Clinical manifestations

Presentation and course

The most frequent sleep disorders observed in childhood are parasomnias, thought to be a CNS sign of immaturity, which tend to be predictable, recurring in the same families and not influenced by environmental stimuli. By definition, parasomnias are defined as undesirable non-deliberate physical or emotional events that accompany sleep. They take place during entry into sleep or during arousals from sleep and may be augmented by the sleep state. The International Classification of Sleep Disorders (ICSD-3) categorizes parasomnias into NREM-related, REM-related, other parasomnia, and normal variants (01).

Table 1. Parasomnia Classification

Confusional arousals are a specific type of parasomnia categorized under “disorders of arousal.” These generally emerge from stage N3 sleep (delta sleep) or relate to arousals occurring during non-REM stage N1 or N2 sleep. They are common in childhood and fairly common in adulthood as well.

The clinical phenomenon of confusional arousals consists of six main symptoms (12):

Confusional episodes most commonly occur with incomplete arousals during the first 2 to 3 hours of sleep. The behaviors can be complex and inappropriate such as sitting up and uttering unintelligible speech, picking up a lamp to talk when the sleeper apparently believes the phone has rung, and so forth. Forced arousal in the first third of the night sometimes precipitates a confusional episode. The episodes can last minutes to hours. Aggression may occur, usually in the form of striking out against the person who induced the arousal.

In the ICSD-3, sleep-related abnormal sexual behaviors are classified as confusional arousals. Sexual behaviors or activities arising from sleep are also called “sexsomnia” and “sleep sex.” Behaviors can include masturbation, sexual intercourse, or even sexual assault, followed by morning amnesia of the event (03).

Less intense confusional arousals may occur after morning awakenings, especially in patients with idiopathic central nervous system hypersomnia. At these times patients may have problems with common activities such as dressing themselves, drinking a cup of coffee, or keeping their balance. The staggering, striking out on awakening, and possible cursing is what gave this disorder the colorful name “sleep drunkenness.” Only rarely do confusional arousals occur after daytime naps; such episodes occur almost exclusively following deep naps associated with recuperation from prior sleep deprivation. Humans are less likely to have sleep inertia after a shorter 10-minute nap as compared to a 30-minute nap (35).

In the study by Ohayon and colleagues, subjects with confusional arousals most commonly exhibited disorientation on awakening (71% of responders), followed by slower mentation and speech (54.4%) and memory impairment (53.9%) (58). Almost two thirds of the 13,057 patients studied reported two or more of these associated features. Another study demonstrated that patients with confusional arousal (and other disorders of arousal) were more likely to have eye opening, head raising, visually exploring the environment, expression of fear or surprise, talking, or interacting with the environment as compared to controls (05).

Prognosis and complications

The prognosis is usually good. Parasomnias can rarely lead to injury to the person or someone who is interacting with them. Rarely, they may produce unintentional injury to self or others. In the case of sleep inertia or drunkenness, it is possible that the person may make a decision or say something after an abrupt awakening that could have negative consequences (ie, a doctor waking up to answer a call and making a decision on a patient). In the case of sexsomnia, it can not only lead to injury, but to legal or ethical issues (37).

Children with confusional arousals often "outgrow" them as they get older. In adults, successful treatment of any underlying condition usually leads to disappearance of the episodes. Patients with NREM sleep parasomnias do report more excessive daytime sleepiness than controls, though there is no correlation between degree of sleep fragmentation noted on overnight polysomnogram and daytime hypersomnia (47). Patients with NREM sleep parasomnias seem to have more sleep pressure (shorter sleep latency and more total sleep time), which may lead to incomplete arousal from stage N3 sleep (16).

Clinical vignette

A 37-year-old man presented to the sleep disorders clinic complaining of unusual nocturnal spells. The spells occurred around 3 AM to 6 AM, four to five times per month. During these spells, his wife witnessed him sitting at the edge of the bed appearing confused for several minutes. He was also witnessed smacking his lips, appearing incoherent, and having no recollection of these events. In the past, some of these episodes were triggered by the alarm clock that was set for 6 AM. Once the alarm sounded, the patient appeared frightened, had mumbled speech, and appeared incoherent and confused.

