Antiepileptic drugs, insomnia, and obstructive sleep apnea may all affect the already complicated relationship between epilepsy and sleep.
As part of the Neuroendocrinology Special Interest Group session at the 2016 American Epilepsy Society Annual Meeting, Dr. Amy Z. Crepeau, Assistant Professor of Neurology at the Mayo Clinic Arizona, presented “Emerging Clinical Aspects of Sleep in Epilepsy.”
Dr. Crepeau began by summarizing recent literature regarding the effects of antiepileptic drugs (AEDs) on sleep architecture. Some AEDs, such as phenobarbital and phenytoin, reduce sleep quality, as indicated by decreased restorative slow wave sleep and/or random eye movement sleep. Other AEDs, such as gabapentin and pregabalin, appear to improve sleep quality, whereas topiramate and vigabatrin have minimal or no effect on sleep architecture.
Dr. Crepeau also discussed the effects of some nonpharmacologic treatments. She noted that although a recent study showed no objective improvement in sleep architecture after epilepsy surgery when all patients were considered, total sleep time improved in the subgroup of patients whose surgery was successful.
Vagal nerve stimulation (VNS) was also discussed. Despite limited evidence suggesting that VNS may improve sleep architecture, Dr. Crepeau emphasized that VNS can increase sleep-disordered breathing in patients with obstructive sleep apnea (OSA). Possible explanations include activation of vocal cord adduction, changes in laryngeal motility, and/or changes in brainstem activity.
The issue of OSA has special relevance, as there is a strong association between epilepsy and OSA. Dr. Crepeau noted that adults with epilepsy have an increased prevalence of OSA (10% overall and up to 30% in those with refractory epilepsy) and individuals with OSA have an increased prevalence of epilepsy. Thus, the possibility of OSA should be considered in all patients with epilepsy. Dr. Crepeau recommended the STOP-Bang questionnaire as a useful screening tool for OSA. Screening is particularly important if VNS is being considered.
Dr. Crepeau also described the close association between epilepsy and insomnia. Approximately 25% to 55% of people with epilepsy have insomnia. In turn, insomnia is associated with reduced seizure control. The cause and effect relationship is unclear – do increased seizures cause insomnia or does insomnia increase the frequency of seizures? Or perhaps, as suggested by Dr. Rama Maganti (another presenter at the session), both factors work in concert to produce a vicious cycle, with seizures causing disrupted sleep, then sleep deprivation leading to further increases in seizure activity.
Strategies to treat sleep disorders in patients with epilepsy were likewise discussed. Dr. Crepeau noted that in patients with OSA, continuous positive airway pressure has been convincingly demonstrated to improve seizure control.
Melatonin has been suggested as a treatment for insomnia in people with epilepsy, based in part on findings that individuals with epilepsy have lower salivary melatonin levels. This is an attractive strategy because of its lack of significant side effects. Dr. Crepeau discussed two studies involving children with epilepsy that demonstrated improved sleep quality with melatonin. However, she noted that these were short-duration studies and the long-term effectiveness remains uncertain.
Poor sleep hygiene may also contribute to insomnia. A recent survey reported that sleep hygiene was poor in adults with epilepsy, but it was also poor in adults without epilepsy. Nevertheless, Dr. Crepeau indicated that it is reasonable to educate patients with epilepsy and their families about strategies to improve sleep hygiene.
Dr. Crepeau also discussed the close association between insomnia and mood disorders, especially depression. Thus, when confronted with a patient with epilepsy who has insomnia, the presence of concomitant depression should be considered.
Reddy DS, coordinator, Special Interest Group: Neuroendocrinology, 2016, American Epilepsy Society Annual Meeting, www.aesnet.org.