Pediatr Clin N Am 51 (2004) 69 88

Parasomnias in childhood
Stephen H. Sheldon, DO, FAAPa,b,*
a b

Department of Pediatrics, Northwestern University, Feinberg School of Medicine, USA Sleep Medicine Center, Childrens Memorial Hospital, 2300 Childrens Plaza, Box 43, Chicago, IL 60614, USA

Parasomnias are classified as dysfunctions associated with sleep, sleep stages, or partial arousals from sleep [1]. These disorders of sleep are strikingly dissimilar in presentation but share many clinical and biologic characteristics. Symptoms appear early in childhood. Steady, gradual transformation and resolution of symptoms suggest that the etiology of parasomnias may be maturational in nature. Few pathophysiologic abnormalities can be identified, despite the severe and often intense symptoms. Spontaneous remission as a child ages is common. Longitudinal observations have shown that many parasomnias may appear gradually or have a sudden onset. Frequency of parasomnic spells can vary and can range from single, rare episodes to nightly events that persist for a protracted period of time. During wakefulness, no obvious clinical abnormalities are present and patients appear medically and developmentally normal, only to express bizarre and sometimes violent behaviors during sleep.

Cause The cause of parasomnias is unknown. Because of the age at which they first manifest and their gradual resolution over time, a maturational origin has been hypothesized. Any theoretical basis of the genesis of parasomnias, however, must address their common features. The International Classification of Sleep Disorders [1] organizes the parasomnias into four major categories: arousal disorders, sleepwake transition disorders, parasomnias usually associated with rapid eye movement (REM) sleep, and other parasomnias. Additional characteristics that affect classification in pediatric patients include parasomnias typically associated with non-REM slow-wave sleep (SWS), parasomnias typically associated with REM sleep, parasomnias typically associated with wake-to-sleep transition, and other
* Sleep Medicine Center, Childrens Memorial Hospital, 2300 Childrens Plaza, Box 43, Chicago, IL 60614. E-mail address: ssheldon@northwestern.edu 0031-3955/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0031-3955(03)00177-9

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parasomnias. Classification is typically made with emphasis on observable behaviors [2].

Clinical and laboratory evaluation of a child with a parasomnia Evaluation begins with a comprehensive history and physical examination. Special attention must be placed on a detailed description of the nocturnal events, includingbut not limited tothe following information: Usual time of occurrence of the spell Description of behaviors, movements, or symptoms manifested Whether intervention efforts by the caretaker improve or exacerbate symptoms Whether the child leaves the bed Recall of or amnesia for the event(s) Occurrence of symptoms during daytime naps Presence or absence of symptoms during wakefulness Presence of stereotypic movements or rhythmic behaviors during the spell Basic neurodevelopmental landmarks must be assessed carefully for the presence of daytime waking behavioral or developmental abnormalities. Typical sleep-wake schedules, habits, and patterns require delineation. Habitual morning wake time, evening bedtime, bedtime rituals, and naptime rituals should be described. The presence of excessive daytime sleepiness, snoring, or other respiratory symptoms [3] may assist in determining exacerbating factors. Presence of concurrent medical illnesses and medication history should be obtained in the clinical interview. A complete physical examination must be performed. Emphasis should be placed on a comprehensive neurologic and developmental evaluation. The existence of developmental delays or symptoms that suggest neurologic disorders might indicate an organic basis for the presenting symptoms. Other sleep disorders are common in children with parasomnias, and resolution of the primary underlying sleep disorder often results in resolution of the parasomnic spells [3]. A urine drug screen might be helpful if symptoms are considered to be side effects of medication. Video recording of the spell by the parents can provide significant information; video polysomnography is often indicated [4,5]. An expanded electroencephalogram (EEG) electrode array assists in differentiating a parasomnia from sleep-related seizures and might provide information localizing focal pathology. Concomitant video recording of the patient while sleeping may demonstrate clinical manifestations and chronicle movements [6]. The study should begin no later than 10:00 PM to avoid artificially short sleep onset latency and end no earlier than 6:00 AM to avoid missing the last REM episode. The patient should be allowed to wake spontaneously so a realistic natural recording may be obtained. It is often helpful to have the patient drink fluids and avoid urination before settling because

