Hereditary Factors in Sleepwalking and Night Terrors

Kales, Anthony; Soldatos, Constantin R.; Bixler, Edward O.; Ladda, Roger L.; Charney, Dennis S.; Weber, Gary R.; Schweitzer, Paula K.

doi:10.1192/bjp.137.2.111

Cited by 234 publications

(91 citation statements)

References 13 publications

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“…The investigation of twin cohorts and families with sleep terror and sleepwalking has led to the suggestion of a genetic factor in parasomnias. 24,25 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.…”

Section: Discussionmentioning

confidence: 99%

Sleepwalking and Sleep Terrors in Prepubertal Children: What Triggers Them?

et al. 2003

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ABSTRACT. Objectives. To evaluate the clinical presentation and polysomnography of prepubertal children with repetitive sleep terrors and sleepwalking, to compare them with a control group, and to evaluate the treatment of associated sleep disorders.Methods. Patients with complaint of sleep terrors with or without sleepwalking were studied retrospectively. A control group was also recruited. Each subject received a standardized evaluation, which included the following: 1) Pediatric Sleep Questionnaire; 2) interview regarding child's medical and sociofamilial history, orthodontic history, schooling, psychological difficulties, medication intake, and family history of medical and sleep disorders; 3) general pediatric physical examination and neurologic, otolaryngological, and craniofacial examination by a specialist; 4) obtaining medical history on variables relevant to early life sleep disorders; 5) polysomnography, which included electroencephalogram (EEG; C3/A2, Fp1/T1, T1/O1, O1/C3, C4/A1, Fp2/T2, T2/ O2, O2/C4), chin and leg electromyelogram, right and left electro-oculogram, and electrocardiogram (modified V2 lead); respiration was monitored with a nasal cannula/ pressure transducer system, mouth thermistor, chest and abdominal bands, pulse oximeter, and neck microphone; respiratory effort was monitored with calibrated esophageal manometry; variables were collected on a computerized sleep system; and 6) available family members with a positive history of sleep terrors and sleepwalking received clinical evaluations similar to those used for index cases; they also underwent ambulatory monitoring with an Edentrace system, which monitors heart rate, body position, oro-nasal flow, chest impedance, breathing noises (neck microphone), and pulse oximetry. Movements are deduced from artifact, and leg movements may be recorded on one channel if the equipment is preset for such recording. Subjects used logs to record "lights out" time, "lights on" time, nocturnal awakenings, and other events that occurred during the night. All original and follow-up recordings were rescored by 2 of 4 randomly selected specialists who were blind to subject identity. Mann-Whitney U test was used for group comparison. Nonparametric 2 test was used to compare percentages of symptoms in symptomatic children versus control children.Results. Eighty-four children (5 with sleep terrors and 79 with both sleep terrors and sleepwalking) and 36 normal control children formed the studied population. All subjects were Tanner stage 1 (prepubertal). None of the control children had any parasomnias. Fifty-one (61%) of 84 children with parasomnia had a diagnosis of an additional sleep disorder: 49 with sleep-disordered breathing (SDB) and 2 with restless leg syndrome (RLS). Twenty-nine of the children with both parasomnia and SDB had a positive family history of parasomnias, and 24 of the 29 also had a positive family history of SDB. Of the 51 children with associated sleep disorders, 45 were treated. Forty-three of 49 children with SDB were treated with...

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Section: Discussionmentioning

confidence: 99%

Sleepwalking and Sleep Terrors in Prepubertal Children: What Triggers Them?

et al. 2003

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“…6 Two modes of inheritance have been proposed, multifactorial 6 and autosomal recessive with incomplete penetrance. 2 However, based on the data reported here, an autosomal dominant mode of inheritance with variable penetrance cannot be excluded.…”

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confidence: 99%

“…4 Some authors have proposed a continuum with other NREM parasomnias such as sleep terrors or confusional awakenings. 5,6 SW can seriously affect the life of a subject by its frequency (one or several episodes per night) or severity (risk of severe injury). Adolescents and adults with SW were found to have an increased prevalence of anxiety and personality disorders.…”

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confidence: 99%

“…Epidemiological surveys including familial and twin studies have suggested a strong genetic implication in SW. 6,[13][14][15] Prevalence of SW in first-degree relatives of an affected subject has been estimated to be at least 10 times greater than that in the general population. 6 Two modes of inheritance have been proposed, multifactorial 6 and autosomal recessive with incomplete penetrance.…”