His bedtime was 11 PM, wake time was 6 AM, and sleep latency less than 15 minutes. There was no history of snoring, apneic episodes, or nocturnal leg jerks. He reported a history of sleepwalking until 5 years of age but denied any current sleepwalking episodes. There was no history of dream enactment behaviors, nightmares, or talking/yelling in the middle of the night. He denied hypnagogic hallucinations, sleep paralysis, and cataplexy, as well as any past history of head injury or loss of consciousness. He was a product of a normal pregnancy and birth. He denied knowing of any history of meningitis or encephalitis. He denied any diurnal seizures spell. There were no blood relatives with history of seizures or unusual nocturnal spells.

His physical and neurologic examinations were normal

His work-up included two 16-channel EEGs at an outside institution that were read as normal with no epileptiform activities. A brain MRI was normal. His primary care physician has tried treating the patient with a variety of medications including zaleplon [Sonata (r)], citalopram [Celexa (r)], zolpidem [Ambien (r)], melatonin, and sertraline [Zoloft (r)] without much success. The patient was subsequently sent to the sleep disorders clinic for further work-up.

The top differential diagnosis at the time was frontal lobe epilepsy and NREM parasomnias. Although unlikely clinically, sleep apnea was also considered.

A 2-night polysomnogram was ordered. The first night was baseline utilizing expanded EEG montage and esophageal pressure monitoring (for the evaluation of upper airway resistance). The nighttime sleep technicians were also instructed to sound the alarm if the patient did not have his typical spell by 3 AM, in the hope of inducing one.

The sleep study revealed two of the patient’s typical events. The first event occurred at 1:22 AM; the patient arose spontaneously from stage N2 sleep, sat up, and looked around the room. He then lay back down for two minutes before starting to move around again, sitting up, and trying to remove his electrodes. He was confused for several minutes afterwards. The second spell was elicited by ringing a bell at 3:05 AM. The semiology was identical except that he also had lip smacking and staring prior to taking off his electrodes. Both instances arose out of stage N2 sleep; the EEG showed desynchronization without any rhythmic or epileptiform activity. In the morning the patient was completely amnesic to the occurrence of these events.

This pattern was determined to be consistent with confusional arousals. There was no evidence of sleep-disordered breathing.

On a follow-up clinic visit, he revealed to be drinking up to 12 cups of coffee per day. He was instructed to discontinue caffeine usage and the spells remitted.

Comments. Parasomnias emerging from NREM sleep such as sleepwalking, sleep terrors, and confusional arousals are considered arousal disorders. Nocturnal video-polysomnography is currently the gold standard to diagnose and differentiate parasomnias from other spells such as nocturnal frontal lobe epilepsy. This form of nocturnal seizure, with prominent dystonic-dyskinetic components, has been identified by means of detailed video analysis of movements during sleep (78). The clinical picture of parasomnias (with onset in early childhood, rare episodes of long duration, absence of stereotypy, general disappearance after puberty) is different from that of nocturnal frontal lobe epilepsy (which first occurs between the ages of 10 and 20 years, manifests frequent, complex, and repetitive behaviors of short duration (excluding rare prolonged seizures), nocturnal agitation, some daytime complaints such as fatigue or sleepiness, and persistence into adulthood). Patients show no difference from classical sleep parameters, whereas microstructure analysis shows sleep instability and arousal fluctuations in parasomnias and nocturnal frontal lobe epilepsy. In children as well, the differential diagnosis between the two disorders is difficult and requires one or more complete nocturnal video-polygraphic recordings. In any case, the diagnosis of nocturnal frontal lobe epilepsy should be considered in children with nocturnal motor episodes or nocturnal motor agitation when the attacks persist; this diagnosis is probably more frequent than expected (78). In this case, with a man in his late 30s, the presence of confusional arousals is atypical and the major initial concern was that of nocturnal frontal lobe epilepsy given the recurrent and stereotyped pattern of the spells. The second issue was heavy caffeine usage and the resolution of symptoms once caffeine was withdrawn.

