Thomas D. Hurwitz, MD

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Nightmare disorder can produce emotional manifestations of fear, anger, and sadness. Here are 7 reasons parasomnias can challenge even the most astute diagnostician.

7 Things to Know About Parasomnias

Parasomnias are undesirable physical, experiential, or behavioral phenomena that occur exclusively during sleep onset, during sleep, or during arousals from sleep. Their manifestations may be easily confused with psychiatric disorders when bizarre motor and/or emotional behavior is mistakenly interpreted as symptomatic of waking aberrance. For some, there may be associations with psychiatric disorders, their treatments, and/or their contribution to predisposition.

In DSM-5, the parasomnias are non–rapid eye movement (NREM) sleep arousal disorders (sleepwalking, sleep terror types), nightmare disorder (formerly known as dream anxiety disorder), and rapid eye movement (REM) sleep behavior disorder (RBD). (Interested readers may refer to the International Classification of Sleep Disorders, third edition, which describes parasomnias in more detail.

Underlying the various parasomnias is the fact that NREM sleep, REM sleep, and wakefulness are not mutually exclusive. Behavioral and electrophysiological components of each may separate and recombine in aberrant ways. For example, when concurrent components of NREM sleep and wakefulness occur, there may be variable juxtapositions or oscillations of consciousness, memory, motor, and/or autonomic activation that result in sleepwalking and sleep terrors. Similarly, complex dream enactment behavior can be liberated during spells of RBD in persons with skeletal muscle atonia.

Although not specified in DSM-5, the simplest of the disorders of arousal is confusional, hence disordered, arousal, which is partial awakening with periods of apparent confusion and inappropriate or absent responsiveness to others while in bed. There is typically amnesia for the event and minimal or no recall of dream mentation. This can evolve into spells including intense autonomic activation with vocalization, tachycardia, tachypnea, mydriasis, diaphoresis, and sleep terrors or sleepwalking.

A recent study found that confusional arousals occurred in 15.2% of a large community sample, and more than half reported at least one episode every week.

 Participants who reported confusional arousal had significant associated mood disorders, alcohol use disorders, panic disorder, PTSD, and generalized anxiety disorder, although no causal relationship was established. Of those who reported confusional arousal, 31.3% were taking a psychotropic drug, mostly an antidepressant. A smaller association was seen with hypnotic, anxiolytic, anticonvulsant, and antipsychotic agents. Other epidemiological evidence suggests some association between sleepwalking, major depression, and obsessive-compulsive disorder, although again with no established causal relationship.

 Generally, there is no need for interventions when confusional arousal occurs in the absence of other sleep disorders, such as obstructive sleep apnea, and without vigorous vocalization or motor activation.

An interesting variant of sleepwalking is sleep-related eating disorder, with episodes of eating during behavioral arousal from sleep without hunger or clearly established wakefulness. These eating episodes typically involve high-carbohydrate and fatty foods, often those that are not ordinarily consumed or toxic; binging is common. Psychiatrists must query patients receiving MAOIs and their families because of the risk of possible hypertensive crisis. Sleep-related eating disorder, in most cases, is distinct from the night eating syndrome, which is distinguished by evening hyperphagia with fully wakeful nocturnal eating.

Another variant of confusional arousals and sleepwalking is sleep-related abnormal sexual behavior (also designated “sleepsex,” “sexsomnia,” and “atypical sexual behaviors in sleep”). Most published cases involve young men with histories of sleepwalking and sleep terrors. Pharmacotherapy (eg, bedtime off-label use of clonazepam) is typically reserved for recalcitrant patients.

Substance-/medication- induced sleep disorder

Parasomnias resembling disorders of arousal can be related to the use of many psychotropic drugs, in particular sedative-hypnotics. Sleepwalking and other amnestic complex sleep-related behaviors have been reported among psychiatric patients taking benzodiazepines. Behaviors can be prolonged and include amnestic nocturnal eating, sexual activity, and even sleep driving. In particular, the hypnotics with short duration of action seem to be associated with these phenomena, whereas longer-duration benzodiazepines tend to suppress them. It is likely that the drugs dull the transition between sleep and wakefulness, permitting behavior unconstrained by executive function in susceptible individuals.

Other drugs associated with sleepwalking and sleep terrors include neuroleptics, such as olanzapine and quetiapine; antidepressants, such as paroxetine, reboxetine, and bupropion; mood stabilizers and antiepileptics, such as lithium, topiramate, and valproic acid combined with zolpidem; stimulants; antihistamines, often in various combinations; metoprolol; and fluoroquinolone.