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HLA and genetic susceptibility to sleepwalking

et al. 2003

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HLA-DQB1 typing was performed in 60 Caucasian subjects with sleepwalking (SW) disorder and their families and 60 ethnically matched subjects without any diagnosed sleep disorder. A total of 21 sleepwalkers (35.0%) were DQB1*0501 positive vs eight (13.3%) controls (P ¼ 0.0056; odds ratio ¼ 3.5, 95% CI ¼ 1.4-8.7). The family data for all HLA subtypes were further assessed for allelic association with SW using the transmission-disequilibrium test. A significant excess transmission was observed for DQB1*05 and *04 alleles in familial cases, strongly suggesting that a DQB1 polymorphic amino acid might be more tightly associated than any single allele. Sequence screening revealed that Ser74 in the second exon shared by all DQB1*05 and *04 was 20 times transmitted against 4 times non-transmitted (P ¼ 0.001) in familial cases of SW. Thus, together with narcolepsy and REM sleep behavior disorder, these findings suggest that specific DQB1 genes are implicated in disorders of motor control during sleep.

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“…The authors of the critique point out that the studies showing high reliability within subjects of the profi le of the R Cartwright and C Guilleminault spectral analysis sleep EEG wave forms, were not conducted on SW subjects and have not been shown to be stable over the extended period that usually occurs between an event that results in a criminal charge and a subsequent sleep study. However the several studies showing night-to-night reliability of delta power within normal individuals 11-14 even under sleep deprivation conditions, along with the several studies showing the significantly lower SWA in SW groups than in C even when no SW events occurred, 3,4,15 makes a low SWA a strong candidate to be a manifestation of the genetic vulnerability to abnormal delta arousals [16][17][18][19] and therefore likely to be a stable characteristic of sleep. Our article was one small step to encourage research needed to test stability of this within SW subjects over time.…”

Section: Was the Methods Appropriate?mentioning

confidence: 99%

Slow Wave Activity Is Reliably Low in Sleepwalkers: Response to Pressman et al. Letter to the Editor

Cartwright

Guilleminault

2014

Journal of Clinical Sleep Medicine

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W e thank the editor for the opportunity to respond to the letter by Pressman et al. 1 This is a critique of the article by Cartwright and Guilleminault 2 recently published in the Journal of Clinical Sleep Medicine. We address the salient points their letter raised: The aim of our article Was the method appropriate?We based the method for our study on the hypotheses proposed by Espa et al. 4 as the conditions necessary to precipitate an occurrence of a SWS parasomnia. "The occurrence of SWS parasomnia requires not only a SWS pressure increase but also SWS arousal enhancement." This is the push/pull model that Pressman argued was a theory that only Cartwright held in the debate he refers the reader to review. [5][6][7][8] He argued forcefully and repeatedly that SW only occurred with an increase of SWS and that this was the accepted wisdom. In fact the two variable model was stated earlier by Broughton et al. 9 in describing the Ken Parks case. "These typical polysomnographic features of sleepwalkers suggest the coexistence of both pressure for deep sleep (SWS) and of heightened arousal causing inability to sustain such sleep." This opposite pressure model was used in the Pilon et al. 10 study which succeeded in eliciting sleepwalking events in the laboratory by combining increasing pressure for SWS by a prior period of sleep deprivation and increasing arousals from sleep by delivering auditory tones during the recovery sleep. Neither of these manipulations was successful when applied singly. It was this opposite pressure model that we tested in the case study reported in our recent paper.The evidence presented in court supported both pressures were present in the defendant on the night of the event (he had a period of prior sleep deprivation and excessive caffeine intake during the day before the event). Thus the conditions for a SW event were present. Furthermore we pointed out that "the additional history of snoring and a mild breathing disorder validated in the PSG may be a contributing cause of his low SWA, high CAP rate and arousal into non-conscious acts when sleep deprived and over-caffeinated."Pressman et al. 1 raise the question whether a low SWA in the fi rst NREM cycle, measured after the fact (not months or years) but specifi cally in this case eight months after the incident, can be a reliable marker of a predisposition to SW. The authors of the critique point out that the studies showing high reliability within subjects of the profi le of the

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Hereditary Factors in Sleepwalking and Night Terrors

Cited by 234 publications

References 13 publications

Sleepwalking and Sleep Terrors in Prepubertal Children: What Triggers Them?

Sleepwalking and Sleep Terrors in Prepubertal Children: What Triggers Them?

HLA and genetic susceptibility to sleepwalking

Slow Wave Activity Is Reliably Low in Sleepwalkers: Response to Pressman et al. Letter to the Editor

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