Abstract
Epilepsy is the fourth most common neurologic disorde in the United States, affecting over 2.2 million people. Epilepsy is associated with a number of medical and psychiatric comorbidities, higher health-care use and cost, and substantial economic burden. OSA is twofold more common in adults with epilepsy than in age-matched control subjects, and the incidence increases with age. Self-reported daytime sleepiness is not helpful in predicting OSA, possibly related to the ceiling effect of general sleepiness among people with epilepsy from diverse causes. Mostly small retrospective series found a significant reduction in seizures in people with epilepsy and OSA adherent with positive airway pressure therapy compared with untreated individuals. This finding illustrates the potential beneficial effects of sleep therapies on epilepsy. Central apnea, oxygen desaturations, and hypercapnia can occur during the ictal and immediate postictal period, especially with generalized tonic-clonic seizures. Central apneas have been produced by electrical stimulation of mesial temporal structures. These respiratory disturbances suggest activation of the central autonomic network and may contribute to sudden unexpected death in epilepsy (SUDEP), the leading cause of epilepsy-related death in people with drug-resistant epilepsy. SUDEP typically occurs during sleep, and patients are more often found in a prone position and have a history of nocturnal seizures. Whether OSA contributes to SUDEP is unknown. Vagus nerve stimulation is a form of neuromodulation for drug-resistant focal epilepsy. When the device activates during sleep it causes reduction in airflow and respiratory effort, airflow obstruction, and oxygen desaturations, sometimes producing a clinical sleep apnea syndrome. The goal of this review is to discuss firmly established and recently recognized clinical, neurobiologic, electrophysiologic, and polysomnographic relationships between sleep-disordered breathing and epilepsy.
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