Clinical manifestations

Presentation and course

Sleepwalking presents with amnestic ambulation and impaired consciousness following an arousal from sleep. As disorders of arousal emanate from deep NREM (N3) sleep, most episodes are noted in the first half of the night. The sleepwalker is usually able to navigate obstacles without difficulty and the eyes are open. The frequency of somnambulism ranges from once every few years to multiple nightly events. There is often childhood history of parasomnias, including night terrors, confusional arousals, as well as sleepwalking (01).

Sleepwalking episodes may end within moments or continue as prolonged episodes lasting an hour or longer (05). Behaviors are typically benign and may include such things as placing a phone in the freezer or moving a bicycle to the living room. The somnambulist is typically unresponsive to redirection. Occasionally, potentially injurious activities, such as walking off a balcony or operating a motor vehicle, may occur (61). Prolonged sleepwalking behaviors are often associated with sedative-hypnotic medication, particularly in the setting of restless legs syndrome (see pathogenesis and pathophysiology) (33). Patients often adopt measures to prevent sleep-related injury, such as locking bedroom doors (33; 01).

Sleepwalking with dysfunctional amnestic eating, often binge-like, is referred to as sleep-related eating disorder. Patients with sleep-related eating disorder will suffer consequences such as weight gain and painful abdominal distension. Of note, less dysfunctional eating that does not meet sleep-related eating disorder criteria is often reported in sleepwalking patients (07). This suggests that sleepwalking and sleep-related eating disorder are not necessarily distinct disorders, but instead that eating is a common nocturnal phenomenon existing on a spectrum with various degrees of caloric intake.

Sleepwalkers typically have only modest impairment in daytime function. Although they often describe fatigue and sleepiness, objective measures have not demonstrated a greater propensity to sleep in the daytime compared to controls (50). After sleep deprivation, sleepwalking patients have poor inhibitory control (an executive function) in comparison to control subjects (46). However, sleep-related verbal memory consolidation is not impaired in sleepwalkers despite having fragmented slow-wave sleep, a state previously correlated with declarative memory tasks (78).

Prognosis and complications

The vast majority of sleepwalking behaviors are benign, and the episodes are self-limited. In children, sleepwalking behaviors typically diminish in frequency or resolve by adolescence. In adults, complications mainly emanate from associated disorders such as obstructive sleep apnea and restless legs syndrome. However, sleep-related injuries might occur, especially with prolonged events due to sedative agents (73). Violence has been noted to be more frequent in males and in cases of childhood-onset sleepwalking as compared to adult-onset (45% for self-injury and 44% for violent behavior versus 33% and 29%, respectively) (06). A sleepwalking fatality was reported after a patient fell into a water tank and drowned (80). Sleepwalking and complex behaviors associated with the use of sedative-hypnotic drugs such as zolpidem can result in serious injuries including death (27).

Clinical vignette

A 38-year-old male presented to the sleep center with his wife, who described a two-month history of unconscious nocturnal wandering. About one to two hours after falling asleep, he would rise from bed and walk downstairs. She would find him engaged in a variety of behaviors that appeared purposeless. On one occasion, she found him staring at a television that was off. Another time, she found him in the kitchen preparing, but not eating, a sandwich made from bread and ice cream. One week prior to the presentation, she was alarmed to find him sitting in the car outside their house struggling to put the keys into the ignition. This event prompted an emergency referral from his primary care physician. These events were the first parasomniac behaviors the patient had experienced since childhood, when he had several episodes of sleepwalking and sleep terrors.

The patient was in good health, except for a longstanding difficulty initiating sleep. Two months prior to consultation, he had sought and been prescribed a sedative-hypnotic medication, zolpidem. On further history, the patient claimed that his inability to sleep was related to never feeling comfortable in bed. He described an uncomfortable sensation in his body that could not be further characterized. This discomfort compelled him to move, and movement relieved the symptoms, although only momentarily.

