Parasomnias in Children

Matthew J. Balog

Stephen H. Sheldon

Darius Loghmanee

Parasomnias are dysfunctions associated with transitions into sleep, partial arousals during sleep, or following arousals from sleep (1, 2). Exclusive to sleep and wake-to-sleep transitions, these phenomena include arousals with abnormal motor, behavioral, autonomic, or sensory symptoms. Parasomnias can be noticeably dissimilar in clinical manifestations, but most share biologic characteristics. Symptoms typically begin early in childhood, gradually transform, and resolve themselves, which suggest a maturation etiology. Although often benign, these sleep disorders can be disruptive and even dangerous to the patient (3). In some cases, psychopathology plays a crucial role in sleep disorders; however, in other cases, recurrent parasomnia episodes induce psychopathology (4). Few pathologic abnormalities or objective diagnostic criteria can be identified, despite the presence of intense and often striking symptoms. Although symptoms are significant, spontaneous remission is typical.

Transitional parasomnias, partial arousals during sleep, or undesirable events or experiences following arousals from sleep may gradually appear or have a sudden and unexpected onset. Frequency can vary from a single isolated episode to multinightly events and persist for a protracted period (5). Patients appear medically and developmentally normal, with no obvious clinical abnormalities present during wakefulness, although unusual motor activity, behavior, or undesirable events or experiences occur during or immediately surrounding the sleep period. In general, sleep disorders in children and adolescents is a topic that is, and remains, neglected in public health and professional education and training. Despite the growing knowledge that has been accumulated in recent years, it has been poorly distributed; therefore, relatively little has been put into practice (6).

ETIOLOGY

The etiology of arousal disorders, partial arousal disorders, and transitional parasomnias is unknown. Because of the natural history and progression of symptoms, a maturation etiology is theorized. Any hypothetical basis of the cause for these phenomena, however, must focus on common features. Classification of these disorders in the child and adolescent separates them into several broad categories (Table 64-1): (1) sleep-wake transition disorders, (2) somniloquy, (3) parasomnias associated with nonrapid eye movement (NREM) sleep, (4) parasomnias associated with REM sleep, (5) sleep-related enuresis (SRE), and (6) sleep-related bruxism. Classification is based on observable behaviors (1).

EVALUATION

Evaluation begins with a comprehensive medical history and physical examination. These are essential and usually result in an accurate diagnosis without elaborate testing. Attention should be placed on a detailed description of the abnormal sleep behaviors. A comprehensive history should include, but not be limited to, the following:

Time of occurrence
Symptoms manifested
Discussion of results of caretaker’s intervention
- Do symptoms quickly improve with intervention?
- Do symptoms worsen with intervention?
Length of spell

Intensity of autonomic nervous system discharge

Table 64-1 Comparison of Parasomnias

Parasomnia	Characteristics	Sleep Period	Polysomnography
Somniloquy	Not associated with any pathologic states May be related to other parasomnias	Any sleep stage	Increased activity in the snore mic and chin EMG Artifact in the EEG may be present
Confusional arousals	Partial awakenings from SWS Confusion and disorientation are prominent	Usually seen in the first half of the sleep period, but may occur at any time during the night	EEG shift from N3 sleep to wake rhythm Vocalization postarousal may occur
Somnambulism	Abrupt arousal from SWS, which can produce sitting up in bed to a full ambulatory session	First third to first half of the sleep period	EEG shift from N3 Significant body movement Muscle artifact in EEG
Isolated sleep paralysis	Inability to move skeletal muscles, but the patient is fully awake	Beginning of a sleep period, or upon awakening	Reduction in general EMG activity with wake EEG rhythm EOG movements may be present
REM sleep without atonia	Considerable motor activity Elaborate, purposeful movements, which may be accompanied by vocalizations	REM sleep	Increased muscle tone and movements while exhibiting REM sleep in other aspects (EEG, EOG)
Sleep-related enuresis	Involuntary and repeated voiding of urine	Any sleep stage, but usually in the first few hours of sleep	Arousals may be more prevalent before the voiding event
Bruxism	Forceful clenching or grinding of teeth, which produces an unmistakable sound EEG arousals may or may not be present	Generally N1 and N2 sleep	Increased activity in chin or masseter EMG Muscle artifact in EEG, typically in the temporal region, but may be found in other channels
EEG, electroencephalogram; EMG, electromyogram; EOG, electrooculogram; REM, rapid eye movement; SWS, slow-wave sleep.