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bladder distension may precipitate some parasomnias [7]. In analyzing the polysomnogram, special emphasis is placed on identification of other sleep-related pathology that might precipitate the parasomnia. Attention also should be paid to analyzing the amplitude of slow wave, synchronization of slow-wave activity [8], arousal rhythms that occur during SWS, and intrusion of 4 to 7 Hz EEG activity into SWS. Partial arousals, frequent arousal rhythms without state change, and hypersynchronous theta intrusion into SWS (theta-delta pattern) have been associated with, but not diagnostic of, arousal disorders [9]. The need for all-night EEG recordings, routine sleep-deprived EEG, and radiographic studies depends on the presenting situation, nighttime manifestations, and clinical symptomatology.

Sleep-wake transition disorders Sleep-wake transition disorders comprise a group of disorders that surround falling to sleep, transition between sleep states, or the movement from sleep to wakefulness. At times they may be thought of as state dissociation or overlapping states. Presentation varies considerably and can vary from rare, mild movements during state transitions to frequent and sometimes injurious movements that have the potential to result in discomfort, pain, anxiety, embarrassment, and disturbance of a youngsters sleep and the sleep of the entire family. Included in this classification of disorders are rhythmic movement disorders (head banging and body rocking), sleep starts, somniloquy and isolated sleep paralysis. Rhythmic movement disorders Rhythmic movement disorders [10 17] involve stereotypic body rocking or head banging that occurs during the transition from wakefulness to sleep. These movements also may occur during arousals from sleep and may persist into nonREM sleep. Movements vary in intensity and sometimes can be violent. The cause is unknown. Rhythmic movements that surround the sleep period are common and have been reported in approximately two thirds of normal children. There seems to be a 4:1 male-to-female ratio. They are typically self-limited and resolve spontaneously in most youngsters by age 4 [18]. Diagnosis of rhythmic movement disorder is based on the identification of characteristic symptoms in the absence of other medical or psychiatric disorders. Polysomnography is rarely required for diagnosis. If conducted, polysomnography demonstrates the typical rhythmic movements during the immediate presleep period that may extend into early stage 1 sleep. They also may be seen during arousals from sleep or during sleep cycle transitions. Occasionally, movements may be seen during SWS, but rarely during REM sleep [19]. Focal, paroxysmal, or other epileptiform activity associated with the stereotypic activity is absent. Video recordings can be helpful in characterizing these rhythmic movements; home video recordings also can be helpful in classification. Occasionally, a sleepdeprived or prolonged EEG recording may be required to rule out seizure

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disorders. Once asleep, sleep architecture, state progression, and stage volumes are typically normal (Fig. 1). Although vigorous head banging may seem aggressive, injury is rare. Occasional bruising or abrasions might occur. Spontaneous degradation of symptoms and spontaneous resolution occurs. Various treatments have been suggested; however, most reports are anecdotal and few treatment regimens have been replicable. Treatments vary and have included intentional rhythmic movements before bedtime, rhythmic sounds in the sleeping environment, and use of antihistamines, benzodiazepines, and carbamazepines. Success in all treatment regimens varies. Children should be protected from injury, and other disorders must be ruled out, such as autism, pervasive developmental disorder, and hypnogenic dystonia. Sleep starts: hypnic myoclonia Sleep starts (hypnic myoclonia) also have been termed hypnogogic jerks [1]. This wake-to-sleep transition problem is characterized by a sudden, single, brief muscular contraction of the legs and occasionally the arms, head, and postural muscles [20]. Sensory hallucinations (hypnogogic hallucinations) often occur before the sleep start, and the subjective perception of falling may occur, ending with the myoclonic jerk. Sleep starts are common, occur in most individuals, and are not pathologic unless they are frequent and result in sleep-onset insomnia [21]. They also must be differentiated from seizure, especially if they occur in patients with known epilepsy [22]. Hypnic myoclonia may occur at any age and may be frightening when observed by a parent, especially if associated with a vocalization or cry. Injury from the massive movement is rare, but foot injuries secondary to kicking a bedpost or crib rail may occur. Somniloquy: sleeptalking Sleeptalking is common during childhood. Although the exact incidence is unknown, it is typically of little concern to parents and caretakers. Significant outbursts of loud talking or utterances are rare but occasionally may be significant enough to disturb the sleep of parents or other family members [23 25]. Somniloquy is not associated with pathologic states but may be associated with other parasomnias, such as sleep terrors, confusional arousals, and sleepwalking. Diagnosis of somniloquy is based on identification of typical manifestations of coherent speech, incoherent mumbling, or utterances during the sleep period. There is typically amnesia for the events. Clinical course is usually self-limited,

