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as a sensation of a creature sitting on the individual’s chest. The condition often
presents in adolescence, with mean age of onset 14–17years old, and most episodes
occur in patient’s teens and 20s [3].
J. T. Standlee and M. A. Kay-Stacey
Risk Factors
A familial form of sleep paralysis has been reported in two families, suggesting that
underlying genetics may play a role; however, most cases do not have a clear familial component. Male and female sexes appear to have equal risk. As with all parasomnias, sleep deprivation and irregular sleep cycles are risk factors [54]. Patients
who sleep supine appear to be at higher risk, though the mechanism for this is not
understood. One case has been reported of isolated sleep paralysis induced by the
abrupt withdrawal of bupropion [55]. As with all parasomnias, psychiatric disease
is a risk factor [24].
Pathophysiology
Like narcolepsy, isolated sleep paralysis is thought to occur from a state dissociation, with the normal expected REM paralysis of skeletal muscles continuing abnormally into wakefulness. Brainstem systems that control serotonin, norepinephrine,
and acetylcholine appear to be affected. Individuals who are sensitive to sleep disruptions may be particularly vulnerable, and abrupt awakenings from REM may
produce an episode [3].
Epidemiology
There are limited global data on the prevalence of recurrent isolated sleep paralysis,
partially due to the various denitions that have been used. When examining for
single occurrences of isolated sleep paralysis, prevalence may range from 5% to
40% [3, 56].
Diagnostic Workup
A polysomnogram (PSG) is not required for diagnosis, and subjective history can be
sufcient. A PSG may be supportive if it demonstrates REM atonia on EMG leads
that persists into wakefulness.
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389
Differential Diagnosis
The primary disease to consider is narcolepsy, which also often includes sleep
paralysis episodes and hypnagogic and/or hypnopompic hallucinations. However,
the prominent features of narcolepsy are extreme daytime somnolence and reduced
mean sleep latency time, whereas these features are absent from recurrent isolated
sleep paralysis. Another related phenomenon, cataplexy, also involves REM atonia
invading the awake state, though it occurs during full wakefulness rather than at
periods of transition to and from sleep; cataplexy also tends to be triggered by
intense emotions, whereas sleep paralysis does not. Similar to cataplexy, atonic
seizures can involve preserved consciousness with inability to move limbs, but
atonic seizures occur during wakefulness rather than only at times of sleep transition.
Periodic paralysis syndromes may resemble isolated sleep paralysis in that the
affected individual is conscious but unable to move the body. These episodes may
occur during wakefulness or at periods of sleep transition; if the latter is the case,
the primary way to differentiate these syndromes from isolated sleep paralysis is
that periodic paralysis lasts for hours rather than seconds. Periodic paralysis is also
less likely to affect bulbar muscles the way sleep paralysis can. These periodic
paralysis syndromes include a hypokalemic, hyperkalemic, and thyrotoxic form,
and involve mutations in skeletal muscle ions channels. Paralysis attacks can be
precipitated by a large intake of carbohydrates, excessive exercise, or alcohol intake.
Most cases of periodic paralysis are hereditary with an autosomal dominant inheritance [57].
Treatment
If sleep deprivation is thought to be a provoking factor, then that component can be
addressed, such as avoiding shift work, addressing jet lag, or other general sleep
hygiene components. Further pharmacotherapy options include tricyclic antidepressants (e.g., imipramine and clomipramine) or SSRIs (e.g., uoxetine or escitalopram), all of which are thought to work by suppressing REM [58, 59].
Nightmare Disorder
Denition
Nightmare disorder is dened as (A) repeated, extended, well-remembered dreams
associated with intensely unpleasant emotions, (B) rapid, full alertness on awakening, and (C) associated distress or impairment in functioning [3].