Biological basis

Etiology and pathogenesis

In most instances there is no apparent etiology, though a study suggests that the majority of individuals who have a confusional arousal also have an underlying sleep disorder or take psychotropic medications, suggesting these as possible triggers (56). Any factor that deepens sleep can in fact be associated with confusional arousals. This includes recovery from prior sleep deprivation, use of central nervous system depressant medications such as hypnotics, tranquilizers, alcohol, and antihistamines, as well as in certain metabolic and toxic conditions. Some studies have shown that the effects of nonbenzodiazepine hypnotics on cognition after awakening may be more common than we suspect, especially in the younger adult population (26). Age is an etiologic factor; the condition is more common in childhood when sleep is normally much deeper than in adulthood in terms of auditory awakening threshold. Confusional arousals may be precipitated exclusively by febrile episodes.

Awakening from slow wave sleep in normal people is often associated with impaired visual evoked potentials indicating abnormal cortical reactivity (12; 65), as well as with unusually prolonged reaction times and impairment on cognitive performance tests, such as the descending subtraction task (20); together these indicate the presence of "sleep inertia." Physiological recordings during actual clinical confusional episodes have generally confirmed arousals beginning in slow wave sleep with the EEG during the episode being that of lighter stages of NREM sleep, often stage N1, but sometimes showing an unreactive alpha rhythm (12). Terzaghi demonstrated that confusional arousals in one patient were not an expression of a global phenomenon, but rather of the coexistence of different local states. Arousal was noted in the cingulate cortex, whereas enhancement of delta activity was noted in frontal and parietal associative areas (72). In a study by the same author, a patient with confusional arousals demonstrated persistence of sleep in the hippocampal and frontal associative cortices in contrast to the presence of awakening in the motor, cingulate, insular, amygdalar, and temporopolar cortices on EEG (73). A study of five patients with intracerebral EEG where confusional arousals were captured also demonstrated awake patterns in most cortical areas of the brain, along with slowing in other parts such as the hippocampus. These researchers also observed a peculiar, hypersynchronous, rhythmic delta (1 to 1.5 Hz) activity in a broad frontoparietal cortical network, which is fundamental for the appearance of consciousness, possibly explaining some of the altered consciousness during an episode (24). This is consistent with what has been seen in ictal SPECT in sleepwalking patients (06). The cyclic alternating pattern (CAP) may also play a role in causing confusional arousals (and other disorders of arousal). CAP is a measure of NREM sleep instability with high level of arousal oscillation. Patients who have disorders of arousal are found to have increases in CAP rate, in number of CAP cycles, and in arousals with EEG synchronization (29; 07). Studies of morning sleep drunkenness in patients with clinical hypersomnia have at times documented repeated "microsleep" episodes until sustained alert wakefulness occurs. There appears to be a genetic component to this disorder as confusional arousals are more frequently seen in families of deep sleepers who may also have episodes of sleepwalking or sleep terrors. One study found a high prevalence of the HLA-DQB1*05:01 genotype in subjects with NREM sleep parasomnias (33). Because the brain in patients with confusional arousals has an unusual degree of difficulty changing from deep sleep to the fully awake state, and because forced arousals can lead predisposed patients to exhibit clinical episodes, the entity has been classified as one of the parasomnias: a "disorder of arousal" (12). There is also suggestion from transcranial magnetic stimulation studies that disorders of arousal arise from immaturity of neural circuits’ synapses or receptors (59).