Fig. 1. This 30-second polysomnographic epoch demonstrates rhythmic body rocking at a frequency of approximately 60 to 65 Hz. This patient was transitioning from wake to sleep and was noted by the technician to rhythmically bang her head into the pillow. (From Sheldon SH, Riter S, Detrojan M. Atlas of sleep medicine in infants and children. Armonk (NY): Futura Publishing Company; 1999. p. 237; with permission.)

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but symptoms may persist. Polysomnography reveals that somniloquy can occur in any stage of sleep.

Arousal disorders: non rapid eye movement motor parasomnias Arousal disorders are believed to be caused by impaired or partial arousal from SWS. Characteristics of arousal disorders stem from their occurrence during this deep sleep state. Symptoms begin in early childhood and resolve spontaneously. Rarely, they may persist into adolescence and adulthood. Arousal disorders share several common features. In general, they occur during the first half of the sleep period, there is some degree of confusion or disorientation, response to parental intervention is often inappropriate, and there is amnesia for the spell. Intensity of manifestations varies considerably, and it is difficult to wake the youngster from the spell. Although typically brief and lasting only a few minutes, with the child rapidly returning to sleep, occasionally the arousal disorders may be prolonged or occur multiple times during the sleep period. Arousal disorders may be exacerbated by factors that result in increased sleepiness. They may be precipitated by stress, anxiety, environmental factors (eg, noise), irregular sleep patterns, sleep deprivation, fever, pain, bladder distension, and other sleep-related disorders. These factors tend to increase brief arousal states in normal individuals. Confusional arousals Confusional arousal occurs upon arousal from SWS. During a spell, youngsters may appear awake but might not recognize parents, and there is considerable disorientation. Children may cry, moan, or speak in unintelligible sentences. They might yell anxiously during the spell. Most common words spoken are No, no! [26]. Diagnosis is based on identification of confusion or disorientation, agitation, or combativeness upon arousal. Amnesia for the event varies, and a child might appear to be frightened after full awaking occurs. Medical or psychiatric disorders are notably absent. Polysomnography reveals a sudden abrupt arousal from SWS. Although muscle artifact often obscures the EEG pattern, there may be stage 1 sleep, theta pattern, or poorly reactive alpha activity noted. Focal, paroxysmal, or epileptiform activity is absent. The clinical course is usually benign; however, it can be frightening to the parent and child. Physical injury, although rare, might occur and is typically accidental. Children must be protected from unintentional trauma during episodes. Sleep terrors Sleep terrors, similar to other arousal disorders, are manifested by an abrupt sudden partial arousal from SWS during the first third to first half of the sleep period. The term sleep terror is preferred to night terror to clearly differentiate it from a nightmare; sleep terrors may occur at any time during the 24-hour continuum when sleep occurs [27]. The onset of a sleep terror is sudden and often