An interesting subset of this category is sleepwalking with sleep- related eating disorder triggered by sedating agents in the presence of restless legs syndrome, which may be a predisposing factor. The most common offending medications include benzodiazepines-zolpidem in particular. Restless legs syndrome may also occasionally present in patients who are taking TCAs, anticholinergics, lithium, triazolam, olanzapine, or risperidone.

Sleepwalking and sleep terrors are treated when they pose risk of injury or prominent disturbed sleep or daytime wakefulness. Treatments include pharmacotherapy-usually long-duration benzodiazepines-and nonpharmacological therapy, such as clinical hypnosis. All drugs to treat these disorders are used off-label.

The first step in treatment is to identify and treat comorbid sleep disorders-in particular, restless legs syndrome and obstructive sleep apnea. Effective therapies for sleep- related eating disorder, such as dopamine agonists and levodopa, are often also used for restless legs syndrome. Codeine combined with clonazepam and combinations of dopaminergic agents with bupropion and trazodone have also been effective. Topiramate monotherapy was found to be effective for suppressing nocturnal eating in patients with sleep-related eating disorder.

Formerly termed “dream anxiety attacks,” nightmare disorder is now recognized as an REM sleep phenomenon, distinct from NREM sleep terrors. As defined in DSM-5, this includes repetitive, extended, extremely dysphoric, and well-recalled dreams that involve threats to survival, security, or physical integrity; episodes usually occur during the second half of the sleep period. Typically, the individual becomes rapidly alert and oriented. Emotional manifestations of fear, anger, and sadness may predominate.

Nightmares occur in 5% to 8% of adults, more commonly women, and individuals with type A personal- ity characteristics. They can be induced by a number of drugs, including antidepressants and neurolep-tics, amantadine, lisuride, clonidine, methyldopa, reserpine, ciprofloxacin, donepezil, and amiodarone. Dopaminergic antiparkinsonian drugs and lipophilic Ã-adrenergic blockers are particularly notable for inducing nightmares. Conversely, withdrawal from REM-suppressing agents, such as TCAs, MAOIs, clonidine, alcohol, and amphetamines, may cause nightmares as a result of REM sleep rebound. Nightmares commonly occur following traumatic experiences, and occasional psychotic episodes may be heralded by their occurrence.

Psychotherapy includes imagery rehearsal therapy.

 A dream scenario is restructured into a more acceptable experience by rewriting the script as a wakeful exercise-lucid dreaming. Pharmacotherapy, based on experience with PTSD, includes cyproheptadine and prazosin.

RBD occurs most frequently in older men and typically involves a prolonged, chronic course. For about 25% of patients, there is a prodromal period with increased action-packed dream content along with vocalization and limb jerking that can progress over several years. As RBD becomes established, there is a tendency for abrupt, often violent movement concordant with recalled dream content, which is much more vivid than with sleepwalking/sleep terrors. This is related to the intensity of mentation and the low arousal threshold of REM compared with NREM sleep.

Patients typically dream of themselves as defenders, rarely as aggressors. Violent dream enactment can result in injury to the patient and/or bed partner whose presence is often incorporated into the dream content. RBD spells are likely to occur during the latter part of the night, when REM sleep tends to be more prolonged and intense, in contrast to sleepwalking/sleep terrors, which occurs earlier in the course of the night, when deeper stage N3 sleep is more likely.

Overnight polysomnography in a sleep laboratory confirms the diagnosis with fluctuating levels of electromyographic tone and limb movement during REM sleep. The loss of skeletal muscle atonia is the key to diagnosis. Over many years of longitudinal observation, it has become clear that idiopathic RBD is an early manifestation of what is likely to emerge later as a neurodegenerative disorder in the family of synucleinopathies, such as Parkinson disease, Lewy body dementia, or multisystem atrophy.

RBD is becoming more frequent in younger individuals and in women, because of its relationship with the use of antidepressant drugs that can cause REM sleep without atonia and, in some cases, frank dream- enactment behavior. This creates ambiguity because the diagnostic criteria technically disallow a diagnosis of RBD if the symptoms are attributable to drug effect. It is suspected, but not yet confirmed, that this form of the parasomnia carries similar risk of neurodegenerative disorders.

Because most RBD is disruptive and includes a threat of serious injury, therapy is usually indicated, typically with clonazepam. However, melatonin has become a frequently used alternative agent. Providing a bed alarm recording of a familiar voice as episodes of RBD start has been shown to modify the extent and intensity of behaviors.