Presence or absence of agitation during the spell
Symptoms following waking
Presence or absence of stereotypic activity

It is important to begin by assessing neurodevelopmental landmarks. The presence of daytime waking behavioral or developmental abnormalities may suggest other underlying disorders. Sleep-wake schedules, habits, and the typical pattern of the appearance of these sleep behaviors require delineation. Morning wake time, evening bedtime, and nap time rituals require description. Sleep logs or sleep diaries are frequently helpful. Video recordings of the episodes often reveal identifiable characteristics and can be very helpful in understanding the nature of the episodes. Evaluating for the presence of excessive daytime sleepiness, unintentional sleep episodes/sleep attacks, restless sleep, limb movements during sleep, and/or snoring may assist in determining precipitating factors (2). A careful evaluation of family history is also quite important as many parasomnias demonstrate a familiar pattern.

Comprehensive physical examination with emphasis placed on neurologic function and developmental assessment is required. Developmental delays, chronic medical or surgical history, or symptoms suggestive of neurologic disorders might indicate an organic cause for symptoms. Comorbid states are often present. Primary sleep disorders such as obstructive sleep apnea (OSA) or periodic limb movement disorder (PLMD) must be first addressed, and treatment may often result in resolution of the symptoms. In some instances, a urine drug screen might be helpful if there is concern that symptoms may be a side effect of or adverse reaction to medication.

Home video recording of the spells may provide important diagnostic information. Under certain circumstances, video polysomnography (PSG) is indicated (7, 8). Using an expanded electroencephalogram (EEG) electrode array during PSG provides additional information and increases sensitivity for identifying neurologic pathology. Concurrent video recording of the patient during PSG may demonstrate symptoms and document movements (9).

If PSG is conducted, it is often helpful to have the patient drink fluids and avoid urination before lights out as bladder distension may precipitate some partial arousals from sleep (10). Analysis of the PSG should place special emphasis on identification of primary sleep-related pathology that may be a factor in the precipitation of spells or fragmentation of sleep (e.g., OSA, PLMD). Increased amplitude of slow waves, synchronization of slow-wave activity (Fig. 64-1) occurring sporadically or just before a spell, as well as arousal rhythms occurring during slow-wave sleep (SWS), and intrusion of 4 to 7 Hz EEG activity may be noted in older patients (2).

Other common PSG findings include movement arousals without state change, frequent arousal rhythms on EEG without state change (Fig. 64-2), and theta-delta sleep pattern (hypersynchronous theta activity intruding into SWS at an age where this hypersynchrony should not still be present; Fig. 64-3). These findings are associated with, but not diagnostic of, disorders of arousal from NREM sleep (2).

Sleep-Wake Transition Disorders

Most commonly noted at the beginning of the major nocturnal sleep period, sleep-wake transition disorders may also occur following arousals, awakenings, or during naps. They may involve stereotypic movements, including but not limited to hypnic jerks, or “sleep starts,” body rocking, head rolling, or head banging. Movements may persist into NREM sleep and may occur following arousals or during waking from sleep. The etiology of these movements is unknown.

Figure 64-1 Hypersynchronous delta activity. This segment demonstrates an episode of hypersynchronous delta activity during slow-wave sleep. This delta hypersynchrony occurred immediately before a partial arousal with agitation and confusion. PSG, polysomnography.

Rhythmic movements surrounding sleep are very common and have been reported in about two-thirds of normal children (11). Predominantly seen in infants and young children, rhythmic movements generally have a frequency of 0.5 to 2 seconds lasting less than 15 minutes. Prevalence is especially high in infants with a 59% incidence rate, which drops to 5% by 5 years of age (12). A strong correlation between rhythmic movement disorders and attention-deficit/hyperactivity disorder has been noticed (12). Institutionalized children, as well as children with neurologic sequelae from brain injury, show an affinity for rhythmic movements. Rhythmic movements typically resolve spontaneously by 4 years of age; however, sleep-disordered breathing (SDB) may act as a trigger for the reemergence of these episodes in adults who experienced rhythmic movements as children (13, 14). If, however, a patient’s head banging continues for a prolonged period, steps should be taken to protect the child from causing any injury to himself or herself. At the same time, efforts should be made to help the child fall asleep without relying on rhythmic movements to calm down. PSG is generally not indicated, because diagnosis can be made by history and physical examination alone; however, when associated with other symptoms that might suggest a primary sleep disorder, a polysomnogram may reveal typical rhythmic movements.