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begins with a blood curdling scream. In contrast to sleepwalking, intense autonomic nervous system discharge results in intense pupillary dilation, diaphoresis, tachycardia, and tachypnea. Intense behavioral manifestations of apparent fear are striking and frightening to the observer. Spells are typically brief, last 3 to 5 minutes, and end spontaneously, and the child rapidly returns to sleep [28]. Occasionally, the spells may be prolonged and there may be multiple episodes during a single sleep period. Similar to other partial arousal disorders, the exact prevalence is unknown. Partial arousals have been reported to occur in approximately 3% of prepubertal (Tanner 1) children and less than 1% of adults. Boys seem to be more frequently affected than girls, and there seems to be a familial pattern of occurrence [28]. Psychopathology is rare in children with sleep terrors. Onset of symptoms of sleep terrors is believed to be between 2 and 4 years of age. Prolonged periods of inconsolable crying in younger children might be symptoms of partial arousal, however, but few objective data are currently available. As with other partial arousal disorders, the frequency decreases as youngsters age, and spells are rare after 10 years of age. Diagnosis is based on identification of characteristic symptoms, exclusion of organic pathology, and other sleep-related disorders that may be precipitating factors. Polysomnography is rarely needed unless there is a suspected primary underlying sleep disorder. Polysomnography typically reveals sudden arousal from SWS during the first third to first half of the sleep period. During a partial arousal, the polysomnogram often reveals muscle artifact superimposed on a background EEG rhythm of 0.5 to 2 Hz. Video recording reveals various behavioral manifestations during the spell. Intensity also can vary from mild to severe. Diagnostic considerations Diagnosis of arousal disorders typically is made by history and physical examination alone. Home video recording of a spell may be helpful in characterizing manifestations. The need for polysomnography is controversial. A decision to obtain a polysomnogram should be based on a patients clinical presentation, frequency of occurrence of episodes, time of spells, characteristics of motor activity, and intensity of symptoms. Risk of injury and resistance to prior therapeutic interventions also should be considered. There are no clearly defined polysomnographic characteristics of partial arousal disorders. A sudden abrupt arousal from SWS during the first third to first half of the sleep period may occur (Fig. 2). Sleep terrors, however, can occur during SWS at any time of the night. Partial arousals without motor manifestations may occur more frequently in children with sleep terrors when compared with children who do not experience these partial arousals (Fig. 3). There is some anecdotal evidence that children who manifest intrusion of hypersynchronous theta activity into SWS (a theta-delta EEG pattern) (Fig. 4), frequent electrocortical arousal rhythms during SWS, or hypersynchronous delta band activity may be prone to partial arousal

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(given the right set of circumstances). These findings are normal variants and are clearly not diagnostic of partial arousal disorders. Sleep terrors require differentiation from sleep-related epilepsy with automatisms. In patients with epilepsy, EEG may show abnormal discharges from the temporal or frontal lobes [6,29]. Epileptic events may be distinguished from disorders of partial arousal by the presence of a combination of clinical features, stereotypic behaviors, and their occurrence during any part of the sleep period or awake state. Identification of epileptiform activity, however, does not completely rule out the presence of partial arousal, because they may occur concomitantly in the same patient. Therapeutic considerations There is no clear consensus regarding when a partial arousal disorder requires treatment. Symptoms are most often mild, occur infrequently, and result in injury to neither children nor parents. In these mild cases, reassurance may be all that is necessary. A comprehensive explanation of the nature of these parasomnias and reassurance that the children are normal mentally and developmentally should be provided. Parents should be encouraged to let the event run its course and intervene minimally. Interventions should be focused on preventing injury and guiding a child back to bed. Too vigorous intervention attempts may prolong the spell. Warning of sleepwalking may be provided by an alarm system. A bell on the doorknob of a youngsters room may alert parents to a childs sleep-related walking. Sleep deprivation should be avoided, and regular sleep-wake scheduling and sleep hygiene should be maintained consistently. Short daytime naps might be attempted, and a period of quiet activity or relaxation techniques should be instituted before bedtime. Fluids after the nighttime meal should be limited, and children should be encouraged to empty their bladder before settling. Fevers, if present, should be evaluated and appropriately treated. Other environmental triggers, medical causes, and psychological precipitants must be addressed appropriately and reinforcing behaviors must be eliminated. Of particular importance, primary sleep-related disorders should be addressed appropriately (eg, sleepdisordered breathing, periodic limb movement disorder) [3]. Severity of partial arousal disorders is considered moderate when symptoms occur less than once per week, the spells do not result in injury or harm to the children, and daytime performance is normal. In these situations, reassurance and a behavioral approach have been successful [26]. When episodes occur almost nightly, there are multiple nightly episodes, or injury has occurred (or there is significant risk of injury), pharmacologic therapy may be indicated. Behavioral and sleep hygiene approaches are still included in the therapeutic regimen, but

Fig. 2. This 120-second polysomnographic epoch demonstrates a sudden arousal from slow-wave sleep precipitated by a periodic limb movement. Note the left leg electromyogram reveals the movement followed by a sudden abrupt arousal from slow wave sleep. The technician noted the patient to be screaming during the sudden arousal.

