Sleep abnormalities in juvenile myoclonic epilepsy—A sleep questionnaire and polysomnography based study. (August 2017)

• Record Type: Journal Article
• Authors: Roshan, Sujata; Puri, Vinod; Chaudhry, Neera; Gupta, Anu; Rabi, Sumit Kumar
• Is Part Of: Seizure. Volume 50(2017)
• Page Start: 194
• Page End: 201
• Publication Date: 2017-08
• Subjects: Juvenile myoclonic epilepsy -- Sleep architect -- Polysomnography -- Drug naïve -- Valproate -- Epileptiform discharges; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2017.06.021
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: Poor sleep quality in patients of JME irrespective of their treatment status. Sleep architecture is disrupted with decreased duration of REM and increased NREM1. Epileptiform discharges are frequent in lighter NREM sleep. AEDs disrupt the NREM sleep however, lowers the epileptiform discharge index. Perhaps GABA receptor dysfunction contributes both for epilepsy and decreased REM. Abstract: Purpose: To evaluate the quality of sleep, its architecture and occurrence of epileptiform discharges with their distribution across various stages of sleep in patients of Juvenile myoclonic epilepsy (JME), both drug naïve as well as those already on treatment. Methods: 99 patients of JME [36 drug naïve, 63 on antiepileptic drug(s) (AED)], and 30 healthy controls were recruited. Sleep quality and daytime sleepiness were evaluated with Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS), respectively.Polysomnography (PSG) was done to assess the sleep architecture. The EDI (Epileptiform Discharge Index) per stage of sleep was calculated. Results: JME patients had significantly poor quality of sleep by PSQI (p = 0.02).PSG revealed reduced sleep efficiency [p < 0.001], increased sleep latency [p = 0.02], increased%WASO [p < 0.001], increased%N1 [p = 0.01] and decreased% REM sleep [p = 0.002] in the patients compared to controls. Epileptiform discharges were frequent among drug naïve JME patients [drug naïve, 868 vs. 727, treatment group]. EDI was higher in N1 (p = 0.001) and N2 (p = 0.007) in drug naïve compared to JME patients on treatment. EDI in valproate treatment group was relatively lower to other AEDs. Conclusion: JME is associated with poor sleep quality and altered architecture, irrespective of treatment status. REM sleep is significantly decreased in JME patients. Epileptiform discharges are frequent in lighter NREM sleep and EDI is higher in drug naïve patients. Although AEDs disrupt the NREM sleep, their use is associated with arousal stability in lighter stages of sleep and lower EDI, in particular with valproate.