Resolution of obstructive sleep apnea with epilepsy surgery? Expanding the relationship between sleep and epilepsy


Address correspondence to Nancy Foldvary-Schaefer, DO, Cleveland Clinic Foundation, 9500 Euclid Avenue, FA20 Cleveland, Ohio 44195, U.S.A. E-mail:


Recent studies suggest a higher than expected prevalence of obstructive sleep apnea (OSA) in patients with refractory epilepsy. In some cases, treatment of OSA improves seizure control. We report a case in which clinically significant OSA disappeared after left frontal lobe resection that produced a near seizure free state. This occurred in the absence of the usual factors, such as weight or medication change or variation in polysomnography (PSG) recording methodology, that often confound the comparison of sequential PSGs over time. Our patient underwent PSG with 18-channel EEG recording pre- and postoperatively using standardized scoring techniques. Baseline testing revealed an apnea-hypopnea index (AHI) of 24 with severe oxygen desaturations reaching a nadir of 62%. Postoperative testing found both the AHI and oxygen saturation normalized as well as a marked reduction in spike rate. We hypothesize that the pathophysiology of OSA in patients with epilepsy may be impacted by frequent, extensive interictal epileptiform discharges (IEDs) and/or seizures altering upper airway control during sleep.

Recent studies suggest that sleep disorders such as obstructive sleep apnea (OSA) are more common than expected in patients with refractory epilepsy. Treatment of OSA has been shown to reduce seizures in some cases. We report a case in which the converse effect was observed; the disappearance of clinically significant OSA after successful epilepsy surgery.

Case Study

AP is an 18-year-old right handed male with intractable epilepsy since infancy. He initially presented with infantile spasms at 7 months of age. Throughout childhood, he experienced daily seizures of various types, including head drops and spasms. At the time of presentation, seizures were characterized by impaired awareness and agitated wandering occurring daily predominately during wakefulness and evolving to right version and generalized tonic–clonic activity a few times per year. He was taking oxcarbazepine 900 mg bid and phenytoin 200 mg bid. Examination was notable for psychomotor delay. He was attending high school with special assistance.

Video EEG evaluation revealed interictal epileptiform discharges (IEDs) in the left frontal (FP1 50%), right frontal (F8, 15%), right temporal (F8, 10%), and right parietal (P8, 10%) regions as well as generalized spike wave complexes (15%), all markedly activated in sleep. Seizures were characterized by sudden arousal from sleep with mumbling or shouting and vigorous bilateral extremity movements at times evolving to an axial tonic phase lasting 10–30 s with rapid return to baseline. The ictal EEG demonstrated diffuse suppression with paroxysmal fast activity lateralized to the right hemisphere, maximum frontal. A single bilateral asymmetric tonic seizure evolving to right face tonic and generalized tonic–clonic activity was recorded having a left hemisphere ictal pattern. Several left frontal subclinical seizures were also recorded. Brain MRI was normal. Fluorodeoxyglucose (FDG)-positron emission tomography (PET) revealed left hemisphere hypometabolism. Ictal single photo emission computed tomography (SPECT) study was attempted but not accomplished. A metabolic workup including skin biopsy was normal. Neuropsychology revealed a full scale IQ of 93, intact memory, and impaired executive functions. A methohexital test revealed right hemisphere language dominance and intact memory bilaterally.

Invasive monitoring was performed with subdural and depth electrodes covering the left frontal and temporal lobes including mesial temporal structures and cingulum. Interictal discharges were recorded from the orbitofrontal and inferior dorsolateral convexity (68%), superior dorsolateral convexity (30%), and anterior subtemporal (2%) regions. Three seizure types were recorded including (1) behavioral arrest with/without oral and manual automatisms associated with paroxysmal fast activity over the dorsolateral frontal region anterior to the motor strip; (2) loss of contact with chin twitching and head jerks to the left in clusters having a nonlocalized EEG; and (3) arousal from sleep with facial grimace and moaning followed by thrashing evolving to right head clonic activity also with a nonlocalized EEG. The patient underwent a premotor frontal lobectomy with guarded prognosis for seizure freedom. Pathology revealed architectural disorganization suggestive of a malformation of cortical development. He had right hemiparesis that resolved over several weeks. In the 4 years since surgery, he had only five seizures despite reduction of AED regimen to oxcarbazepine (OXC) monotherapy semiologically distinct from his preoperative seizures.