Sleep paralysis is essentially the atonia of REM sleep that has become dissociated and occurs at times other than the typical periods of REM sleep during the night. It can either intrude at sleep onset or persist into awakening at sleep offset, and it is often experienced as discomforting or frightening. It is classically found in association with narcolepsy, but not exclusively. Lifetime prevalence of isolated sleep paralysis appears to be 2.3% to 40%, depending on the population under study. Unless the history includes hypersomnia or cataplexy, there is no need for polysomnography. Treatment is usually unnecessary unless there is significant sleep disruption of subjective distress. In that case, an REM-suppressing agent, such as fluoxetine or imipramine, may be indicated.

Sleep-related events not specified in DSM-5

Up to 69% of individuals with panic disorder have had a sleep-related panic attack, and 33% report recurrent sleep-related spells.

 Clinical features of nocturnal spells resemble those of diurnal attacks. They arouse the patient, who rapidly achieves full wakefulness with anxiety, difficulty in returning to sleep, and full recall of the events. Diagnostic caution must be emphasized because of the myriad other disorders that can masquerade as nocturnal panic, such as sleepwalking/sleep terrors, RBD, seizures, gastroesophageal reflux, obstructive sleep apnea, bruxism, nocturnal asthma, and nocturnal cardiac arrhythmias.

Dissociative disorders may also occur during sleep, typically in individuals with daytime syndromes such as dissociative identity disorder and dissociative amnesia. In one report, 6 of 21 patients (28.5%) with daytime dissociative disorders had nocturnal dissociative episodes, and 2 of them showed a clear transition to an alter personality.

 The nocturnal behaviors resemble sleepwalking/sleep terrors or RBD that can be prolonged, often with amnesia. If observed in the sleep laboratory, these complex, lengthy, and repetitive behaviors are clearly seen to follow the development of electroencephalographically documented wakefulness in spite of no obvious behavioral awakening. Therapy is typically that which would be provided for wakeful dissociative disorder.

Sleep disturbances have figured prominently in descriptions of PTSD. These include initial insomnia; sleep discontinuity with increased arousal; limb movements; night terrors; nightmares; and even purposeful behavior, which can result in injury to a bed partner when a threat is perceived. PTSD nightmares tend to occur less frequently in the laboratory than in the naturalistic environment. They can occur during REM and NREM sleep and tend to be recurrent, usually with imagery recalling the traumatic event.

There appears to be no definitive, descriptive, polysomnographic pattern that characterizes PTSD. Patients often sleep well in the laboratory, without nightmares or behavioral spells. Motor activation during REM sleep that suggests the possibility of RBD was reported in only 2 cases.

 Repetitive body movements seen in other stages may resemble those seen in non-PTSD patients with sleepwalking/sleep terrors and rhythmic movement disorder. It is important to rule out other distinct sleep disorders in these patients.

A striking finding in the PTSD sleep literature is the elevation of auditory arousal thresholds in affected persons during NREM as well as REM sleep. Kramer

 interprets these findings as evidence that in chronic PTSD there is a heightened responsiveness to internal events while individuals are less arousable by external stimuli. Increased depth of sleep may represent a chronic adaptation to trauma. Consistent with this idea, Kaminer and Lavie

 describe diminished dream recall of more resilient Holocaust survivors. The common subjective sleep complaints of patients may reflect a breakdown of this adaptation but with enough resilience to allow intact sleep in a safe, neutral environment such as a sleep laboratory.

Other rare but relevant disorders with sleep-related manifestations that can confound psychiatrists include sleep-related epilepsy, which should be considered for any sleep-related behavior that is recurrent, inappropriate and, most importantly, stereotyped. Exploding head syndrome is a sudden sensation of a loud noise or a violent, though painless “explosion” in the head occurring as the affected person is falling asleep or waking during the night. It is a rare, benign but frightening event during the transition between wake and sleep. Sleep-related hallucinations can be related to narcolepsy, Ã-adrenergic receptor blocking medications, dementia with Lewy bodies, visual loss (Charles Bonnet hallucinations), and other brain pathology (peduncular hallucinosis).

Dr Hurwitz is Director of Sleep Medicine in the Mental Health Service Line at the Minneapolis Veterans Affairs Health Care System and Assistant Professor of Psychiatry at the University of Minnesota Medical School in Minneapolis. Dr Schenck is Professor of Psychiatry at the University of Minnesota Medical School and staff psychiatrist at the Minnesota Regional Sleep Disorders Center at Hennepin County Medical Center in Minneapolis. Dr Khawaja is Associate Professor of Neurology at the University of Minnesota Medical School and Medical Director at the Minnesota Regional Sleep Disorders Center. The authors report no conflicts of interest concerning the subject matter of this article.

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Articles

Here's an update on parasomnias-the undesirable physical, experiential, or behavioral phenomena that occur exclusively during sleep onset, during sleep, or during arousals from sleep.

Thomas D. Hurwitz, MD

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