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pharmacotherapy might be prescribed for a short period. Treatment with medication should be conducted in conjunction with a behavioral approach. When indicated, benzodiazepines are the most commonly prescribed medication [30]. Small nightly doses of clonazepam, lorazepam, or diazepam can be effective. Prolonged use of medication increases the potential for side effects, tachyphylaxis, complication, and chronic disruption of sleep structure. Young children generally respond well to behavioral and pharmacologic approaches.

Parasomnias usually associated with rapid eye movement sleep Parasomnias also occur during REM sleep. In most cases, manifestations are markedly dissimilar to the non-REM sleep parasomnias and sleep-wake transition disorders. Most parasomnias can be differentiated on clinical evaluation alone. On occasion, certain REM sleep parasomnias may share similar symptoms with partial arousal disorders. Frequency varies considerably from commonly seen REM sleep parasomnias (nightmares) to others that are rarely described in childhood (REM sleep behavior disorder). Disorders rarely encountered during childhood are included because their importance to the practitioner might become clear when they are more completely understood and dysfunction associated with the sleeping state is further delineated in children. Nightmares: anxiety dreams A nightmare occurs during REM sleep and is characterized by a frightening dream that often results in a prolonged period of wake [31,32]. There is typically clear recall for the dream, manifestations of anxiety, and some mild autonomic nervous system discharge. A sudden arousal from REM sleep occurs, there is arousal to full waking state, and there is full orientation to the environment and clear sensorium. Nightmares most commonly occur during the last half to one third of the sleep period, during the longest and most intense REM episode. The dream story is often complex and may involve credible threat to survival, security, or self-esteem. The dreams are usually vivid and there is a clear, action-packed story line. Dream recall is appropriate to the childrens developmental and maturational level. Children most often are fully awake and alert after the nightmare, and the reaction is emotional rather than associated with the intense autonomic nervous system discharges seen in association with sleep terrors. Children are often easily comforted after an arousal from a nightmare, and return to sleep is delayed. Nearly all children experience nightmares. Prevalence data are not clear. The age of onset seems to parallel development of dreams in childhood. There seems to be equal sex distribution and no clear familial pattern. Movements are rare
Fig. 3. This 30-second polysomnographic epoch demonstrates slow-wave sleep. Note that during the last third of the epoch there is a burst of theta activity that represents an arousal rhythm, without state change.

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Box 1. Sleep terrors versus nightmares Sleep terrors

      

Occur during first third to first half of the night Occur during non-REM (SWS) Child has brief and rapid return to sleep Child resists parental interventions Child has poor to absent recall for the event Child experiences intense autonomic nervous system discharges Child has confusion upon awakening

Nightmares
      

Occur during second half to last third of the sleep period Occur during REM sleep (dream sleep) Child has prolonged return to sleep Child is easily comforted by parents Child has clear recall of dream/detailed story Child experiences mild autonomic nervous system activity Child is alert upon awakening

during nightmares because of normal REM sleep hypotonia; however, arousal from sleep with clear mentation is typical. Manifestations are generally mild and vocalizations are rare. Diagnosis of anxiety dreams is based on the identification of the mild and characteristic manifestations of disturbing dreams that occur during the early morning hours, absence of intense autonomic activation, clear recall of the dream, a story-like quality to the dream report, appropriate functioning and alertness upon waking, and a good response to parental interventions. Rarely are other diagnostic techniques required, and nightmares are typically easily differentiated from sleep terrors on clinical grounds alone (Box 1). If polysomnography is conducted, an abrupt awakening from REM sleep is seen followed by a prolonged period of wake. Children may have mild tachycardia. Increased REM sleep eye movement density may be present during the nightmare. Muscle tone is low, and there may be increased frequency of phasic muscle twitches. Focal, paroxysmal, and epileptiform activity is absent.