Polysomnography after 24 hours of sleep deprivation and an auditory alarm during N3 sleep demonstrated a confusional arousal with attempted ambulation (not successful due to restraint from the polysomnography wires). Immediately prior to the episode the patient had a 10-second burst of synchronous slow-wave (delta) activity noted on electroencephalography. No other abnormalities, such as sleep-disordered breathing or periodic limb movement events, were noted.

The patient was diagnosed and treated for restless legs syndrome. Zolpidem was discontinued, and the patient was prescribed gabapentin 300 mg, which resolved restless legs syndrome and difficulty with sleep initiation. No further sleepwalking episodes were reported at a 6-month follow-up.

Biological basis

Etiology and pathogenesis

Sleepwalking arises when a patient predisposed to ambulation has an incomplete arousal from N3 sleep (25; 67). Disorders that fragment sleep or promote the homeostatic sleep drive lead to impaired cortical arousal (65). One high-risk pathology is obstructive sleep apnea, which both fragments sleep and increases sleep drive (06).

Somnambulism peaks in frequency between the ages of eight and 12 years, with most cases spontaneously resolving. This apex is likely related to the intensity of the slow-wave sleep prior to adolescence (64).

Importantly, sleep is not a homogenous state of unconsciousness, but is instead characterized by routine arousals. These include ultradian awakenings every 90 minutes as well as the more frequent, every 30 to 90 seconds arousals of the cyclic alternating pattern. During a normal transition from NREM sleep to wakefulness, consciousness emerges quickly, typically within seconds. Whether an arousal will progress to full alertness, recede to NREM sleep, or pathologically result in a disorder of arousal depends on an intricate combination of variables, including duration of prior wakefulness, current sleep duration, depth of NREM sleep, circadian rhythm phase, effects of sedating or stimulating medications, presence of comorbid sleep disorders, as well as multiple environmental factors (60). Activating neurons in the brainstem and basal forebrain promote wakefulness through direct activation of the cerebral cortex and by inhibiting thalamic reticular neurons, blocking spindle oscillations. These alerting phenomena normally lead to suppression of slow-wave activity and more predominant fast cortical activity consistent with wakefulness.

Disorders of arousal occur when the cortex incompletely activates from deep NREM sleep. Pressman’s “3P model” suggests that predisposed patients are primed by conditions that impair normal arousal. Parasomnias are then subsequently precipitated by events that lead to sudden wakefulness (67). Priming factors include sleep deprivation and sedative medications (76). Precipitators can be internal pathologies (eg, sleep-disordered breathing) or external factors (eg, noise) (25; 65).

Changes in slow-wave activity immediately preceding sleepwalking episodes provide further evidence of impaired arousal during sleepwalking. A spike in slow-wave activity is often noted on electroencephalography immediately preceding a disordered arousal (63). In tandem, there is a fast activation of EEG in the regions of the motor cortex (42). These findings are not noted among control subjects when they wake from sleep, nor is it seen when sleepwalkers have a normal, no disoriented arousal from sleep (41; 63). It has been speculated that cortical neurons, having received an internal stimulus, attempt to block the arousal by increasing the density of slow-wave activity. Ultimately, the internal stimulus partially overcomes the brain’s attempt to maintain sleep, awakening the individual in a disoriented state and leading to sleepwalking (25; 63; 40).

Scalp EEG analysis of patients of disorders of arousal including sleepwalking has shown decrease in slow-wave activity in centroparietal region specifically cingulate, motor, and sensorimotor associative cortices (10). An EEG connectivity study of sleepwalkers demonstrated coexistence of arousal and deep sleep brain processes immediately preceding a somnambulistic episode (18). The spectral analysis revealed in the 20 seconds preceding a sleep-walking episode the following findings: (1) decreased delta EEG functional connectivity in parietal and occipital regions, (2) increased alpha connectivity over fronto-parietal network, and (3) increased beta connectivity involving symmetric inter-hemispheric networks (18). Another study revealed changes in K-complexes in N2 sleep in pediatric cases (70). A single-photon emission computed tomography study revealed decreased regional cerebral perfusion in frontal and parietal areas in sleepwalkers as compared to controls. Also reduced perfusion in the dorsolateral prefrontal cortex and insula during recovery. Slow-wave sleep is consistent with the clinical features of impaired consciousness and reduced pain perception noted in somnambulistic episodes (17).

