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Irregular Respiratory Rhythm: A Physiological Biomarker of SUDEP Risk in Patients with Nocturnal Seizures?

Commentary A subset of patients with temporal lobe epilepsy (TLE) have been identified as at greater risk for sudden unexpected/unexplained death in epilepsy (SUDEP), specifically, those with generalized tonic-clonic seizures, nocturnal seizures, early onset epilepsy, and long duration of epilepsy that is refractory to antiseizure drugs (ASDs). A few prototypical ASDs (e.g., carbamazepine) have also been associated with SUDEP risk (1). Over 30% of patients with TLE have seizures that are refractory to commonly used ASDs and 9 in 1000 of these intractable patients will die yearly from SUDEP (2). Given these contributing factors, there is a need for the 1) identification of reversible indicators (i.e., physiological biomarkers) of SUDEP risk in animal models of epilepsy and most importantly, 2) development of novel therapies to modify SUDEP biomarkers to prevent fatalities in this relatively large patient population. Hajek and Buchanan have identified changes in measures of respiration during potentially important sleep states and demonstrated that animals with baseline susceptibility to respiratory dysfunction have an increased mortality rate following maximal electroshock (MES)-induced seizures. This is particularly exciting given that data from epilepsy patients included in the Mortality in Epilepsy Monitoring Unit (MORTEMUS) study (3) suggests that respiratory and cardiac mechanisms contribute to SUDEP. Every case of monitored SUDEP in the MORTEMUS study followed a generalized tonicclonic seizure (GTCS), and a pattern of seizure-induced events leading to death was identified. GTCS is followed by postictal generalized EEG suppression (PGES) that is associated with depression of cardiorespiratory function (apnea/hypoventilation) and finally, asystole. Additionally, baseline abnormal cardiac and autonomic features were observed in epileptic patients that may facilitate or trigger SUDEP in the absence of epileptic seizures. Hajek and Buchanan have used a well-designed, simple approach to determine whether sleep state, a known risk factor for SUDEP, contributes to autonomic dysfunction following a single, evoked seizure. C57bl6 mice were outfitted with EEG, EKG, electromyography (EMG), and a temperature transponder to assess multiple physiological measures. Sleep-state was determined in real time prior to stimulus delivery using standard EEG/EMG frequency definitions of vigilance state. Respiratory and cardiac function was assessed before, during, and after evoked seizures. Seizure susceptibility, respiratory function, and cardiac function are regulated by sleep transitions. Animal models and patients with TLE demonstrate more frequent seizures during non–rapid eye movement (NREM) sleep, and relatively infrequent seizures during REM (4). However, Hajek Influence of Vigilance State on Physiological Consequences of Seizures and Seizure-Induced Death in Mice.