Epidemiology

Confusional arousals are common and probably a normal phenomenon in young children until the age of about 5 to 7 years. They become much less common in older children and are more rare in adulthood. Seven percent of adolescents were found to have disorders of arousal (including confusional arousals), and higher if they smoked, used alcohol, or had a depressed mood (38). Roth states that 50% to 60% of patients with idiopathic hypersomnia have morning sleep drunkenness (64). Parasomnias were noted to be higher in children with developmental disorders (54). In an epidemiological study of adults with sleep disorders, 4.2% of the study participants identified themselves as currently experiencing confusional arousals; they are more prevalent in the 15- to 24-year-old group, and there was no gender difference in prevalence (55). In yet another study by Ohayon that consisted of 13,057 subjects, 2.9% reported confusional arousals (58). One cross-sectional study in Norway conducted by telephone reported a lifetime prevalence of confusional arousals at 18.5% in adults, with a current prevalence of 6.9% (10). One study looking at prevalence of confusional arousals in the United States found that 15.2% of respondents had a confusional arousal in the last year (56). In a cross-sectional study of 342 medical students (age range 18 to 35 years), Hidalgo and Caumo found that daytime sleepiness, arousal, insomnia, and sleeping less than seven hours per night were associated with minor psychiatric disorders (34). There is no evidence for gender difference. There have been higher rates of NREM sleep parasomnias including confusional arousals seen in shift workers, likely from their disruptive and irregular sleep schedules (42).

Prevention

Preventive measures include regular sleep/wake habits (known as good sleep hygiene) and avoidance of predisposing factors such as sleep deprivation, stimulants (that can disrupt sleep), or central nervous system depressants. Sleep-related eating disorder and sexsomnia have been reported after use of sodium oxybate (27). One study showed higher rates of confusional arousals and other parasomnias in shift workers working evening or night shifts (11).

Differential diagnosis

Confusing conditions

The present diagnostic criteria distinguish confusional arousals from other parasomnias, such as sleepwalking, by the absence of the behavior of leaving the bed and walking about, and from night terrors by the absence of signs of acute fear and of a bloodcurdling cry. REM sleep behavior disorder is distinguished by the explosive nature of the behaviors that characterize these attacks, as well as by their typical occurrence during the second half of the night during an episode of REM sleep rather than during an episode in the first half of the night during slow-wave sleep. Many times the patient will remember dream content that matches the nocturnal motor activity (isomorphism), which would not be expected in confusional arousals or other NREM sleep parasomnias. Occasionally, confusional amnesic behaviors are observed during nocturnal complex partial epileptic seizures of infero-mesial temporal or frontal lobe origin. These may cause diagnostic questions. However, in most cases an ictal EEG discharge accompanying such episodes and a history of more or less similar epileptic attacks in waking may be documented (30; 41; 61; 13). Parasomnias usually have an earlier age of onset and decrease in frequency after puberty, whereas frontal lobe seizures tend to occur first between the ages of 10 and 20 years and persist into adulthood. Often the behaviors in parasomnia cases are less stereotyped in nature and may last over longer periods of time than those associated with frontal lobe seizures (78). One case series also identified the following semiological features favoring a NREM parasomnia versus nocturnal frontal lobe epilepsy: interactive behavior, failure to wake after event, coherent speech, and indistinct offset (19). Adding to the difficulties in correctly distinguishing parasomnias from frontal lobe epilepsy is the fact that families with nocturnal frontal lobe epilepsy were found to have a higher frequency of arousal disorders, suggesting a possible common pathophysiological mechanism (09). Seizures also need to be considered in the differential diagnosis of sexsomnia, as there was a case series published of complex sexual behaviors as part of an ictal phenomenon in temporal or frontal seizures (77).

There has been some concern about the limited EEG montage of the standard polysomnographic recording and its sufficiency in identifying seizure activity and differentiating it from arousals of other types. In a study by Foldvary and colleagues, frontal lobe seizures could be detected without additional EEG channels, but temporal lobe seizures needed at least seven sites to be identified with high sensitivity (25). Another issue is the possible misdiagnosis of confusional arousals as Kleine-Levin syndrome. Although these patients share the symptoms of being difficult to arouse from sleep, mental confusion, and incoherent speech, the Kleine-Levin patient has the distinctive features in wakefulness of hypersexuality and hyperphagia. Also, the long sleep periods have an episodic occurrence pattern with a return to normal sleep and wake functioning between episodes that may be widely spaced in time (53).