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J. T. Standlee and M. A. Kay-Stacey
Clinical Features
Nightmares entail a realistic and vivid dream sequence that tends to become increasingly frightening, though other negative emotions can be predominant such as
anger, disgust, guilt, or embarrassment. There is often a theme of imminent bodily
harm, though this is not universally true. On awakening, affected individuals are
quickly oriented, and can vividly recall dream content. There is often difculty
returning to sleep after an episode, and individuals may note signs of increased
sympathetic activity such as rapid heart rate or piloerection. These episodes tend to
occur in the latter third of a sleep session, as this is when REM sleep is most prominent. Nightmares associated with PTSD may be more variable in their timing within
a sleep cycle, and can occur at sleep onset or from NREM sleep [3].
While occasional nightmares are quite common among the general population, a
diagnosis of nightmare disorder is only made if these occurrences are persistent and
affect a person’s daily functioning. Distress can be manifested by any of the following: mood disturbances, sleep resistance, cognitive impairment such as concentration difculties, negative impact on family functioning, behavioral disturbances,
daytime somnolence, low energy, impairment in one’s education or occupation, or
impaired social function [3].
Risk Factors
The greatest risk factor for nightmare disorder is exposure to severe psychosocial
stressors. This is particularly true in children, though in all age groups there is an
association between physical or sexual abuse and nightmares. Trauma often precedes the onset of nightmares, though there may be a prolonged delay prior to nightmare onset. In acute stress disorder, symptoms occur immediately after a trauma,
whereas in posttraumatic stress disorder, symptoms may arise more than a month
after the event [3, 60].
Individuals who had recurrent nightmares as children are more likely to report
recurrent nightmares as an adult, suggesting that predisposition to nightmares may
be a component of one’s personality traits. Twin studies also demonstrate that there
are genetic predispositions to nightmares, analogous to the pattern seen with NREM
parasomnias such as sleepwalking and sleep talking [61].
Nightmares can be induced by pharmaceuticals that affect neurotransmitter concentrations and function, particularly for serotonin, dopamine, and norepinephrine
[62, 63]. Medications of interest include antidepressants of all classes; antihypertensive agents including beta-blockers and calcium channel blockers; dopaminergic
drugs including levodopa and methylphenidate; atypical antipsychotics including
risperidone and olanzapine; sedatives including alcohol and barbiturates (particularly withdrawal from these); acetylcholinesterase inhibitors, including donepezil
and rivastigmine; and varenicline, which is a nicotinic acetylcholine receptor
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antagonist. Another class of implicated medications is antimicrobials (e.g., ciprooxacin, ganciclovir, and meoquine) which, in contrast to the above list, are
thought to act via modulation of cytokines that are involved in sleep such as IL-1B
and TNF-alpha. Implicated medical conditions include hypoglycemia induced by
nocturnal insulin use [64], as well as all mood disorders including major depression,
bipolar affective disorder, and schizoaffective disorder [24, 65]. As with all parasomnias, sleep deprivation and OSA can be a predisposing factor [66].
391
Pathophysiology
The pathophysiology of nightmares is not known.
Epidemiology
Occasional nightmares occur in 60–75% of children, and in most cases these nightmares are sporadic. Only in a small minority of children are nightmares frequent
and extensive, occurring in 1–5% of children [3]. Among the general population,
2–8% report distress related to nightmares, and the age most likely to be affected is
between 6 and 10years old [67–69]. However, the incidence is increased among
adults with psychopathology, most notable among those with PTSD where 80%
report recurrent nightmares.
Diagnostic Workup
Patient history is sufcient for diagnosis of nightmare disorder, and further PSG
evaluation is not required [70]. However, it may be considered if during the patients’
nightmares they perform actions that either cause harm to self or others, or are
highly stereotyped in nature, as this would raise clinical suspicion for other conditions, as described below.
Differential Diagnosis
The main conditions to distinguish from nightmare disorder are sleep terrors, nocturnal panic attacks, seizures, RBD, and sleep paralysis.
Sleep terrors also involve an awakening from sleep with appearance of distress.
However, with sleep terrors there is a prominent component of confusion and disorientation, which is not seen with nightmares. Further, in sleep terrors there is a
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lack of recall of dream content, whereas dream recall tends to be vivid with nightmares. Prominent autonomic activity (e.g., diaphoresis, pupillary dilatation) is more
common with sleep terrors than nightmares. As sleep terrors arise from NREM
sleep, they tend to occur earlier in the night, while nightmares occur later in the
night. Similarly, nocturnal panic attacks tend to arise from NREM sleep, occurring
earlier in the night and are not typically associated with vivid dream content.
