Original articleIdentification and treatment of obstructive sleep apnea in adults and children with epilepsy: a prospective pilot study☆
Introduction
Obstructive sleep apnea (OSA) and epilepsy are both common conditions that are interrelated. In prior work, we reported that up to one-third of adults with medically refractory seizures have OSA, defined by an apnea–hypopnea index (AHI) of five events or more per hour [1]. Twelve percent of subjects in this report had moderate OSA, defined by an AHI of 20 or greater. Patients with epilepsy may have coexisting OSA not only because this sleep disorder is so common but also because of the effects of epilepsy treatments on breathing during sleep. Antiepileptic drugs (AEDs) may promote weight gain [2] or affect upper airway tone [3], thereby contributing to OSA. Devices such as the vagus nerve stimulator (VNS) may affect upper airway musculature or brainstem networks that regulate respiration during sleep [4].
Several case series in adults and two in children have reported the coexistence of OSA with epilepsy and the improvement in seizure control or daytime sleepiness when OSA was treated [5], [6], [7], [8], [9], [10]. Limitations of these studies, inherent to small case series, include: (1) only small numbers of selected patients treated for OSA are reported; (2) none of the studies systematically screened large groups of epilepsy patients to identify and treat those with OSA; (3) sleepiness was not assessed using physiologic measures; and (4) apart from the study by Vaughn et al. [7], subjects did not keep seizure calendars and AEDs were not monitored with serum levels.
In this pilot study, we screened patients with epilepsy seen in adult and pediatric clinics for the presence of sleep-disordered breathing with validated questionnaires followed by comprehensive sleep evaluations. Those meeting study criteria were invited to participate in a longitudinal study of the effects of treating OSA on epilepsy and underwent polysomnography (PSG). Throughout the study, seizure calendars were used to document seizure occurrence. AED doses were kept constant throughout the study and AED levels were checked during the baseline and treatment phases. Our hypothesis was that treating OSA would improve seizure frequency.
Section snippets
Methods
This study was approved by the University of Michigan Institutional Review Board and conducted between May 2000 and June 2002. Clinic rosters were used to identify epilepsy patients aged 5 and older coming for return visits at the Adult and Pediatric Neurology Clinics at the University of Michigan. Adult patients completed the University of Michigan Adult Sleep and Epilepsy Questionnaire, developed for this study, if (a) had a history of recurrent epileptic seizures; (b) were able to provide
Adult subjects
A total of 398 adult subjects, aged 18 and older, were surveyed. Fifty-two subjects surveyed met our primary study criteria of four or more seizures a month and an SDQ score of 27 or greater in women or 30 or greater in men. Thirteen adults agreed to participate in this trial and met complete entry criteria, confirmed at the comprehensive sleep evaluation and screening visit.
These subjects consisted of 12 with partial epilepsy, with or without secondary generalization, and one (subject #1) with
Discussion
Our results show that treatment of OSA in epilepsy patients may reduce seizure frequency. The 3 adults and 1 child who were compliant with CPAP treatment showed at least a 45% reduction in seizure frequency, with the adult treated with an oral appliance showing a reduction in nocturnal seizures. Even subjects with mild OSA (AHI<20) showed improvement. Identification and treatment of sleep disorders in epilepsy patients represents a novel therapeutic avenue for the 30% of patients with epilepsy
Acknowledgements
Mr Jason Cannon performed a portion of the polysomnograms.
This work was supported by the University of Michigan General Clinical Research Center (MO1 RR00042), the University of Michigan Medical School Venture Investment Fund, and NINDS KO2 NS2099.
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Cited by (0)
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Presented in part at the 55th annual meeting of the American Academy of Neurology, Honolulu, Hawaii.