Ictal apnea linked to contralateral spread of temporal lobe seizures: Intracranial EEG recordings in refractory temporal lobe epilepsy

Abstract

Respiratory mechanisms are implicated in sudden unexpected death in epilepsy (SUDEP). We previously demonstrated a high incidence of ictal hypoxemia in temporal lobe seizures. We now report on the temporal relationship between ictal apnea and seizure onset and spread in patients undergoing video-EEG (electroencephalography) telemetry (VET) with intracranial electrodes. Ten patients with medically refractory temporal lobe epilepsy (TLE) undergoing VET were studied. Data from synchronously recorded digital pulse oximetry (SaO(2)), end-tidal CO(2) (ETCO(2)), nasal airflow, abdominal excursions, and electrocardiography were obtained. Sixty-one seizures were captured. SaO(2) in the ictal/postictal period was available for 52 seizures, apnea onset times for 27 seizures, and ETCO(2) for 16 seizures. Apneas occurred only when seizures spread to the contralateral temporal lobe. The mean delay to apnea onset was significantly shorter after contralateral seizure spread (2.87 s) than after seizure onset (58.4 s); p < 0.001. The mean SaO(2) nadir with partial seizures or partial seizures prior to secondary generalization was 89.4 +/- 8.6% (91.5, 69-100). Following generalized convulsions the mean oxygen saturation nadir was 75.8 +/- 10.6% (78.5, 58-90). ETCO(2) elevations occurred with each ictal desaturation below 85%. There is a close temporal relationship between spread of seizures to the contralateral hemisphere and the onset of seizure-associated apnea. Apnea onsets are more tightly linked to time of contralateral spread than to time of seizure onset. Patients with TLE in whom there is evidence of contralateral seizure spread may be at higher risk for ictal-related respiratory dysfunction than those in whom seizures remain unilateral.