Although much is known about priming and precipitating causes, we have only modest insight into which patients are predisposed to NREM parasomnias. There is a genetic component, as sleepwalking runs in families. A longitudinal study demonstrated that although only 22.5% of children without a family history of sleepwalking will sleepwalk, among children with two sleepwalking parents 61.5% sleepwalk themselves (64). One study has identified a gene for sleepwalking on chromosome 20q12-q13.12 (47; 32). High prevalence (41%) of the HLA DQB1*05:01 genotype has been noted in disorders of arousal including somnambulism (29). However, little is known about the mechanisms driving behavioral expression. For example, why do some patients sleepwalk and others only have only confusional arousals? The presence or absence of underlying motor restlessness, such as that seen in restless legs syndrome, may explain why some patients ambulate after an incomplete arousal from sleep (sleepwalking) and others do not (confusional arousal alone) (33; 33).

Restless legs syndrome and medication-induced sleepwalking. Many cases of NREM parasomnias, particularly sleepwalkers who eat (sleep-related eating disorder), are driven by restless legs syndrome. This relationship is most notable when patients are misdiagnosed with psychophysiological insomnia (34).

Restless legs syndrome is common, 8% to 10% of the adult population, and easily mistaken for psychophysiological insomnia (01; 33). The commonly prescribed GABA agents and opioid analgesics will obscure the diagnosis by masking symptoms. Hence, it is not unexpected that many patients with restless legs syndrome will be mistakenly treated with therapies developed for psychophysiological insomnia, such as benzodiazepine receptor agonists (33).

In addition to the classical symptoms of motor restlessness, restless legs syndrome is characterized by various non-motor nocturnal urges (68). Wakeful evening and nocturnal (after an arousal from sleep, but prior to final morning awakening) eating is common (60%) in restless legs syndrome, and the feeding behavior closely resembles motor activity. This means, like the compulsion to move, restless legs syndrome patients will describe an urge to eat, not driven by hunger, but instead by the perception that eating will allow for sleep initiation (33). This restless eating is unique to restless legs syndrome. For example, patients with psychophysiological insomnia do not frequently eat at night (33). Notably, Ekbom described nocturnal eating in his original 1960 paper defining restless legs syndrome (21).

To summarize, as patients with restless legs syndrome are predisposed to ambulation and eating, it is expected that parasomnias characterized by walking (sleepwalking) or eating (sleep-related eating disorder) would emerge when primed with a sedative agent that impairs memory and executive function (53). Studies have confirmed this. Among patients with restless legs syndrome who have been treated with sedative-hypnotic agents, a high incidence of sleepwalking and sleep-related eating disorder has been noted. In one investigation, 80% of restless legs syndrome patients that had been exposed to sedative-hypnotic agents had subsequent sleepwalking or amnestic sleep-related eating disorder (33). Conversely, zolpidem-induced NREM parasomnias are rare when prescribed to patients with psychophysiological insomnia, less than 1% in clinical trials where restless legs syndrome is carefully excluded (31).

Some studies have helped explore the CNS pathogenesis of sleepwalking. A neuroimaging study revealed decreased cerebral blood flow in the region of the inferior temporal gyrus among sleepwalkers after a night of sleep deprivation compared to controls (15). Patients with parasomnias (both sleepwalking as well as those with nightmares) demonstrate changes in exploratory excitability while awake, consistent with changes in the mesolimbic dopaminergic system (62). Another technique, transcranial magnetic stimulation, provides a method of evaluating the excitability of the motor cortex, and preliminary findings demonstrate that sleepwalkers have changes similar to patients with restless legs syndrome. In particular, sleepwalkers have reductions in short-interval intracortical inhibition, cortical silent periods, and short-latency afferent inhibition (58). These changes, suggestive of a hyperexcitable motor cortex, have also been demonstrated in restless legs syndrome (10).

