M, Guilleminault C.Hypnagogic and hypnopompic hallucina-
tions: pathological phenomena? Br J Psychiatry. 1996;169(4):459–67.
bjp.169.4.459
63. Harari MD. Nocturnal enuresis. J Paediatr Child Health. 2013;49(4):264–71. https://doi.
org/10.1111/j.1440-
64. Graham KM, Levy JB. Enuresis [published correction appears in Pediatr Rev. 2009
Sep;30(9):369]. Pediatr Rev. 2009;30(5):165–73. https://doi.org/10.1542/pir.30- 5- 165.
65. Kuwertz-Bröking E, von Gontard A. Clinical management of nocturnal enuresis. Pediatr
Nephrol. 2018;33(7):1145–54. https://doi.org/10.1007/s00467- 017- 3778- 1.
66. Singh S, Kaur H, Singh S, Khawaja I. Parasomnias: a comprehensive review. Cureus.
2018;10:e3807. PMID: 30868021.
67. Pressman M, Mahowald M, Schenck C, etal. Alcohol-induced sleepwalking or confusional
arousal as a defense to criminal behavior: a review of scientic evidence, methods and forensic
considerations. J Sleep Rev. 2007;16:198–212.
68. Papadimitriou GN, Linkowski P.Sleep disturbance in anxiety disorders. Int Rev Psychiatry.
2005;17:229–36.
69. Khachiyants N, Trinkle D, Son SJ, Kim KY.Sundown syndrome in persons with dementia: an
update. Psychiatry Investig. 2011;8:275–87.
70. Kushida CA, Littner MR, Morgenthaler T, etal. Practice parameters for the indications for
polysomnography and related procedures: an update for 2005. Sleep. 2005;28:499–521.
71. Schenck CH, Boyd JL, Mahowald MW.A parasomnia overlap disorder involving sleepwalk-
ing, sleep terrors, and REM sleep behavior disorder in 33 polysomnographically conrmed
cases. Sleep. 1997;20:972–81.
72. Proserpio P, Loddo G, Zubler F, Ferini-Strambi L, Licchetta L, Bisulli F, Tinuper P, Agostoni
EC, Bassetti C, Tassi L, Menghi V, Provini F, Nobili L.Polysomnographic features differentiating disorder of arousals from sleep-related hypermotor epilepsy. Sleep. 2019;42(12):zsz166.
73. Foldvary N, Caruso AC, Mascha E, etal. Identifying montages that best detect electrographic
seizure activity during polysomnography. Sleep. 2000;23:221–9.
https://doi.org/10.1016/j.sleep.2005.03.002.
https://doi.org/10.1016/j.
.
https://doi.org/10.1192/
.
1754.2012.02506.x.

Chapter 17
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Rapid Eye Movement Parasomnias
JordanTaylorStandlee andMargaretA.Kay-Stacey
Keywords
sleep paralysis · Nightmare disorder
REM parasomnias · REM sleep behavior disorder · Recurrent isolated
REM Sleep Behavior Disorder
Denition
REM Sleep Behavior Disorder (RBD) is clinically dened as having all of the following: (A) repeated sleep-related vocalizations and/or complex motor behaviors,
(B) the episodes are documented to occur in REM sleep either based on PSG or
clinical history, (C) PSG demonstrates REM sleep without atonia (RSWA), and (D)
the episodes are not better explained by an alternative disorder [1– 3].
