The impact of sleep loss on the facilitation of seizures: A prospective case-crossover study.
The relationship between sleep and seizures is intricate. The aim of this study was to assess whether sleep loss is an independent seizure precipitant in a clinical setting.



In this prospective, observational cross-over study, 179 consecutive hospital admissions for epileptic seizures were included. A semi-structured interview regarding several seizure precipitants was performed. The sleep pattern prior to the seizure, as well as alcohol, caffeine and drug use, were recorded. The interview was repeated by telephone covering the same weekday at a time when there had been no recent seizure. The Hospital Anxiety and Depression Scale (HADS) and a visual analogue scale for perceived stress were applied at admission. Student's t-test, Fisher exact test and ANOVA were used for statistical analyses.



Complete data for analysis were retrieved in 144 patients. The sleep-time during the 24h prior to the seizure was lower (7.3h) compared to follow-up (8.3h; p<0.0005). Caffeine consumption and use of relevant non antiepileptic drugs (AED) were not different. HADS and stress scores at admission did not correlate with sleep-time difference. In ANOVA, controlled for alcohol consumption and AED use, the sleep-time difference remained significant (p=0.008). The interaction with alcohol intake was high, but the sleep-time difference remained highly significant also for the non- and low-consumption (≤2 units per day) subgroup (n=121, 7.50h vs 8.42h, p=0.001).



Epileptic seizures are often precipitated by a combination of various clinical factors, but sleep loss stands out as an independent seizure trigger.
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, Trondheim, Norway; Department of Neuroscience, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. Electronic address: christian.samsonsen@stolav.no.
Christian
C
Samsonsen
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, Trondheim, Norway; Department of Neuroscience, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Trond
T
Sand
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, Trondheim, Norway; Department of Neuroscience, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Geir
G
Bråthen
Department of Neuroscience, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Grethe
G
Helde
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, Trondheim, Norway; Department of Neuroscience, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Eylert
E
Brodtkorb
D000328:Adult; D019973:Alcohol-Related Disorders / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology; D000927:Anticonvulsants / Q000627:therapeutic use; D018592:Cross-Over Studies; D004198:Disease Susceptibility; D004827:Epilepsy / Q000150:complications / Q000453:epidemiology* / Q000503:physiopathology / Q000628:therapy; D005260:Female; D005500:Follow-Up Studies; D006760:Hospitalization; D006801:Humans; D007407:Interviews as Topic; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012640:Seizures / Q000150:complications / Q000453:epidemiology* / Q000503:physiopathology / Q000628:therapy; D012890:Sleep / Q000502:physiology; D012892:Sleep Deprivation / Q000150:complications / Q000453:epidemiology* / Q000503:physiopathology
D000927:Anticonvulsants
Alcohol; Antiepileptic drugs; Epilepsy; Non-adherence; Seizure precipitants; Seizures; Sleep