Epidemiology

Disorders of arousal usually peak in childhood, with a reported prevalence of approximately 15%, and then decrease to 1% to 4% in adulthood (45; 64; 01). Of note, one study reported that 12% of healthy adult sleepers admitted to occasional, nondistressing sleepwalking, suggesting that the true prevalence of these phenomena is higher than previously assumed (23). According to one study, the incidence of sleepwalking in patients with mental health disorders was reported at 8.5% (81). A meta-analysis reports the estimated lifetime prevalence of sleepwalking at 6.9% (95% CI, 4.6% to 10.3%) (75). A study revealed an association of male gender, European American race, and genetic factors with a higher prevalence of sleepwalking in youth (12). It also demonstrated a genetic risk locus with genome-wide significance at rs73450744 on chromosome 18 in African Americans.

As noted earlier, sleepwalking is frequently associated with other sleep disorders. Restless legs syndrome and obstructive sleep apnea are the most identified conditions in patients with sleepwalking disorder (25; 33). Others include behavioral insufficient sleep syndrome, circadian rhythm disorders, environmental sleep disruption, and periodic limb movement disorder (33). Environmental sleep disruptions, particularly those from electronic technologies, lead to an increased risk of parasomnias in adolescents. Frequent television viewers are four times more likely to report higher sleepwalking frequency (03).

Not unexpectedly, there has been an increase in sleepwalking reports in parallel to the contemporary rise of prescription sedative use. Zolpidem is the most frequently reported agent to induce sleepwalking; however, it is also the most frequently prescribed. In one year (2011), zolpidem was prescribed more than 39 million times for nine million individuals in the United States (22). Injurious sleep-related complex behaviors have been reported as a result of sedative-hypnotic use, and hence, caution is advised (27).

Sleepwalking has also been associated with a variety of other medications and medical conditions. Implicated classes of drugs include antidepressants amitriptyline, bupropion, paroxetine, and mirtazapine; mood stabilizer lithium; antipsychotics quetiapine, clozapine, and olanzapine; antihypertensives propranolol and metoprolol; antiseizure agent topiramate; the antiasthma agent montelukast; antibiotic fluoroquinolone; GABA modulator sodium oxybate and stimulants mixed amphetamines (33; 37; 66; 76; 13; 16; 01). Sleepwalking is more common among patients with chronic pain syndromes (49). Other associated medical conditions include febrile illness, vitiligo, hyperthyroidism, hypoglycemia, encephalitis, and stroke (33; 01).

Although studies have noted a higher degree of mood and anxiety symptoms among sleepwalkers compared to controls, the vast majority of sleepwalking patients do not report clinically significant levels of anxiety or depression (77). Further, the association may be accounted for by the increased exposure among these individuals to agents known to induce sleepwalking. Because of this notion, most subjects can be reassured that sleepwalking does not represent an underlying mental health disorder.

Prevention

Treating the predisposing, priming, and precipitating factors can prevent disorders of arousal, including sleepwalking (67). Decreasing sleep debt by addressing sleep deprivation is critical, and a 2-week period of sleep extension ad-lib is recommended to unload homeostatic sleep drive. Effective strategies include careful scrutiny for restless legs syndrome, particularly among patients on a benzodiazepine receptor agonist for difficulty initiating sleep. Discontinuing the sedative-hypnotic and treating with anti-restless legs syndrome therapies will typically resolve the amnestic behaviors as well as address sleep initiation failure (33; 33). Avoiding and minimizing all sedating agents when appropriate is recommended. Finally, eliminating conditions that suddenly fragment sleep, such as sleep-disordered breathing and bedroom noise (eg, televisions, phones) can prevent sleepwalking episodes (26; 65).

