A Comparative Study of Architecture and Quality of Sleep among Juvenile Myoclonic Epilepsy Patients and Healthy Individuals Attending Tertiary Care Hospital in Central India

Ashwin Lathiya; Dilip Maheshwari; Bharat Bhushan; Vijay Sardana; Vaibhav Somvanshi; Shubham Garg; Vinod Jatav

doi:10.18502/jss.v7i(3-4).15248

Ashwin Lathiya Department of Neurology, Government Medical College, Kota, Rajasthan, India
Dilip Maheshwari Department of Neurology, Government Medical College, Kota, Rajasthan, India
Bharat Bhushan Department of Neurology, Government Medical College, Kota, Rajasthan, India
Vijay Sardana Department of Neurology, Government Medical College, Kota, Rajasthan, India
Vaibhav Somvanshi Department of Neurology, Government Medical College, Kota, Rajasthan, India
Shubham Garg Department of Neurology, Government Medical College, Kota, Rajasthan, India
Vinod Jatav Department of Neurology, Government Medical College, Kota, Rajasthan, India

DOI: https://doi.org/10.18502/jss.v7i(3-4).15248

Keywords: Sleep quality; Polysomnography; Juvenile myoclonic epilepsy

Abstract

Background and Objective: Primary sleep disorders are common in patients with epilepsy. Seizures, epileptiform discharges, and antiepileptic drugs alter the sleep architecture of patients with juvenile myoclonic epilepsy (JME). We evaluated sleep architecture and its quality in these patients.

Materials and Methods: Thirty patients with JME (11 men and 19 women with mean age of 21.10 ± 4.55 years) and 30 healthy controls underwent overnight polysomnography (PSG). Sleep quality and daytime sleepiness were assessed using Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS), respectively.

Results: Myoclonus and generalized tonic-clonic seizures (GTCS) were present in all patients with JME, while absence seizures were in 13.3%. Sleep deprivation was the most frequent precipitating factor for seizures (56.6%) followed by fatigue, sound, and photic stimulation. Patients with JME reported a statistically significant drop in sleep efficiency (P<0.001) with prolonged sleep onset latency (P<0.001). There was prolongation in the N1 stage of non-rapid eye movement (NREM) sleep (P=0.002), and reduction in the N2 stage of NREM (P<0.001) and rapid eye movement (REM) sleep (P<0.001). The median PSQI score was higher in patients with JME, suggesting poor sleep quality (P<0.001), and the daytime sleepiness was not different as indicated by the similar median ESS score (P=0.033).

Conclusion: Our results suggest a significant alteration in the sleep architecture of patients with JME with reduced sleep efficiency and poor sleep quality. The possible role of the disease itself is suggested for these alterations as a simi- lar trend was also observed in drug naïve patients.