Nocturnal seizures can, in rare cases, present only with recurrent nightmares
[71]. These can be difcult to distinguish from true nightmares by history, though
suspicion should be raised in patients with underlying cerebral disease or a history
of epilepsy. Nightmares from epilepsy are more likely to resemble classic temporal
lobe auras, such as déjà vu or intense panic without any associated dream content to
induce the fear. These episodes come from NREM sleep rather than true REM sleep.
A PSG, preferably with an extended EEG montage, is required to capture and prove
that episodes are epileptic in nature.
REM sleep behavior disorder (RBD), as discussed in section “REM Sleep
Behavior DisorderS30”, involves involuntary acting out of dream content, much of
which tends to involve frightening and life-threatening situations. While the dream
content can be analogous between these two conditions, nightmare disorder does
not involve any physical action, movement, or injury, so the presence of these would
be strongly suggestive of RBD.RBD is most common in older age, whereas nightmare disorder is most common in childhood, though there are exceptions in both
directions, as discussed above.
Sleep paralysis, whether occurring as part of isolated recurrent sleep paralysis
(see section “Recurrent Isolated Sleep Paralysis”) or narcolepsy, occurs at periods
of transition to or from sleep and can often be associated with anxiety during the
episode. Hallucinations commonly co-occur and can be disturbing in nature. While
nightmares can occasionally involve an inability to move or speak, a recurrent experience of total paralysis with simultaneous wakefulness is much more suggestive of
sleep paralysis.
J. T. Standlee and M. A. Kay-Stacey
Treatment
Nightmares on their own do not necessitate treatment, as they can often be selflimited. In particular, nightmares occurring in the context of recent bereavement
tend to resolve over time [72]. For those patients who do require treatment, the next
step is to address general sleep hygiene and any predisposing medications or medical conditions. When this approach is insufcient, then a choice or combination
between cognitive behavioral therapy (CBT) and pharmacotherapy can be
employed [73].
CBT interventions for nightmare disorder emphasize stress management and
repeated exposures [74]. As with other forms of CBT, it consists of a limited set of
therapy sessions, aimed at addressing the maladaptive thoughts, emotions, and
behaviors that disrupt patients’ lives. One option is image rehearsal therapy, where
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patients recall the nightmare while awake, write down its details including emotional content, modify the story to have a more positive ending, and then rehearse
the new narrative with the goal of replacing the nightmare if the dream recurs [73,
75, 76]. Another option is lucid dreaming treatment, where the patient is taught to
identify that they are dreaming during a nightmare and then actively change the ending of the nightmare to a positive one [77]. Hypnosis has also been shown in small
case studies to be effective in decreasing nightmare frequency [78]. Finally, systemic desensitization, where patients are gradually exposed to cues associated with
their nightmares and taught stress management techniques, can be used [79].
The best-studied pharmacotherapy option is prazosin, which is a centrally active
alpha1-adrenergic antagonist, and has been well-described to be effective in both
PTSD and other nightmare disorders [73, 80–83]. It is thought to act via blunting of
the sympathetic arousal state associated with nightmares. The only other medications recommended by the American Academy of Sleep Medicine (AASM) are triazepam and nitrazolam [84]. If these medications are ineffective or not tolerated,
then there are many other options, which have primarily been studied in the context
of PTSD nightmares: topiramate [85, 86], trazodone [87], risperidone [87], gabapentin [73, 88], olanzapine [89, 90], clonidine [73], aripiprazole [84], cyproheptadine [84], phenelzine [84], tricyclic antidepressants [84], and synthetic cannabinoids
[91, 92]. Two medications which the AASM specically recommends against using
are venlafaxine and clonazepam, as the limited studies looking at these two have
shown no efcacy [84]. Once a patient has attained prolonged relief from nightmares, pharmacotherapy can be tapered off.
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