Differential diagnosis

Sleepwalking typically presents with a history of prolonged, ambulating, nonviolent activities emanating from the first half of the sleep period. It is often associated with other complex amnestic behaviors, such as sleep-related eating disorder and sleep smoking (33; 01). The differential diagnosis of sleepwalking includes either another NREM disorder of arousal (confusional arousals, sleep terrors), REM sleep behavior disorder, nocturnal epilepsy, or sleep-related dissociative disorder.

Other disorders of arousal are limited to the bed and do not involve ambulation. Confusional arousals are often benign episodes with inappropriate behaviors, vocalizations, and subsequent amnesia (01). Prolonged events, usually due to sedating medications, can be more serious and involve activities such as electronic communication (sleep texting) or sexual behaviors (sexsomnia). Sleep terrors occur most often in preadolescent children and are characterized by inconsolable episodes of intense fear initiated by a sudden scream. Patients with sleepwalking have less autonomic activation than patients with sleep terrors, who have increased heart rate, tachypnea, diaphoresis, and facial flushing. Attempts to awaken and calm a child in a sleep terror often result in a paradoxical increase in agitation (33; 01).

Due to its association with deep NREM sleep (N3), several features distinguish sleepwalking from REM sleep behavior disorder. Sleepwalking episodes typically arise earlier than those in REM sleep behavior disorder. Further, patients with REM sleep behavior disorder usually exhibit a rapid return to alertness and orientation on awakening from an episode, whereas sleepwalkers have prolonged residual confusion (33). Unlike REM sleep behavior disorder, sleepwalking behaviors are not predominantly characterized by dream enactment. However, a word of caution is warranted as many sleepwalking patients have noted dream mentation during nocturnal behaviors prompting a preliminary diagnosis of REM sleep behavior disorder, which is later reversed after polysomnography notes normal REM sleep atonia (72; 38; 01).

Parasomnia overlap disorder, a combination of sleepwalking and REM sleep behavior disorder, may occur. In one series, 28% of all sleepwalking/sleep terror cases were later determined to also have REM sleep behavior disorder and, thus, were ultimately diagnosed with parasomnia overlap disorder (72).

Other etiologies include sleep-related dissociative disorder or nocturnal epilepsy. The behavior in sleep-related dissociative disorder is often prolonged, and polysomnography demonstrates wakefulness throughout the episode. Nocturnal epilepsy is characterized by stereotyped, recurrent, abnormal behaviors, and the EEG may demonstrate epileptiform activity (33; 01).

Diagnostic workup

Diagnosing sleep disorders in general, and sleepwalking requires a comprehensive clinical evaluation. This includes a review of the presenting complaint and establishing the patient’s underlying circadian rhythm, sleep deficit, medication exposure, and other comorbid sleep disorders. Careful consideration should be given for possible underlying motor restlessness, or sleep-disordered breathing, or both. These symptoms may appear only marginally relevant, and thus, patients can frequently minimize their importance. In addition, a bed partner report is helpful as many patients are unable to recall sleep-related events (33; 39).

There are a few helpful tools to evaluate sleepwalking such as the Munich Parasomnia Scale developed by Fulda, which is a self-assessment questionnaire consisting of 21 questions related to sleep related behaviors including sleepwalking and other disorders of arousals (24). The Munich Parasomnia Scale has sensitivity of 83% to 100% and specificity of 89% to 100% for detection of disorders of arousals. The Paris Arousal Disorders Severity Scale is another scale for assessing the presence and severity of arousal disorders (02). Ranging from 0 to 50, a Paris Arousal Disorders Severity Scale score higher than 13 suggests an active sleepwalking problem with a high risk for injury. This cutoff demonstrated a sensitivity of 84% and a specificity of 88%. A recently proposed Arousal Disorder Questionnaire (ADQ), which is a 2-part survey based on ICSD-3 criteria, demonstrated sensitivity of 73% (95% CI: 60–82) and specificity of 96% (95% CI:89–98) (01).