Fig. 4. This 30-second polysomnographic epoch depicts theta intrusion into slow-wave sleep. This occurrence is sometimes termed theta-delta sleep and can be seen as a normal variant in younger children. (From Sheldon SH, Riter S, Detrojan M. Atlas of sleep medicine in infants and children. Armonk (NY): Futura Publishing Company; 1999. p. 210; with permission.)

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Occasional nightmares are common during childhood. If they become frequent, persist for prolonged periods of time, or are associated with daytime behavioral or performance dysfunction, however, underlying medical or psychological causes should be considered. Treatment is based on reassurance and education. Maintenance of appropriate sleep hygiene is essential. Identifying and minimizing underlying causes, especially those that are anxiety or stress related, are essential for appropriate management. Additional medical or psychological evaluation and management may be required. Sleep paralysis Isolated sleep paralysis [33,34] is characterized by a period of inability to move voluntarily that occurs at the beginning of the sleep period (hypnogogic) or immediately upon awakening from sleep (hypnopompic). Children are conscious and awake and vigilant to the environment. All muscle groups, except the diaphragm and the extraocular muscles, are typically involved. Active inhibition of alpha motor neurons is present, and this inhibition is similar (if not identical) to that which is associated with normal REM sleep. Patients often have a sensation of difficulty breathing because of inhibition of accessory muscles of respiration, and episodes are characteristically frightening. Sleep paralysis spells are most often brief, last only a few minutes, and subside spontaneously. Spells sometimes can be aborted by another person touching the patient or by volitional rapid movements of the eyes. Hypnogogic or hypnopompic hallucinations are unusual during spells of sleep paralysis but can occur and increase anxiety related to the episode. Isolated occurrences of sleep paralysis occur in normal individuals. More frequent events are seen in patients with narcolepsy syndrome (as part of the tetrad of excessive daytime sleepiness/sleep attacks, cataplexy, hypnogogic hallucinations, and sleep paralysis) and in familial sleep paralysis. There is equal sex distribution in the isolated form and a female preponderance in the familial form. Onset of sleep paralysis usually occurs during adolescence, but symptoms may begin during childhood. Children have difficulty describing the events and may seem to be asleep throughout the duration of the event. Parents may be unaware of the occurrence because touching or shaking might abort the hypotonia. Symptoms may be mistaken for resistance to waking. Children who resist waking arouse cranky and obstinate; conversely, children who wake from an episode of sleep paralysis might be frightened and cry. Clinical course varies significantly among individuals. Most cases are isolated and are provoked by sleep deprivation, excessive sleepiness, stress, irregular sleepwake schedules, and acute changes in sleep phase. Sleep paralysis runs a more

Fig. 5. This 30-second polysomnographic epoch demonstrates rhythmic temporalis muscle artifact in the EEG leads. The frequency of teeth grinding is approximately 1 Hz. (From Sheldon SH, Riter S, Detrojan M. Atlas of sleep medicine in infants and children. Armonk (NY): Futura Publishing Company; 1999. p. 228; with permission.)

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chronic course in patients with narcolepsy syndrome or the familial form of the disorder. Diagnosis is based on identification of presenting symptoms, which may not be obvious. Sleep paralysis associated with narcolepsy syndrome can be differentiated from the isolated form by the absence of other symptoms related to the clinical tetrad. Atonic generalized seizures occur during wakefulness and may or may not be associated with changes in levels of consciousness. Syncope also occurs during wakefulness and is commonly associated with altered levels of consciousness. Polysomnography might reveal significant decrease in chin muscle tone in the presence of normal waking EEG rhythm. Conjugate eye movements also may be present. Occasionally, patients may enter sleep during an episode of sleep paralysis and reveal an EEG pattern consistent with stage 1 sleep. True sleep-onset REM periods may occur at night, and a multiple sleep latency test may be required to differentiate these episodes from the narcolepsy syndrome.