Clinical Features
The usual presentation of RBD is dramatic, aggressive physical activity during
sleep. Patients may punch, kick, scream, curse, or even run or fall out of bed. It is
not uncommon for these activities to be associated with injury to the individuals and
bed partners, or to damage to objects around the bedroom. The movements tend to
be brief and can appear purposeful to observers. Bruises, fractures, and even legal
issues can result from these activities. In contrast to NREM parasomnias, it is
J. T. Standlee · M. A. Kay-Stacey (*)
Northwestern University Feinberg School of Medicine, Department of Neurology,
Chicago, IL, USA
e-mail: Jordan.standlee@northwestern.edu; Margaret-stacey@northwestern.edu
M. S. Badr, J. L. Martin (eds.), Essentials of Sleep Medicine,
Respiratory Medicine, https://doi.org/10.1007/978-3-030-93739-3_17
381© Springer Nature Switzerland AG 2022

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uncommon for the behaviors to be elaborate or involve leaving the room, though
relatively complex behaviors have occasionally been described in children and teenagers, and in non-Western populations [4, 5]. When questioned afterward, patients
report vivid dreams that commonly obtain life-threatening, action-lled content. As
a distinction from a confusional arousal, the patient will rapidly reorient upon awakening and have clear recollection of dream content. There is usually no associated
daytime somnolence. As is true with all REM-related conditions, they are much
more common in the middle or latter third of the night, though this may not be the
case in patients with narcolepsy, as those patients often have REM abnormally early
within a sleep period. Frequency of events can be quiet variable, ranging from multiple events per night to one every few months. The onset of symptoms tends to be
gradual and slowly progressive, with usually a long lag between initial symptom
onset and diagnosis. When asked in retrospect, patients often report a gradual prodrome of limb jerking, teeth grinding, or sleep talking for years prior to RBD diagnosis [3, 6–9].
As will be discussed below, there is a strong association between idiopathic RBD
and alpha-synucleinopathies, and RBD is often one of the cardinal prodromal symptoms portending later neurodegeneration. As such, at the point where patients are
diagnosed with RBD, they often have other signs of early alpha-synucleinopathies:
loss of olfaction, chronic constipation, autonomic dysfunction (particularly orthostasis), and impaired visuospatial abilities [2, 10–13].
J. T. Standlee and M. A. Kay-Stacey
Risk Factors
There is a clear association between RBD and neurodegenerative diseases, particularly alpha-synucleinopathies (idiopathic Parkinson disease, dementia with Lewy
bodies, multiple system atrophy), though a huge range of other non-synuclein
degenerative diseases have been implicated including tauopathies like Alzheimer
disease, frontotemporal dementia, and progressive supranuclear palsy; Huntington
disease; amyotrophic lateral sclerosis; myotonic dystrophy; paraneoplastic and
autoimmune encephalitides; and spinal cerebellar ataxia [2, 3, 14–17]. Given the
association of RBD with neurodegenerative disease, it is unsurprising that the strongest risk factor for RBD is older age, particularly age greater than 50 [3], and the
median age of diagnosis is 60–70years old [18]. However, the absence of a comorbid neurodegenerative syndrome should not rule out clinical suspicion for RBD,
since RBD tends to be part of the initial prodrome of the syndrome and can precede
development of further symptoms by up to 50years [19]. Often, the only comorbid
symptoms are anosmia and constipation which, together with RBD, make up the
classic prodrome for alpha-synucleinopathies. A 2019 meta-analysis found that
among patients diagnosed with RBD, at 5-year follow-up, a third (33.5%) had
developed a neurodegenerative disorder, whereas by 14-year follow-up, nearly
everyone (96.6%) had developed one [20]. This nding speaks to both the robust

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association between RBD and neurodegenerative diseases, as well as the relatively
long lag time that can separate the two.
Male sex is another very strong risk factor, though the mechanism for this is
unknown [3]. Some case series report a male-female prevalence of 9:1, though this
is likely inated due to both the fact that women generally express less injurious
dream enactment behaviors, which makes them less likely to seek medical attention,
and that older women often outlive their spouses and therefore do not have a bed
partner to report their symptoms [21]. Other risk factors include the presence of
comorbid psychiatric conditions and antidepressant use, especially in cases where
RBD has a relatively rapid onset [22–24]. Antidepressants of nearly all categories
have been observed to acutely precipitate or exacerbate RBD episodes, including
SSRIs, SNRIs, tricyclic acids (TCAs), monoamine oxidase inhibitors (MAOIs), and
mirtazapine, though notably this has not been seen with bupropion [3, 23, 25, 26].
