Factors that predispose, prime and precipitate NREM parasomnias in adults: Clinical and forensic implications
ABSTRACT Sleepwalking and related disorders are the result of factors that predispose, prime and precipitate episodes. In the absence of one or more of these factors sleepwalking is unlikely to occur. Predisposition to sleepwalking is based on genetic susceptibility and has a familial pattern. Priming factors include conditions and substances that increase slow wave sleep (SWS) or make arousal from sleep more difficult. These factors include sleep deprivation, alcohol, medications, situational stress and fever among others. The patient with a genetic predisposition to sleepwalking and with priming factors still requires a precipitating factor or trigger to set the sleepwalking episode in motion.
- SourceAvailable from: Ann L Sharpley
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- "The behaviour is most commonly walking around, but can include other behaviours which are highly familiar to the subject such as dressing, washing, making tea, arranging objects in the house, etc. Some cases of sleepwalking seem related to use of certain drugs, for example alcohol and hypnotics, especially zolpidem and triazolam (Pressman, 2007). It is rare for affected individuals to present for treatment, except if they have injured themselves or a partner, have put themselves into potential danger, or have excessive daytime fatigue because of nighttime disturbance. "
ABSTRACT: Sleep disorders are common in the general population and even more so in clinical practice, yet are relatively poorly understood by doctors and other health care practitioners. These British Association for Psychopharmacology guidelines are designed to address this problem by providing an accessible up-to-date and evidence-based outline of the major issues, especially those relating to reliable diagnosis and appropriate treatment. A consensus meeting was held in London in May 2009. Those invited to attend included BAP members, representative clinicians with a strong interest in sleep disorders and recognized experts and advocates in the field, including a representative from mainland Europe and the USA. Presenters were asked to provide a review of the literature and identification of the standard of evidence in their area, with an emphasis on meta-analyses, systematic reviews and randomized controlled trials where available, plus updates on current clinical practice. Each presentation was followed by discussion, aimed to reach consensus where the evidence and/or clinical experience was considered adequate or otherwise to flag the area as a direction for future research. A draft of the proceedings was then circulated to all participants for comment. Key subsequent publications were added by the writer and speakers at draft stage. All comments were incorporated as far as possible in the final document, which represents the views of all participants although the authors take final responsibility for the document.Journal of Psychopharmacology 11/2010; 24(11):1577-601. DOI:10.1177/0269881110379307 · 2.81 Impact Factor
Journal of Sleep Research 01/2009; 17(4):473-4. DOI:10.1111/j.1365-2869.2008.00694.x · 2.95 Impact Factor
- "Their comments suggest they are unfamiliar with the extensive research that supports the role of increased SWS in sleepwalking. The role of increased SWS in sleepwalking is very well established and supported by numerous published empirical studies in the sleep laboratory that address this question directly and have highly significant statistical results (Pressman, 2007a; Zadra et al., 2008; Joncas et al., 2002; Pilon et al., 2006). On the other hand, there is no generally accepted alternate theory of sleepwalking. "
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- "There are significant variations between the studies reporting HSD and SWS arousals in DOA (Blatt et al., 1991; Broughton, 1991, 2000; Espa et al., 2000, 2002; Gadreau et al., 2000; Joncas et al., 2002; Pilon et al., 2006) supporting the concept that HSD and SWS arousals have low specificity and sensitivity for the diagnosis of DOA (Pressman, 2007). In summary, data indicate that HSD is not specific for the diagnosis of NREM parasomnias (Pressman, 2007) in adults and even less in children. CAP represents a more refined tool for the analysis of NREM sleep structure, and we prospectively explored if the neurophysiological alteration of NREM sleep in subjects with DOA could be more accurately defined. "
ABSTRACT: To evaluate NREM sleep instability, as measured by the cyclic alternating pattern (CAP), in children with sleep terrors (ST) vs. normal controls. Ten boys (mean age: 8.5 years, range 5-13) meeting the following inclusion criteria: (a) complaint of ST several times a month, (b) a history of ST confirmed by a third person, and (c) a diagnosis of ST according to the ICSD-2 criteria. Eleven age-matched control children with parental report of at least 8.5h of nightly sleep, absence of known daytime consequences of sleep disorders were recruited by advertisement from the community. Sleep was visually scored for sleep macrostructure and CAP using standard criteria. Sleep macrostructure showed only a significantly increased number of awakenings per hour and reduced sleep efficiency in ST subjects. CAP parameters analysis revealed several significant differences in ST vs. controls: an increase of total CAP rate in SWS, of A1 index in SWS and of the mean duration of A phases while B phases had a decreased duration, exclusively in SWS. The normalized CAP interval-distribution graphs showed significant differences in SWS with interval classes 10< or = i < 35s higher in children with ST and intervals classes above 50s higher in normal controls. Children with ST showed faster alternations of the amplitude of slow EEG bursts during SWS. This abnormally fast alternation of the EEG amplitude in SWS is linked to the frequent intrusion of CAP B phases interrupting the continuity of slow delta activity and could be considered as a neurophysiological marker of ST. This abnormal alternation of the EEG amplitude in SWS is associated with the occurrence of parasomnias and might be considered as a neurophysiological marker of disorders of arousal.Clinical Neurophysiology 05/2008; 119(5):985-92. DOI:10.1016/j.clinph.2008.01.015 · 2.98 Impact Factor