The parasomnia categories of sleepwalking, sleep terrors, confusional arousals, Kleine-Levin, and even REM sleep behavior disorders share some overlapping symptoms (49; 50). The rapid or delayed shifting between the basic states of wakefulness, NREM sleep, and REM sleep in these clinical cases opens the possibility that the diagnostic criteria are in need of revision. There has even been a case report description of a possible confusional arousal out of REM sleep (08). Also, the presence of sleep eating and sleep sexual activity further blurs the distinction between confusional arousal and Kleine-Levin syndrome (22; 74; 63; 67).

The following table provides a comparison between confusional arousals and other nocturnal spells, modified from (13; 40).

Confusional arousals are associated with mental health disorders as 51% of patients reported comorbid symptoms of anxiety, 60% reported depressed mood, and 22% were diagnosed with bipolar disorder (55). Ohayon also reported that 13% of patients with confusional arousals had obstructive sleep apnea compared to 2% of those without confusional arousals.

Table 2. Comparison of REM Sleep Behavior Disorders and Confusion Arousals

Associated or underlying disorders

One report by Vela Bueno and colleagues (76) described the occurrence of episodic sleep arousal disorders in an 18-year-old patient with fever. The patient had a temperature elevation of up to 40 degrees C. His EEG tracing demonstrated slow wave sleep with the onset of increased autonomic activity associated with bizarre confused behavior while febrile (76). Another report by Larsen and colleagues documented the presence of episodic confusional spells in a patient with a febrile illness (43). The patient, a 12-year-old boy experienced five episodes of confusional arousals in the setting of a febrile illness over the course of one year. During the onset of fever, the patient experienced sudden arousals from sleep and proceeded to engage in bizarre behaviors (43). During the spells he was witnessed to have episodes lasting as long as 15 to 20 minutes during which he would fluctuate between feelings of terror and hilarity (43).

One of the most frequent sleep disorders coexisting with confusional arousals is obstructive sleep apnea. In a study by Ohayon and colleagues (58), obstructive sleep apnea was present in 13.3% of subjects who had confusional arousals. Patients with obstructive sleep apnea may experience frequent arousals that may serve to trigger arousal-induced precipitous motor activity (32). The observed behavior, a confusional arousal, may be the result of an underlying primary sleep obstructive sleep apnea. This is a good example of why overnight polysomnography (PSG with extensive physiologic monitoring, multi-channel EEG, limb EMG) may be essential in the evaluation of problematic motor parasomnias.

Psychophysiologic insomnia was observed in 10.7% of patients with confusional arousals, and disorders of hypersomnia were present in 6.2% of patients reporting confusional arousals. The most common parasomnias prevalent in patients with confusional arousals include sleep talking (37.6%) and sleep bruxism (13.2%) (58).

Many patients with reported confusional arousals also report having underlying psychiatric disorders. The rates of these mental illnesses were six to seven points higher than those observed in subjects without confusional arousals (58). According to the International Classification of Sleep Disorders, mood disorder was the most frequent psychiatric disorder associated with sleep disturbances, and it was observed in one fourth of patients having confusional arousals with associated features (58). Alcohol ingestion at bedtime was also frequent (7%) in patients reporting confusional arousals (58). Behavioral/emotional problems are surprisingly common (in more than a third) in children/adolescents with disorders of arousal in a multicentered study (17).