History alone may be unable to distinguish sleepwalking from other nocturnal events, and further scrutiny is often needed to identify the predisposing, priming, and precipitating mechanisms underlying sleepwalking behaviors. Thus, an objective evaluation of the circadian sleep-wake cycle using wrist actigraphy and in-laboratory polysomnography may be necessary (20). Prior to polysomnography, a protocol of 25 hours of sleep deprivation, with forced awakenings during N3, increases the likelihood of inducing parasomnia from slow-wave sleep (65). Frequent slow/mixed arousals in slow-wave sleep (slow/mixed arousal index of 6/hr and slow-wave sleep fragmentation cutoff value of 6.8/hr) and video-based behavioral analyses can assist with correct identification of disorders of arousal in 91.3% of cases (51).

However, even when abnormal behavior does not occur, polysomnography is often helpful by identifying or ruling out sleep-disordered breathing or periodic limb movement disorder as a precipitant of the nocturnal behaviors. In addition, the frequency of arousals during slow-wave (N3) sleep can predict more frequent sleepwalking episodes at home (09). Finally, an extended electroencephalographic montage should be added if nocturnal epilepsy is suspected with a history of stereotyped, abnormal, and repetitive behaviors (33).

Investigators have demonstrated the utility of long-term home video monitoring in the characterization of sleepwalking. In the case of a 33-year-old woman with sleepwalking since childhood, home video monitoring was employed after two nights of in-laboratory video polysomnography failed to illustrate the diversity of her sleepwalking behaviors. Over the course of 36 nights, 199 motor episodes were captured and her activity was documented, which ranged from handling the cat to shaking her husband (54).

Management

Various treatment options depending on the morbidity associated with sleepwalking episodes can be attempted as follows. If non-injurious, without any implicating consequences, the patient and family should be reassured and counseled about ensuring safety.

Environment modification. Management should initially focus on environmental safety by modifying the sleeping environment. Removal of bedside firearms and other weapons is of paramount importance. Windows, or other exits that could result in a fall, should not be easily accessible. Automatically locking doors are to be avoided as sleepwalkers may ambulate outside of their residence without means of reentry. If necessary, a door alarm is often useful to alert other family members that the patient is ambulating through the house (14).

Cessation of the offending agent. Attempts should be made to eliminate sedating agents as well as to identify and treat comorbid sleep and circadian disorders. Most cases of sedative-induced sleepwalking behaviors are self-limited following discontinuation of offending medications. Counseling of patients who may be initiated on medications that can induce disorders of arousal should be performed (76). In April 2019, the US Food and Drug Administration (FDA) released box warnings for eszopiclone, zaleplon, and zolpidem in an attempt to regulate the use of these drugs, warning patients to discontinue taking these medications if they found themselves engaged in any nocturnal activities while not fully awake when taking these drugs (22).

Management of other sleep disorders. Further, sleepwalking typically resolves once the underlying sleep deprivation, obstructive sleep apnea, or restless legs syndrome are effectively addressed (25; 33; 33; 39).

Pharmacotherapy. When serious nocturnal behaviors persist despite these interventions or in situations with a high probability of injury, pharmacotherapy may be considered. A variety of different therapies, typically benzodiazepines, have been reported as effective for sleepwalking. However, at present, there is a paucity of clinical trial data. Instead, a consensus has arisen, based on case series and small clinical trials. Importantly, national and international agencies that regulate drug approval do not recognize these treatments (33).

The most frequently used pharmacological treatments for sleepwalking are intermediate- or long-acting benzodiazepines. The efficacy of these agents would be paradoxical as other sedative-hypnotics, such as benzodiazepine receptor agonists, frequently induce amnestic nocturnal behavior (76).

The most extensively reported medication for the treatment of sleepwalking is clonazepam. In two series of parasomnia patients who were treated with clonazepam, similar response rates were noted (74% to 84%). However, not all patients sleepwalked. Other parasomnias were included in both series and separate data for sleepwalking were not reported (73; 04). Another investigation reported that all patients treated with clonazepam dropped out of the study within one year and reported persistence of sleepwalking (25). Limiting side effects of clonazepam include morning sedation as well as gait impairment and pertain to its prolonged duration of action.

