Epilepsy and Sleep Apnea
Abstract & Commentary
By Charles Pollak, MD, Professor of Clinical Neurology, Weill Cornell Medical College; Dr. Pollak reports no financial relationships relevant to this field of study.
Synopsis: Obstructive sleep apnea may be both a cause and a consequence of uncontrolled epileptic seizures.
Sources: Malow BA, Foldvary-Schaefer N, Vaughn BV, et al. Treating obstructive sleep apnea in adults with epilepsy: a randomized pilot trail. Neurology 2008;71:572-577; Foldvary-Schaefer N, Stephenson L, Bingaman W. Resolution of obstructive sleep apnea with epilepsy surgery? Expanding the relationship between sleep and epilepsy. Epilepsia 2008; 49:1457-1459.
It is well known to neurologists that convulsive seizures are more likely to occur during REM (rapid eye movement) or deep non-REM sleep, so much so that sleep is used as an activating condition in the diagnostic electroencephalography (EEG) laboratory. At the same time, sleep deprivation is a potent activator of seizures and of status epilepticus. The relationship of seizures to sleep, therefore, is complex.
The two papers cited above illustrate this complexity. Foldvary-Schaefer et al report the case of an 18-year-old epileptic man with interictal epileptiform discharges (IEDs) that were markedly activated in sleep. Subdural and depth electrode recordings from the left frontal and temporal lobes showed interictal discharges and three seizure types: behavioral arrest with and without automatisms, loss of contact with chin twitching and head jerks, and arousal from sleep with grimacing and head clonic activity. He underwent a premotor frontal lobotomy. In four postoperative years, he has had only five seizures despite the reduction of antiepileptic drugs. At the time of presentation, he reported daytime sleepiness and snoring and was found to have moderate obstructive sleep apnea (apnea-hypopnea index = 24 apneas or hypopneas per hour, not temporally related to epileptiform activity).
Use of continuous positive airway pressure (CPAP) resulted in abolition of apneas. Remarkably, not only was the apnea-hypopnea index (AHI) normal postoperatively, but the spike rate also was markedly reduced compared to the preoperative baseline.
Previously, small case series have shown that treatment of obstructive sleep apnea (OSA) may reduce seizures, possibly by reducing sleep-wake transitions and correcting sleep deprivation; however, amelioration of OSA following curative epilepsy surgery has never before been reported. The authors were unable to explain this outcome of surgery, though they speculated that the abundant interictal discharges and seizures prior to surgery might have affected upper airway control during sleep in a vulnerable patient.
The second study, by Malow et al, was described as a pilot study meant to provide critical information for planning a trial to test the hypothesis that treating OSA in epileptic patients would improve seizure control. Because 30% of patients with epilepsy continue to have seizures despite antiepileptic drugs (AEDs), eliminating factors such as sleep deprivation that may promote seizures could provide important new strategies for seizure control. Epileptic subjects selected for this study had to have two or more seizures a month after optimization of AEDs, as well as coexisting OSA.
Those subjects meeting criteria for OSA after two nights of polysomnography were randomly assigned to either therapeutic or sham-CPAP treatments. Sham CPAP was accomplished by providing a CPAP machine modified to include a large hidden leak in the exhaust port of the mask to disperse the therapeutic pressure. The sham treatment provided normal blower noise and airflow resistance, making the patient's experience similar to that of therapeutic CPAP. Subjects assigned to sham CPAP slept with the sham CPAP for two consecutive nights. Those assigned to therapeutic CPAP were titrated to the pressure needed to resolve their apneas and hypopneas. Therapeutic or sham treatment was then continued at home for 10 additional weeks. The second night of therapeutic CPAP was found to be significantly more effective in reducing AHI than the sham CPAP. It was not significantly more effective in reducing seizures; however, a greater reduction of seizures was observed in the therapeutic group.
Commentary
We must be cautious about drawing conclusions from the finding by Foldvary-Schaefer et al that curative epilepsy surgery in one patient resulted in an apparent resolution of sleep apnea. For one thing, the length of follow-up was not clear. We are told only that a follow-up polysomnogram 6 months postoperatively showed the AHI to be normal (1.1 events/hour). The mechanisms by which apneas were controlled are not known. It also is not clear whether the improvement lasted longer than 6 months, when a follow-up polysomnogram was done. The apneas and hypopneas had been occurring at a rate of 24 per hour and were easily controlled by a CPAP pressure of only 5 cm of water.
Malow et al billed their study as a "pilot" that provided information regarding the feasibility of a planned comprehensive trial to test the hypothesis that treating OSA in patients with epilepsy improves seizure control. Had the difference in seizure rate between therapeutic and sham CPAP groups been statistically significant, I suspect that this study of 68 subjects for which 865 candidates were screened would have been portrayed as solid evidence for detecting and treating sleep disorders such as OSA in epileptic patients. Instead, the need for a larger sample is evidence that the effect of OSA on seizure frequency is rather modest.
Taken together, these interesting studies contribute to our appreciation of the complexity of the relationship between sleep disorders and seizures. We may anticipate further exploration of this area, with clinical benefits as a likely result.
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