At the time of presentation, the patient reported daytime sleepiness and snoring and underwent polysomnography (PSG) in March 2004. He was found to have moderate OSA with an apnea-hypopnea index (AHI) of 24, worse in rapid eye movement (REM) sleep and associated with severe oxygen desaturations. Respiratory events were not temporally related to epileptiform activity. He had a typical seizure arising from slow wave sleep (SWS) consisting of bilateral asymmetric tonic activity with more prominent right sided motor involvement and right head version followed by generalized clonic activity associated with rhythmic delta activity lateralized to the left hemisphere. He subsequently underwent a continuous positive airway pressure (CPAP) titration study during which respiratory events and oxygen desaturations were abolished with a CPAP pressure of 5 cm H2O. He underwent repeat baseline PSG 6 months postoperatively in May 2005 due to CPAP noncompliance. Both PSGs were performed with simultaneous 18-channel EEG recording. On this study, the AHI was normalized and spike rate was markedly reduced compared to baseline (867 vs. 27 spikes per hour). No seizures were recorded. Pre- and postoperative PSG findings are shown in Table 1. AEDs and dosage were unchanged across studies.

Table 1.  Polysomnographic parameters
 Preoperative PSGPostoperative PSG
  1. aInterictal epileptiform discharges per hour, quantified over the first sleep cycle.

Body mass index (kg/m2)21.223.1
Recording time (min)374.1 491.0 
Total sleep time (min)367.4 367.0 
Supine sleep time (%)100.0 97.0
Sleep efficiency (%)98.274.7
Sleep latency (min) 0.2111.0 
REM latency (min)301.5 76.0
Stage 1 (%) 7.3 3.8
Stage 2 (%)37.353.0
Stages 3–4 (%)52.322.1
Stage REM (%) 3.121.1
Arousal index11.314.4
AHI24.3 1.1
REM AHI47.1 2.3
Mean/Minimum SaO292/6298/91
% TST with SaO2 < 90%30.60
Periodic limb movement index 1.015.2
Periodic limb movement arousal index0  2.9
No. of recorded seizures10
Spike ratea867  27 


OSA affects up to 24% of men and 9% of women (Young et al., 1993) and appears to be even more common in epilepsy, affecting over 30% of patients with intractable seizures (Malow et al., 2000). A recent study found older adults with new onset seizures or worsening epilepsy more likely to have OSA than similarly-aged patients with well-controlled seizures (Chihorek et al., 2007). Untreated OSA is associated with a variety of potentially life-threatening conditions including cardiac arrhythmias, hypertension, stroke, and myocardial infarction. Treatment of OSA has been shown to reduce seizures in small series (Devinsky et al., 1994; Vaughn et al., 1996; Malow et al., 1997) possibly by consolidating sleep and reversing the effects of sleep deprivation.

We report the case of a young male with intractable focal epilepsy and moderate OSA that resolved after successful left premotor frontal resection. This finding is not explained by variation in recording technique (thermister and nasal pressure recordings were obtained on both PSGs), amount of supine sleep time, sleep architecture variations, change in body mass index (BMI) or medications. In fact, comparison of BMI and sleep architecture across studies would have predicted the AHI to worsen postoperatively as the BMI was slightly higher, the REM percentage increased (muscle atonia during REM predisposes to more frequent and severe upper airway obstruction), and SWS percentage reduced (SWS is protective of upper airway obstruction). Normalization of the AHI postoperatively was associated with seizure freedom and a marked decline in spike rate.

While there is growing evidence that sleep apnea increases excitability in the epileptic brain, the converse effect of amelioration of OSA following curative epilepsy surgery has not been previously reported. It is possible that cessation of seizures and reduction of interictal discharges stabilize sleep thereby reducing respiratory events. However, respiratory events were not restricted to sleep–wake transitions, so this effect would not be sufficient to explain our findings. It is also possible, though entirely speculative, that abundant interictal discharges and/or seizures, as observed in this case, adversely affect upper airway control during sleep in vulnerable patients. Patients with epilepsy are often less physically fit and therefore, more overweight than their counterparts in the general population and take medications that either cause weight gain or reduce upper airway tone (benzodiazepines and barbiturates predominately). While these factors likely contribute to the observed increase of OSA in intractable epilepsy patients, neither applies in this case. This case illustrates yet another example of the complex relationship between OSA and epilepsy, and highlights the need for routine screening for sleep disorders in patients with epilepsy. Further understanding of the mechanisms underlying these findings is required.

Conflict of interest: We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. None of the authors has anything to disclose.