Further medications which have been implicated include beta-blockers and selegiline, and anticholinesterase inhibitors [3]. PTSD has an association with RBD,
though it is more commonly associated with a different REM parasomnia, nightmare disorder, as discussed in section “Nightmare Disorder”. There is also a clear
association with narcolepsy, primarily narcolepsy type 1 [27]. Up to 50% of patients
with narcolepsy type 1 may demonstrate RBD, though the mechanism for this is
distinct from other causes of RBD, as discussed below. Unfortunately, treatments
aimed at reducing cataplexy in narcolepsy patients, such as TCAs or SNRIs, may
exacerbate RBD symptoms. While patients commonly report dreams with aggressive content, in waking life there is no clear association with aggressive personality
traits; therefore, no particular personality traits are thought to impart risk [28–30].
Traumatic brain injury is a risk factor for all types of parasomnia (both NREM and
REM), with one study estimating new onset of RBD in 8% of TBI patients [31].
Family history is also a risk factor, with one study showing that among patients with
conrmed idiopathic RBD, 14% had a close family member with a history of dream
enactment [32]. Tobacco smokers are also more likely to develop RBD, both among
those with Parkinson disease and among the general population [33, 34].
383
Pathophysiology
While numerous distinct neurodegenerative diseases have all been associated with
RBD, the underlying pathophysiology connecting them appears to be disruption of
the dopaminergic and noradrenergic pathways through the pons, striatum, and frontal lobes, as demonstrated by functional neuroimaging [3, 20, 35–42]. These pathways are integral to normal sleep physiology, involving the usual paralysis of
skeletal muscles during REM sleep. Alpha-synucleinopathies tend to target these
pontine nuclei of sleep early-on, which explains their strong association with
RBD.The exception to this physiology is in narcolepsy, where orexin deciency
from the hypothalamus is the culprit, leading to destabilization of sleep architecture.

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J. T. Standlee and M. A. Kay-Stacey
Epidemiology
Prevalence of RBD in the general population is thought to range from 0.5% to 1%,
though some studies estimate a higher prevalence in the elderly population, around
2% [3, 43, 44]. As discussed above, it is more common in elderly males, though it
has been reported in women, children, and teenagers.
Diagnostic Workup
In-laboratory video polysomnography (PSG) demonstrating REM sleep without
atonia (RSWA) is required for a diagnosis of RBD; this entails capturing REM sleep
with simultaneous capturing of excessive EMG activity on chin or limb leads. When
RSWA occurs in the setting of a clinical complaint of dream enactment, then the
diagnosis of RBD can be made. Practically speaking, when setting up for an RSWA
screen, EMG leads should be placed on upper and lower limbs as well as the chin in
order to increase sensitivity for muscle activity. RSWA tends to occur in all REM
periods throughout the night, though it is often most prominent in latter portions of
the night, when REM sleep is more emphasized. Home sleep apnea testing is not a
useful screen for this condition, as the lack of sleep stage identication prevents an
evaluation of RSWA.
Though there is a strong association between RBD and neurodegenerative diseases, identication of such processes is not necessary for a diagnosis of RBD.As
such, it is not required to send diagnostic tests such as a dopamine transport scan
(DAT) or a neuropsychological battery to evaluate for neurodegeneration, though
these tests could be considered as part of a patient’s larger multidisciplinary care
plan, and would generally be coordinated by a neurologist.
The presence of signicant autonomic activation such as tachycardia during a
behavioral episode should raise a diagnostic red ag because while this does not
rule out RBD, it is uncommon in this condition whereas it is quite common in the
NREM parasomnias associated with arousals. Also, in RBD, general sleep architecture is preserved between wake, NREM, and REM stages, which differentiates it
from status dissociatus (as discussed in 17.1.9).
