Slow wave sleep disorders (SWSD) are unwanted nocturnal behaviors that affect 2% to 5% of adults.1 The role of alcohol in the pathogenesis of SWSD is controversial,2 and it has recently been removed as a trigger for these behaviors in the International Classification of Sleep Disorders, Third Edition (ICSD-3).3
We undertook an audit in our patients with SWSD (n = 126) to examine for association between alcohol and SWSD. A questionnaire reviewing lifestyle factors and triggers that might affect symptom frequency and severity was mailed to patients meeting ICSD-33 criteria for non-rapid eye movement parasomnia, identified through a clinical database at our tertiary referral sleep center. Formal ethical approval was deemed unnecessary because this was an audit and questionnaire-return implied consent.
The overall response rate was 31% (n = 39). The mean age of responders (40.7 ± 12.7 years) compared to that of nonresponders (36.3 ± 11.1 years) did not differ significantly (P = .39), nor did the sex of the responders (56.4% male, 41.0% female, and 2.6% other) versus nonresponders (48.3% male and 51.7% female) (P = .2).
Responders reported the following types of SWSD: 59.0% sleepwalking, 28.2% sleep talking, 23.1% sexsomnia, 20.5% night terrors, 23.1% other (eg, sleep eating). Almost half (46.2%) suffered from more than one type of SWSD.
Twelve individuals reported consuming alcohol regularly and 11 (91.7%) of these individuals reported that alcohol increased the frequency of their SWSD (P < .001). Two responders reported that an increase in alcohol intake increased their behaviors, two responders reported that decreasing their alcohol intake decreased their behaviors, and one reported that a decrease in alcohol intake increased the behaviors.
Alcohol has been shown to influence both sleep quality and symptoms in patients with SWSD.4,5 Consuming alcohol increases the amount of slow wave sleep in the first half of the night while increasing arousals in the second half of the night. Chronic alcohol use can lead to significant sleep fragmentation that can persist in the long term, resulting in chronic sleep deprivation.
We believe alcohol intoxication can act as a trigger for SWSD because of its effects on sleep architecture, whereas low doses of alcohol could have the opposite effect. Our survey provides support that alcohol can influence symptom expression in patients with SWSD. Irrespective of the mechanism, we believe that alcohol should be reintroduced as a trigger for SWSD in future editions of the ICSD.
All authors have seen and approved the final manuscript. The authors report no conflicts of interest.
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