In a study from 1996, Ohayon also reported a strong association between confusional arousals and hypnopompic and hypnagogic hallucinations (57). Whereas hypnopompic and hypnagogic hallucinations are phenomena of REM sleep intrusion, confusional arousals are a phenomenon of non-REM sleep intrusion into wakefulness. This suggests that in many individuals this combination represents an overlap syndrome, an admixture of both wakefulness and sleep (REM and non-REM). This has been named the “parasomnia overlap syndrome” (66). Forced awakenings can often trigger a confusional arousal episode, especially if this takes place early during the sleep cycle (02).

Confusional arousals may appear from restless legs syndrome or periodic limb movement disorder and have been described in the newly described restless sleep disorder. Senel and colleagues demonstrated that restless sleep disorder was present in almost one third of the children with NREM parasomnias at their center over a year (69).

Two specific variants of confusional arousals are presently identified including sleep drunkenness (severe morning sleep inertia) and sleep-related abnormal sexual behavior. Sleep inertia is defined as a transitional state of reduced arousal occurring immediately after awakening from sleep typically induced by sudden awakening from slow wave sleep (71). This can be a normal phenomenon but is more commonly seen in patients with idiopathic hypersomnia or circadian rhythm disorders where patients are awoken during their normal sleep period. Sleep-related abnormal sexual behavior is also known as “atypical sexual behavior during sleep,” “sleepsex,” and “sexomnia.” Reports characterize these atypical behaviors as variants of sleepwalking disorder where the overwhelming majority of these patients have a history of parasomnia and a family history of sleepwalking (21). Sexual behavior during the episode may range from explicit sexual vocalizations, to violent masturbation, to complex sexual acts including anal, oral, and vaginal penetration (21). In a case from England, a patient was acquitted on three charges of rape on the basis of automatism due to somnambulistic sexual behavior. In a paper from Canada, Shapiro and Trajanovic first suggested “sexsomnia” as a new parasomnia citing a series of patients with distinct behaviors of sexual nature during sleep most common during non-REM sleep (70).

Diagnostic workup

One publication suggests that diagnosis using clinical criteria from the ICSD-3 has good interobserver reliability for disorders of arousal, including confusional arousals (45). The Arousal Disorders Questionnaire has been proposed by one group as a new diagnostic tool for confusional arousals and other disorders of arousal. The Arousal Disorders Questionnaire had a sensitivity of 72% (95% CI: 60-82) and a specificity of 96% (95% CI: 89-98) for disorders of arousal diagnosis when used in groups of patients with NREM and REM sleep parasomnias as well as seizures (44). Polysomnography may be helpful when clinical history is not entirely consistent with a disorder of arousal or if there are atypical features or concerns about other disorders on the differential diagnosis such as REM sleep parasomnias or seizures. Polysomnography can also be helpful to evaluate for other disorders such as sleep apnea or periodic limb movement disorder, which can trigger parasomnias. Nocturnal polysomnography during a confusional episode will confirm the patterns described above. Some reports have shown increased slow wave activity prior to NREM sleep parasomnias captured in laboratory polysomnography as compared to prior other arousals during the night without parasomnia activity (60). One study demonstrated that confusional arousals captured on polysomnography displayed higher slow wave activity and lower beta activity in frontal and central brain regions after movement onset (18). Forced awakenings during slow wave sleep in the early part of the night may precipitate a recorded episode. A study has demonstrated that calculating an elevated “slow wave sleep fragmentation index” from polysomnography as a way to measure disruption of stage N3 sleep may help identify patients with disorders of arousal as compared to health controls, especially if used with concurrent video analysis of spells (48). In rare patients full scalp EEG and possibly mini-sphenoidal electrodes as part of the polysomnographic recording may be indicated to exclude an epileptic mechanism. Use of home video recording can be particularly useful as it both permits full movement during an episode and visually documents behavioral patterns for subsequent analysis. Patients suspected of having an underlying sleep disorder, such as sleep-disordered breathing, should be evaluated with overnight polysomnography (PSG with extensive physiologic monitoring, multi-channel EEG, limb EMG) because sleep apnea, when untreated, may trigger nocturnal arousals that may predispose the patient to having a confusional arousal (32).