Differential Diagnosis
Other conditions that can manifest as dramatic sleep-related behaviors are NREM
parasomnias such as sleepwalking and sleep terrors, sleep-related hypermotor epilepsy (SHE), rhythmic movement disorders, and OSA.
To distinguish REM from NREM parasomnias, PSG and clinical history can be
used to elucidate the stage of sleep associated with the behavior. Often the dramatic

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behavior itself is not captured on a single night PSG, so clinical history is relied on
to clarify how early in the sleep cycle the behavior emerges. Typically, NREM parasomnias occur within the rst one-third of the night, and REM parasomnias occur
in the latter two-thirds of the night [3]. Further, RBD is characterized by rapid alertness and orientation, whereas NREM parasomnias may have a prolonged period of
confusion [45]. Individuals with RBD tend to report vivid dream content, whereas
those with NREM parasomnias have at most a fragmentary, limited recall of dream
content. Vocalizations can be seen in both RBD and NREM parasomnias, but those
due to RBD are often loud and feature expletives or aggressive content, whereas
NREM vocalizations more often resemble usual conversation, though this can be
seen in REM as well [45]. NREM parasomnias tend to present in childhood or
young adulthood, whereas REM parasomnias traditionally present in older age,
though as discussed above, there are exceptions in both directions [3].
Sleep-related hypermotor epilepsy (SHE), formerly known as Nocturnal Frontal
Lobe Epilepsy (NFLE), is characterized by recurrent motor behaviors arising from
sleep which can sometimes by dramatic or injurious in nature, similar to RBD.A
key feature to screen for, especially from bed partners who can better describe the
specic motions being performed, is whether the behaviors are stereotyped, as RBD
tends to involve a range of vocalizations and actions, whereas epilepsy-induced
behaviors tend to be a very stereotyped action or set of actions which can occur
more than a dozen times throughout the night [46, 47].
Rhythmic movement disorder tends to be seen in childhood and only rarely
occurs in adults. It consists of rhythmic movement of large muscle groups, such as
body rocking or head-banging during sleep. These movements often occur in developmentally normal children and do not cause harm or distress to the affected individuals. When seen in adults, it may be related to other underlying sleep disorders
such as restless leg syndrome or obstructive sleep apnea.
Periodic limb movements of sleep (PLMS), while also consisting of movements
during sleep, are differentiated from RBD in that they predominantly occur during
NREM and often consist of a stereotyped triple exion of a leg (hip exion, knee
exion, ankle dorsiexion) that can occur frequently through the night around once
per minute [3]. These movements do not have an association with dream content.
Untreated obstructive sleep apnea (OSA) should be considered in any case of
parasomnia, given that it is a common condition that causes fractured sleep, which
can provoke parasomnias. Pseudo-RBD, as it is known, occurs when a patient with
sleep apnea presents with symptoms of RBD. However, the RSWA and dream
enactment are secondary to apneas and hypopneas disrupting REM sleep. Treatment
of OSA with CPAP or other therapies leads to resolution of the RBD symptoms [2].
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Treatment
The predominant goal of all treatment strategies is to prevent injury by reducing the
burden of behavioral events.

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First, clinicians should screen for any factors that may have provoked secondary
RBD and address those triggers. For instance, in cases of OSA-provoked parasomnias, appropriately treating the OSA generally resolves the symptoms [48, 49].
Further, if a medication, such as an antidepressant, is thought to be contributing,
then that medication should be discontinued if possible.