There have been sporadic reports with mixed results on other benzodiazepines and neuropsychiatric agents. One diazepam study, a small double-blind crossover trial, reported no significant difference between placebo and treatment groups (69). In another report, flurazepam resolved sleepwalking in two patients, and a combination of clonazepam with phenytoin eliminated abnormal nocturnal behavior in a third report (44). Interestingly, the nondopaminergic antiparkinsonian drug biperiden has successfully treated four cases of adults with sleepwalking (30). On occasion, antidepressants including fluoxetine, citalopram, and mirtazapine have also been proposed to benefit, as indicated in a study showing improvement in 11.7% of patients (14; 19). Drakatos also posits the use of melatonin to improve NREM parasomnias (noted in 10.7% of cohort) suggesting mechanisms of sleep consolidation, treatment of sleep deprivation, and concomitant insomnia, although further studies are required to support the findings (19). A case series showed resolution of sleepwalking episodes with osmotic controlled-release oral delivery system (OROS) methylphenidate (56).

Behavioral therapies. There have been some reports to suggest that behavioral techniques, such as cognitive-behavioral therapy, hypnosis, psychoanalysis, and anticipatory awakening in the setting of sleepwalking may be helpful, but results are not consistent (59; 82; 57). Among 23 sleepwalking patients who underwent hypnosis training, 20 described improvement after more than 6 months of follow-up (36). Conversely, a separate investigation reported that only three of 11 sleepwalkers treated with hypnosis described significant improvement after 18 months (28). A study showed promising results with Cognitive Behavioral Therapy for Insomnia (CBT-I) and Mindfulness-Based Stress Reduction in 30 of 40 patients without obstructive sleep apnea and periodic limb movements during sleep (19).

In conclusion, the most effective sleepwalking therapy is to identify and treat comorbid predisposing, priming, and precipitating conditions. Even subtle sleep-disordered breathing or motor restlessness should be considered as a potential target to resolve sleepwalking (25; 33; 34). The patient should also attempt to optimize the duration and circadian timing of sleep. Finally, if pharmacological therapy is utilized, patients should be made aware that evidence supporting these treatments is minimal.

Special considerations

As discussed in the treatment section, in most cases of benign sleepwalking episodes, reassurance is sufficient. Nonetheless, if the patient faces serious safety and morbidity consequences like injuries or impact on quality of life (fatigue, sleepiness, effect on mood), treatment is warranted. Environment adaptation can significantly reduce the risk of injuries, and addressing the precipitants like sleep deprivation, obstructive sleep apnea, and offending drugs can successfully alleviate the frequency of nocturnal episodes. According to a study, a significant proportion (53 out of 60) of sleepwalkers demonstrated obstructive sleep apnea; the treatment of which resulted in the resolution of sleepwalking in all adequately treated cases (25). If still present, a trial of clonazepam can be initiated based on case series, small studies, and expert consensus (74). Although there are some data guiding clinical decision-making, larger adequately controlled trials are still lacking. A retrospective study with 103 out of 232 adults revealed an efficacy of 73% with clonazepam (04). Alprazolam, temazepam, and flurazepam have also shown some benefit in a few case reports (14), but diazepam has yielded mixed results (69). Although behavioral strategies like hypnosis have shown an efficacy of 64% in disorders of arousal (74), data show benefit approaching the equivalence of clonazepam (04).

Pregnancy

Disorders of arousal have been reported in pregnancy and in postpartum women. Sleepwalking and sleep-related eating disorder have been reported and may be related to the high prevalence of restless legs syndrome in this population (33; 33). Postpartum parasomnias are often characterized by frightening confusional arousals (without ambulation). The women typically describe a frantic feeling that something has happened to their newborn child (55). After correction of concurrent sleep disturbance, behavioral strategies such as Cognitive Behavioral Therapy for Insomnia (CBT-I) and Mindfulness-Based Stress Reduction have been proposed by a study showing efficacy in two pregnant patients (19).