A newly developed and well-validated scale to assess the severity of arousal disorders (Paris Arousal Disorders Severity Scale, PADSS) can be helpful in the assessment and evaluation of treatment efficacy for arousal disorders (PADSS). The scale may be used by general practitioners to patients referred for nocturnal violence and abnormal behaviors to enhance recognition of arousal disorders and evaluate their severity. This would help ensure that patients referred for the assessment of disorders of arousal, including confusional arousals, receive the correct diagnosis and management, and it would prevent waste of resources and time (04).

Management

During a confusional arousal, efforts to curtail the behavior should be avoided because they may lead to aggression. The episode should simply be allowed to run itself out, unless there is an attempt to leave the bed or to leave the premises. Many of the violent behaviors directed against other individuals associated with disorders of arousal most frequently appeared to follow direct provocation by, or close proximity to, another individual (62). Educating family members about how to react to a spell and securing the area around the bed from any dangerous items is also an important management strategy. There is no specific management for confusional arousals. Patient or family self-report (or logs) of confusional arousals are likely underestimated, and there is one study suggesting that use of home nocturnal infrared video may be more accurate in detecting episodes at home (46). Some patients are helped by tricyclic antidepressants such as clomipramine. Benzodiazepines (clonazepam or diazepam) have also been suggested as treatment options (68). Patients should avoid any known precipitating factors, such as sleep deprivation, shift work, or central nervous system depressants—particularly alcohol. In idiopathic hypersomnia associated with the morning form of sleep drunkenness, Roth reports success by having patients use an alarm to wake them about an hour before their desired morning wake time and to take methylphenidate (10 to 20 mg) before going back to sleep. This, he reports, helps avoid subsequent morning sleep drunkenness (64). There is one report of simulating dawn (a gradual increase in illumination of low-intensity light prior to waking from sleep) 30 minutes before normal wake time to improve motor and cognitive skills on awakening (75). One trial demonstrated that saturated red light delivered through closed eyelids (through a red light mask) at levels that do not suppress melatonin helped mitigate sleep inertia upon waking (23). Exposure to polychromatic short-wavelength-enriched light immediately after waking from slow-wave sleep at night did demonstrate improvement in vigilant attention and subjective alertness in one study of 12 patients with sleep inertia in a sleep lab environment (36).

A study by Guilleminault and colleagues showed that children with chronic parasomnias such as confusional arousals may often also present with sleep-disordered breathing or, to a lesser extent, restless legs syndrome (31). Furthermore, the disappearance of the parasomnias after the treatment of the sleep disordered breathing or, to a lesser extent, restless legs syndrome and periodic limb movement syndrome suggests that the latter may trigger parasomnias (31).

The high frequency of sleep disordered breathing in family members of children with parasomnias provides evidence that sleep disordered breathing may manifest as parasomnias in children. The clear, prompt improvement of severe parasomnia in children who are treated for sleep-disordered breathing provides evidence that subtle sleep disordered breathing can have important health-related significance. There has been a case report of a patient whose sexsomnia resolved after treatment of obstructive sleep apnea with a mandibular advancement device (52).

Some evidence suggests that melatonin therapy (at dosages of 5 mg, 30 minutes prior to sleep) may be helpful for patients with sleep walking and night-terrors and that L-5-hydroxytryptophan at a dose of 2 mg/kg administered at bedtime may be helpful in children with sleep terrors (15; 39). These two studies did not include patients with confusional arousals. However, because sleep terrors, sleepwalking, and confusional arousals all represent disorders of arousal, treatment options and responses may be similar.

Outcomes

Avoiding precipitating factors and treating any underlying sleep disorders (sleep apnea, restless legs) typically reduces the frequency of confusional arousals. Safety measures and education about how to react to a spell also help avoid injury to the patient or family members. If pharmacotherapy is used in the form of benzodiazepines such as clonazepam or diazepam, the patient should be warned about morning sedation and risk of falls at night, along with tolerance and the controlled nature of the medication.