Rapid eye movement sleep motor disorder REM sleep motor disorder, originally described in adults as REM sleep behavior disorder, also has been described in childhood [35]. REM sleep motor disorder is an unusual abnormality seen in REM sleep characterized by elaborate, sometimes purposeful movements accompanied by vocalizations. There is a paradoxic increase in muscle tone that might be considered the absence of REM sleep atonia, which results in patients acting out their dreams. Occasionally, violent behaviors occur, with patients punching, kicking, or leaping out of bed. These behaviors are associated with vivid dream recall. Injuries to the patient or bed partner are common. Episodes usually occur during the first REM period of the night, approximately 90 minutes after sleep onset. REM sleep motor disorder usually begins during late adulthood and progresses over a variable period of time. Children also may be affected, and further understanding of this disorder may reveal the incidence and prevalence to be higher than current description suggests. Most cases are idiopathic; however, neurologic disorders have been reported in approximately 40% of affected adults. Signs and symptoms also have been reported in posttraumatic stress disorder. Polysomnography reveals increased muscle tone that persists throughout sleep, especially REM sleep. There is increased phasic muscle activity, excessive limb movements and body jerking, and periodic limb movements. Complex behaviors occur during REM sleep. No epileptiform activity is noted on EEG. REM sleep motor disorder in children and adults responds well to benzodiazepines, especially clonazepam.

Fig. 6. This 60-second polysomnographic epoch demonstrates bruxism after an obstructive apnea during the first third of the epoch and bruxism after an obstructive hypopnea during the last third of the epoch.

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Sleep bruxism: teeth grinding Sleep bruxism [36] is forceful grinding or rhythmic clenching of the teeth or rhythmic movements of the mandible during sleep (Fig. 5). These rhythmic movements are a result of involuntary repetitive contractions of the masseter, temporalis, and pterygoid muscles. When teeth grinding occurs, a loud, unmistakable noise is produced. Predisposing factors for the development of bruxism have been reported to include minor abnormalities of the teeth, malocclusion, stress, and anxiety. Some anecdotal data have shown that rhythmic movement and protrusion of the mandible also occur during arousals associated with occlusive sleepdisordered breathing (Fig. 6). Researchers have estimated that 5% to 20% of children have manifested symptoms of bruxism. Bruxism has been reported in more than 50% of children, with a mean age of onset of 10.5 years. Dental evidence of bruxism can be identified in 10% to 20% of the general population. There seems to be an equal sex distribution, and the condition is most commonly seen in children and young adults. Similar to many parasomnias, a familial pattern can be demonstrated, without clear genetic transmission. No longitudinal studies have demonstrated the natural course of bruxism. Episodes of rhythmic jaw movements occur either periodically or paroxysmally in bursts of 5 to 15 seconds or longer and are often repeated many times during the sleep period. Daytime symptoms are common and include jaw pain, craniofacial pain, painful teeth, morning headaches, chronic wear to the crowns of the teeth, periodontal tissue damage, and bleeding from the gums. Resorption of alveolar bone, hypertrophy of the masseter and temporalis muscles, and temporomandibular joint dysfunction can occur. Sleep bruxism also can be mistaken for atypical migraine cephalgia, especially when response to traditional treatment has been poor. Diagnosis is made by identification of the loud, unmistakable sound of bruxism in the absence of other medical or psychiatric disorders that may produce abnormal movements during sleep. Presence of obstructive sleep-disordered breathing also should be assessed, especially if morning headaches, frequent nocturnal wakings (with or without headaches), snoring, restless sleep, daytime sleepiness, hyperactivity, attention span problems, or performance difficulties are present. Polysomnography reveals paroxysmal, rhythmic muscle activity manifested by approximately 1 Hz muscle artifact over the temporalis muscle. This rhythmic activity also may be seen in the chin muscle electromyogram or masseter muscle groups. If associated with obstructive sleep-disordered breathing, the muscle activity occurs during the arousal that immediately follows the obstructed respiratory event. Several therapeutic approaches have been recommended, yet a most important factor is appropriate dental management. A mouth guard may be worn to prevent damage to the teeth. The mouth guard does not seem to prevent episodes of bruxism, however, and is used primarily as a preventive dental intervention. If

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stress or anxiety is prominent, efforts to minimize precipitating causes may be helpful. Treatment of dental or other anatomic abnormalities, if present, may not alter the course of bruxism. If bruxism is associated with sleep-disordered breathing, it should be managed appropriately.

References
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