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Abbreviations. NREM, non-rapid eye movement; SWS, slow wave sleep; EEG, electroencephalogram; SDB, sleep-disordered breathing; RLS, restless leg syndrome; AHI, apnea-hypopnea index; RDI, respiratory disturbance index; PLMS, periodic limb movement syndrome.
Sleep terrors and sleepwalking, 2 common childhood parasomnias, are arousal disorders that arise from deep non-rapid eye movement (NREM) sleep. In a landmark study, Klackenberg followed for 20 years >200 children who were born in Stockholm and documented these parasomnias and their pattern of occurrence and potential association with psychopathology. He described the evolution, in some cases, of atypical, rare nocturnal behaviors into clinical syndromes in need of treatment: sleepwalking can lead to self-inflicted injuries or, in teenagers, involuntary aggression toward others. Sleep terrors and sleepwalking are states of confusion and partial arousal that emerge during the first third of the night when children exit slow wave sleep (SWS; ie, stages 3 and 4 of NREM sleep). Patients rarely remember the events in detail, but if actively probed after 4 years of age, they often report vague memories of having to act-run away, escape, or defend themselves-against monsters, animals, snakes, spiders, ants, intruders, or other threats. Children may report feeling complete isolation and fear. Parents often describe terrified facial expressions, mumbling, shouting, and inability to be consoled.
Despite widespread prevalence of these disorders and the recognition that they may arise from incomplete arousal, their pathophysiology is not well understood. Recent polysomnographic recordings of these events have shown that they are associated with 2 abnormalities during the first sleep cycle: abnormally low Δ electroencephalogram (EEG) power and frequent, brief, nonbehavioral EEG-defined arousals. One study also showed that most abnormal behaviors were preceded by a short-lived increase in Δ EEG frequency, a pattern that can also reflect physiologic activation. However, none of these studies of sleep terrors and sleepwalking has identified a cause for frequent arousals or decreased Δ EEG power in the first sleep cycle.
To explore what might precipitate sleep terrors and sleepwalking in children, we performed a retrospective analysis of clinical and polysomnographic data from 84 prepubertal children, aged 2 and 11 years, who were referred for these behavioral problems during sleep. We compared their findings with those of 36 normal children who were recruited from the community.
Sleep terror and sleepwalking episodes are disturbing to parents. Depending on the degree of confusion, bedroom location, furniture, and strength of the subject, sleepwalking may lead to accidents and self-injury. As shown by Klackenberg, up to 50% of children may experience 1 event during childhood, and these children, with a rare or isolated event, are not among those reported here. Our patient population is biased toward more severe, recurrent symptoms that disturb family life. Our study provides little information on the frequency of SDB or PLMS/ RLS in patients who have parasomnia and are seen at general pediatrics clinics. However, one third of our patients was self-referred: the recurrent parasomnia was disturbing the family life, and the associated sleep disorder was discovered at the sleep clinic. SDB and RLS were unsuspected by parents. In view of the frequency with which SDB was found in our patients, questions about signs and symptoms of SDB and RLS may be important in clinical practice when recurring sleep terrors or sleepwalking is reported.
Although past studies suggested that brief EEG arousals are increased and early night Δ power decreased, in patients with sleep terrors or sleepwalking, several reasons could explain why SDB and RLS/PLMS have not been implicated previously as a common cause of these changes in sleep architecture. Children with parasomnias, even if recurrent, are not systematically monitored during sleep. Breathing events during sleep in children rarely are apneas, and one must look for more discrete patterns. Arousals <15 seconds in duration are not systematically tabulated, are difficult to recognize visually, and are not mentioned in any sleep scoring atlases published before 1992. However, these short-lived EEG disturbances, indicated by bursts of high θ or slow α EEG frequencies in the central EEG leads (depending on the age of the child), should have underlying causes. Our study shows that at least 2 can be identified: SDB and RLS/PLMS. The possibility remains that we missed other causes of sleep fragmentation in some children. We did not perform, for example, esophageal pH measurement during sleep, although we had no history to suggest esophageal reflux.
Two other points deserve emphasis. One important aspect of childhood SDB is that obstructive sleep apnea is an uncommon feature in polysomnography: nasal flow limitation, abnormal respiratory effort, and bursts of tachypnea during sleep are more frequently noted. For facilitating recognition of these patterns, children’s respiration during sleep should be monitored with equipment such as nasal cannula/ pressure transducer systems or esophageal manometry, which are more sensitive than the thermistors or thermocouples currently used in many laboratories. One common limitation in the interpretation of pediatric sleep studies is the lack of sufficient data that link health-related outcomes with specific polysomnographic findings. Previous authors have pointed out that breathing abnormalities more subtle than those commonly found in adult SDB may have significance in children, but these assertions most often have been based on the rarity of overt, adult-defined apneic events in normal children. The current study used highly sensitive equipment, liberal definitions of apneic events, and inclusive definitions of SDB. Without outcome data, the high frequency of SDB in our sample (58%) might have been considered inflated, and clinical relevance would have been questionable. However, the clear, prompt improvement of severe parasomnias in children who were treated for SDB-as currently defined -provides important outcome-based evidence that SDB that is more subtle than that commonly recognized to be abnormal can have substantial health-related significance.
Also noteworthy is the report of a familial presence of parasomnia. The investigation of twin cohorts and families with sleep terror and sleepwalking has led to the suggestion of a genetic factor in parasomnias. The RLS has been shown to have familial recurrence and genetic involvement, particularly in early-onset cases. Familial aggregation also has been demonstrated in SDB. Thus, the question raised is whether a genetic factor directly influences sleep terror and sleepwalking or instead influences other disorders that fragment sleep and lead to confusional arousals. Among our patients, 2 individuals had a positive family history of RLS. The ambulatory Edentrace unit with which we tested relatives is not the state of the art for recognizing mild SDB. However, we can affirm that chronic snoring and some symptoms and signs of SDB were present in siblings and parents of patients who were reported to have had sleepwalking and sleep terrors. Additional studies are needed to address the association between SDB and these NREM parasomnias in the general population.
Reflection Exercise #2
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