Rhythmic movements may be seen in NREM sleep but are rare in REM sleep (15). Focal, paroxysmal, or epileptiform activity is notably absent. Rarely, prolonged EEG recording may be required to rule out a seizure disorder. Sleep architecture, progression of states, and state percentages as proportions of the total sleep time are normal for age.

Figure 64-2 Arousal rhythm in slow-wave sleep (SWS). This segment is from the same patient as depicted in Figure 64-1. There is an arousal rhythm lasting about 10 seconds, occurring without state change during SWS. PSG, polysomnography.

Figure 64-3 Theta-delta sleep. This segment of a 30-second polysomnography (PSG) epoch was recorded from an 8-year-old child with a history of agitated sleepwalking. There is considerable 4 to 7 Hz activity superimposed upon 0.5 to 1 Hz activity.

SOMNILOQUY

Somniloquy, typified by talking during sleep, is almost universal, with some studies suggesting a prevalence of 84.4% during childhood (16). Somniloquy is most frequently of little concern to parents or health care practitioners, but rare episodes of vocal outbursts, loud talking, or unintelligible speech may occasionally be significant enough to disturb the sleep of other family members (17). Somniloquy is not associated with pathology but can occur during sleep terrors, confusional arousals, or sleepwalking.

Diagnosis is based on typical manifestations of either apparent coherent speech or incoherent mumbling during sleep. The child is typically amnestic for the event, and somniloquy is most often self-limited. PSG is rarely indicated unless other clinical manifestations are present. When noted outside of the context of a primary sleep disorder, treatment is unnecessary.

PARASOMNIAS ASSOCIATED WITH NREM SLEEP

Parasomnias during NREM sleep (typically, SWS) are considered to be part of a continuum of undesirable manifestations of arousal or partial arousal that occur during sleep. Symptoms typically begin in childhood and resolve spontaneously. Rarely do they persist into adolescence or adulthood. Manifestations can be alarming and, in certain circumstances, injury might occur. Spontaneous resolution and benignity of most signs and symptoms suggest a maturational etiology. Stereotypic movements characteristic of some parasomnias most likely arise from a disinhibition of subcortical central pattern generators. Genetic predisposition, an inherent instability of NREM sleep, and underlying sleep disturbances such as OSA may predispose to the activation of confusional arousals, sleepwalking, or sleep terrors. Inherited anatomic risk factors, present at birth, and even subtle SDB can lead to sleep disruption, instability of NREM sleep, and an increase in the number of parasomnia activities (18). Many of these parasomnias can be recognized by history alone, but some require nocturnal PSG to guide further evaluation and treatment (19).

Arousal and partial arousal disorders can cause simple symptoms, such as briefly sitting up in bed with rapid return to sleep or bizarre, dramatic symptoms. Nonetheless, these phenomena share several common features, which seem to occur during or following abrupt arousals from SWS. Confusion, disorientation, and amnesia for the event are common.

Arousal disorders occur more frequently during periods of anxiety or stress, with bladder distension, following periods of sleep deprivation, in the context of fever, or with hypersomnolence due to sleep deprivation or prolonged sleep fragmentation. Stress can increase the number and frequency of brief partial arousals in normal children. SWS rebound (increased time spent in SWS following sleep deprivation) can exacerbate partial arousals. These events may also be precipitated by external environmental stimuli. Computer-assisted identification of nonvisible arousals, cyclic alternating patterns, or respiratory cycle-related EEG changes may complement what can be accomplished by human scorers. Addition of autonomic arousal measures, such as heart rate variability, pulse transit time, and peripheral arterial tonometry, into standard reports may help discover more subtle sleep fragmentation (20).

CONFUSIONAL AROUSALS

Confusional arousals consist of partial awakenings from SWS usually occurring in the first half of the sleep period, but may happen at any time during the night (2, 21, 22). Episodes are sudden and startling, and may be precipitated by environmentally induced awakenings. Children may appear fully awake during the spell, but may not respond appropriately to commands or may resist being consoled. Confusion and disorientation are prominent. Attempts to abort the spell may make the symptoms more severe. These differ from agitated sleepwalking in that the patient is more aware of the environment, and the EEG may abruptly progress from SWS to wake following a very brief period of partial arousal.

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