Excessive daytime sleepiness could be multifactorial in adults with epilepsy

Citation:

Khachatryan SG, Attarian, HP. Excessive daytime sleepiness could be multifactorial in adults with epilepsy. J Clin Sleep Med. 2020;16(8):1395–1396.

We appreciate the commentary by Urquhart and colleagues regarding our article on sleep disorders in adults with epilepsy (AWE).¹ Our primary focus was on sleep-related movement disorders in AWE; however, we also assessed other important sleep complaints such as excessive daytime sleepiness (EDS). EDS was defined as an Epworth Sleepiness Scale (ESS) score of > 10. We found no significant difference between our AWE and control groups. Urquhart et al rightfully point out that higher EDS prevalence is seen more consistently in children with epilepsy than in AWE. In their study they found significantly higher degree of EDS in children with epilepsy than in controls using the modified pediatric ESS scale (30 vs 5%, P < 0.05), with other studies presenting similar findings using different scales.^2,3

Studies in AWE have produced mixed results.⁴ There are several factors that would potentially cause EDS in AWE. This was not, however, seen in our sample. The symptom of EDS and ESS score of > 10 was the same in both groups of our cohort. No difference was also seen between AWE taking antiepileptic drugs vs. patients not on therapy. Interestingly, treated AWE reported more unpredictable sleep attacks than did those who were not on antiepileptic drugs treatment.

Urquhart et al highlight sleep-disordered breathing (SDB) as a possible cause of EDS. It is arguably the best-established sleep disorder in all patients with epilepsy. Both groups of our cohort had equally high snoring prevalence. Self-reported or witnessed apneas, however, were significantly higher in our AWE than controls (23.7 vs 9.2%, P < 0.05). Berlin Questionnaire results similarly showed higher SDB risk among AWEs (26.95 vs 19.2%, P > 0.05). Although we realize that this is not readily convertible into polysomnographically diagnosed SDB, it does suggest higher prevalence of SDB in our AWE cohort. It is important to point out that the ESS is not a reliable tool to assess EDS in SDB.⁵ Our EDS assessment was also skewed because of higher prevalence of poor sleep hygiene among our control participants, which can lead to increased EDS. Although not included in our paper, the mean ESS scores were higher in our control group than in our AWE group (4.9 vs 5.95, P < 0.05). In Armenia, we have significant psychosocial issues connected to epilepsy, especially social stigma. Parental overprotection remains significant well into adulthood, with frequent interference in the lives of those with epilepsy. This potentially could lead to better sleep hygiene practices among those with AWE than the controls. In contrast to children, sleep hygiene in adults is usually better, independent of epilepsy.

We agree with the notion that polysomnographic assessment of SDB and other sleep disorders would bring more clarity to this question.

DISCLOSURE STATEMENT

All authors have seen and approved the manuscript. Work was performed at Somnus Neurology Clinic’s Sleep and Movement Disorders Center and Republic Epilepsy Center, Erebouni Medical Center, Yerevan, Armenia. The authors report no conflicts of interest.