This disorder is almost universal in children younger than 5 years of age and becomes progressively less common with age. The prevalence of confusional arousals in adults is approximately 4% (14). A strong familial pattern exists in the cases of the idiopathic confusional arousals.

Confusional arousals consist of episodes of confusion and disorientation during and following arousals from non-REM sleep, typically SWS, in the first part of the night (7,9,15). Patients often exhibit inappropriate behaviors such as talking nonsense, have decreased mentation, and respond poorly and slowly to questionings. In children, they may be characterized by movements in bed and sometimes thrashing about, or inconsolable crying (16). Retrograde and anterograde amnesia may be present. The confusional behavior generally lasts a few minutes but can be as long as several hours. Confusional arousals can be precipitated by forced awakenings, mainly in the first third of the night. The course of the childhood form is usually benign. The underlying etiology may be related to recovery from sleep deprivation; circadian rhythms sleep disorders (e.g., shift work, jet lag); the use of
CNS depressants (i.e., hypnotics, sedatives, tranquilizers, alcohol, and antihistamines); and underlying metabolic, hepatic, renal, and toxic encephalopathies. Confusional arousals are often seen in conditions characterized with pathologic hypersomnia, such as in patients with narcolepsy or OSA. Episodes of confusional arousals are frequent in patients with sleep terrors and sleepwalking. Organic causes of confusional arousals are rare but may include lesions in arousal generators, such as the periventricular gray, the midbrain reticular area, and the posterior hypothalamus.

Polysomnography (PSG) recordings during the episodes demonstrate arousals from SWS or non-REM sleep, most commonly during the first third of the night. Electroencephalography (EEG) monitoring during the spell may show brief episodes of delta activity, stage N1 theta patterns, repeated micro-sleeps, or a diffuse and poorly reactive alpha rhythm. Figure 5.3 demonstrates the induction of confusional arousal in a patient with excessive sleepiness and shift work disorder, who presented to the sleep disorders laboratory with a history suggestive of this parasomnia. The episodes required differentiation from nocturnal seizures (hence the expanded EEG montage) due to the unusual frequency of the spells. Please see confusional arousal clinical vignette for more information.

Differentiation from other parasomnias with mental confusion during the sleep period is essential.

The prevalence of sleepwalking in the general population is between 1%-to-17%. It is common in children between ages 4-to-8 years, and occurs in nearly 4% of adults (14,17). Sleepwalking may occur as soon as a child is able to walk.

Sleepwalking consists of complex behaviors during SWS ranging from simple sitting up in bed to walking and rarely, when extreme, to “escape” behaviors. Once awaken, the patient may be confused and amnestic for the episode. Sleepwalking can occur several times a week or only when precipitating factors are present (1,4). The semiology of sleepwalking may include inappropriate behavior, and may result in falls and injuries during attempts to “escape” or when walking into dangerous situations (e.g., an open window). Attention has been given to episodes resulting in death that may be erroneously deemed suicides (sleep pseudosuicide) (18). Other parasomnias, such as sleep terrors, can coexist as a “hybrid” in sleepwalking.

Precipitating factors include the use of medications, such as thioridazine, hydrochloride, chloral hydrate, and desipramine. Factors such as sleep deprivation and fever can induce sleepwalking episodes. Underlying primary sleep disorders such as OSA may produce severe SWS disruption and can potentially induce sleepwalking. Internal stimuli, such as a full bladder, or external stimuli, such as outside noises, can also precipitate these spells.

Sleepwalking originates from SWS and is common during the first third of the night or during times of SWS rebound, such as following abrupt sleep deprivation. The PSG shows that sleepwalking begins during SWS, most commonly toward the end of the first or second episode of SWS. The EEG reveals the presence of both hypersynchronous slow delta, burst of delta waves and cyclic alternative pattern, the latter of which is thought to be a sign of arousal instability during sleep (19).

The prevalence of sleep terrors is approximately 3% of children between the ages of 4 and 12. Sleep terrors can occur at any age, but are most common in prepubertal children. In adults, they are probably more prevalent than generally acknowledged (4%-to-5%) (20), most commonly occurring between 20-to-30 years of age with a predisposition in males compared to females. They can occur in several members of a family.

Sleep terrors are the most dramatic disorder of arousal. Spells are characterized by a sudden arousal from SWS with a piercing scream or cry and extreme panic, accompanied by severe autonomic discharge (i.e., tachycardia, tachypnea, diaphoresis, mydriasis, and increased muscle tone) and behavioral manifestations of intense fear as depicted in Figure 5.4. The typical spells demonstrate that the patient sits in bed, is unresponsive to external stimuli, and, if awakened, is disoriented and confused. The episodes are sometimes followed by prominent motor activity such as hitting the wall, running around or out of the bedroom, even running out of the house, resulting in bodily injury or property damage (1,4,21). Sleep terrors are characterized by amnesia for the episode, which may be incomplete, accompanied by incoherent vocalizations (22). Sometimes, attempts to escape from bed or to fight can result in harm to the patient or parents responding to the child. Mental evaluations of adults indicate that psychopathology may be associated with sleep terrors. Sleep terror episodes may become violent and may result in considerable injury to the patient and bed partners, at times with forensic implications (18,23,24). Psychopathology is rare in affected children, but may play a role in adult sufferers. Sleep terrors typically resolve spontaneously during adolescence. Precipitating factors include fever, sleep deprivation, or the use of CNS depressant medications.

The PSG shows episodes emanating out of SWS, usually in the first third of the major sleep episode. However, episodes can occur in SWS at any time. The recordings demonstrate episodes of tachycardia and other signs of increased sympathetic activation. Differentiating between sleep terrors and sleep-related epilepsy (temporal-lobe epilepsy) is sometimes difficult and the use of expanded EEG monitoring is helpful.

There is no definite agreement between studies as to the specific frequency of nightmares in the general population. Approximately, 10%-to-50% of children ages of 3
to 5 have clinically significant nightmares that disturb their parents. Up to 75% of the population can remember at least one or a few nightmares in the course of their childhood. About half of adults admit to having an occasional nightmare. About 1% of the adult population is afflicted with frequent nightmares of more than one per week. Nightmares usually start at age 3 to 6 years but can occur at any age. In children, the gender ratio is equal, while in adults there is a male: female ratio of 1:2 to 1:4 favoring females.

Nightmares typically consist of a long, complicated dream pattern that becomes increasingly frightening toward the end, causing patients to arouse from REM sleep. The vivid dreamlike feature is an essential feature in distinguishing them from sleep terrors (see Table 5.2

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