Second, if no provoking factor is identied, then the patient is considered to have
idiopathic primary RBD and warrants symptomatic treatment. Pharmacotherapy is
a mainstay of treatment, though optimizing the sleeping environment to minimize
injuries and property damage should also be part of treatment. For example, walls
should be padded, dangerous or breakable objects should be moved away from the
bed, and bed partners may be counseled to sleep in a separate bed. The primary
pharmacologic agents are melatonin and clonazepam [50, 51]. Both medications
have shown efcacy in reducing or eliminating RBD.Many clinicians prefer melatonin as an initial agent given its favorable side effect prole, especially since clonazepam’s sedating properties can predispose elderly patients to falls, particularly
those with dementia or gait disorders, which is a large portion of the RBD population [51]. There has never been a head-to-head trial between these agents, but clonazepam may be more likely to eliminate symptoms than melatonin, so it is a
reasonable second-line agent if patients do not respond to an adequate melatonin
trial (3–15mg of melatonin).
Other medications which have some evidence suggesting their efcacy toward
RBD include “z-drugs” such as zopiclone, benzodiazepines other than clonazepam,
acetylcholinesterase inhibitors such as donepezil and rivastigmine, carbamazepine,
sodium oxybate, clozapine, pramipexole, levodopa, and paroxetine. Many of these
drugs have only been studied in case reports or limited populations and are rarely
used. However, they could be considered when both melatonin and clonazepam
have been ineffective.
J. T. Standlee and M. A. Kay-Stacey
Subtypes
Status Dissociatus
Status dissociatus is a subtype of RBD where the individual expresses clinical
behaviors suggestive of classic RBD (e.g., aggressive dream enactment), but on
PSG, there is a lack of identiable sleep stages. The PSG has a mixture of markers
for wakefulness, NREM, and REM, without a clear delineation between these
stages. Even more than in classical RBD, individuals with status dissociatus are
often interpreted by observers to be awake when engaging in dream enactment
behaviors, and these individuals may often be confused about whether they are
awake or asleep [3]. If this condition is accompanied by generalized motor overactivity during wakefulness, loss of slow wave sleep, and sympathetic overactivation,
then this would be consistent with a syndrome called “agrypnia excitata” and raises

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concern for an autoimmune/paraneoplastic encephalitis, delirium tremens, or fatal
familial insomnia [3]. The prevalence of this subtype is unknown.
Parasomnia Overlap
Parasomnia overlap disorder refers to patients who meet clinical criteria for RBD
and, in addition, have an NREM-related parasomnia or rhythmic movement disorder. Unlike isolated RBD, overlap syndrome is much more common in younger
ages, often beginning during childhood and adolescence, though any age range
could be affected. The associated pathophysiology is not as clear as with isolated
RBD, and many diverse causes have been implicated, including pharmacotherapies,
substance use, various psychiatric disorders, multiple sclerosis, narcolepsy, and
traumatic brain injury [3]. As with status dissociatus, the prevalence is unknown.
While this disorder may sound like status dissociatus in that REM and NREM conditions are blended, parasomnia overlap disorder does not feature involvement of
the awake state, and affected individuals do not report confusion about whether they
are awake, asleep, or dreaming.
387
Recurrent Isolated Sleep Paralysis
Denition
Recurrent isolated sleep paralysis is dened as (A) a recurrent inability to move the
trunk and all limbs at onset or offset of sleep, (B) the episodes last seconds to minutes, (C) the episodes cause distress, and (D) the episodes are not better explained
by a different medical condition [3].
Clinical Features
Recurrent isolated sleep paralysis is a recurrent distressing sensation of an inability
to move one’s body while transitioning to or from sleep [52, 53]. While it is benign,
it can be associated with signicant anxiety during and after an episode. Affected
individuals are unable to speak or move, though they are fully conscious. Respiratory
muscles are unaffected. These episodes tend to resolve spontaneously within a short
period, usually seconds though it can last up to a few minutes, and sometimes an
episode can be ended early if an observer speaks to or touches the patient. These
episodes are not classied as a disease unless they are associated with signicant
distress to the patient, such as inducing bedtime anxiety or fear of sleep.
Hallucinations often occur, including visual, auditory, or tactile hallucinations such
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