Sudden Death and Epilepsy—Closing in on Causes?
abstracts & commentary
Sources: Blum AS, et al. Oxygen desaturation triggered by partial seizures: Implications for cardiopulmonary instability in epilepsy. Epilepsia 2000;41:536-541; Nei M, et al. EKG abnormalities during partial seizures in refractory epilepsy. Epilepsia 2000;41:542-548.
Although post-mortem studies have identified abnormalities in patients experiencing sudden unexpected death in epilepsy ([SUDEP], see Neuro Alert, 2000;18:29), the specific cause has remained elusive. Most helpful to clinicians would be information identifying patients at high risk for SUDEP, as well as interventions to reduce the risk. Two studies examining cardiopulmonary function in epileptics may lead to future solutions. Examining patients with partial seizures, Blum and colleagues evaluated the association between attacks and arterial oxygen saturation, while Nei and colleagues identified the relationship with EKG abnormalities.
Blum et al reviewed 166 consecutive admissions and identified 17 patients who experienced a total of 49 partial or generalized seizures while undergoing video-EEG evaluation with continuous pulse oximetry. Generalized attacks accounted for 29 of 49 events, partial seizures affected 20. The data, however, were skewed by the fact that in a single patient 23 of the 29 generalized seizures were nonconvulsive. More interesting were the findings that 12 of 20 (60%) of partial seizures were accompanied by oxygen desaturation below 92%. Complete recordings were available for nine complex-partial seizures in six patients. Average maximal desaturation reached 83%. The length of desaturation lagged seizure onset by an average of 35 seconds and usually lasted throughout the seizure. EKG recordings monitored tachycardia during most periods of oxygen desaturation, but did not identify abnormal rhythms.
Nei et al evaluated the EKG in 43 patients during refractory partial seizures. Patients received a baseline 12-lead EKG prior to video-EEG monitoring that included continuous recording of a single EKG lead (lead I). Fifty-one seizures were monitored, 35 were complex-partial and 16 secondarily generalized. The EKG recorded minutes prior to ictal onset, during the seizure, and immediately following and was analyzed for abnormalities of heart rate, rhythm, conduction, repolarization, and corrected QT interval.
Seventeen of Nei’s 43 patients (39%) expressed ictal or postictal abnormalities on EKG. Three-quarters of patients with ictal abnormalities, however, had a normal baseline EKG. Six patients had a potentially serious seizure-related EKG change, including ST segment elevation, asystole, junctional rhythm, and supraventricular tachycardia (SVT). The remaining had more benign EKG changes, with the most common being atrial premature depolarizations (APDs) and sinus arrhythmia. Secondary generalization and prolonged duration were both independent predictors of EKG abnormalities. Neither laterality of seizure onset, choice of number of anticonvulsant medications, corrected QT interval, nor sleep state was significantly associated with the occurrence of EKG abnormalities.
Commentary
Striking is Nei et al’s finding that three-quarters of their patients with normal baseline EKGs undergo ictal or postictal EKG abnormalities. One can imagine that the coincidence of ictal EKG changes and ictal hypoxia may create the milieu for more malignant cardiac arrhythmias. Nei et al speculate that recurrent sympathetic hyperactivity-produced seizures may cause subtle yet progressive changes in the myocardium that increase the potential for lethal arrhythmias. The largest problem in understanding the causes of SUDEP has been its relatively low incidence despite the fact that it may cause as much as 50% of direct epileptic mortality. The studies of Blum and Nei represent first steps in finding possible etiologies of SUDEP. To find definitive causes will require prospective collaborative studies. —fal
Patients with complex-partial seizures without generalization are at risk for:
a. serious EKG changes including asystole, ST-segment elevation, SVTs, and junctional rhythms.
b. benign EKG changes including APDs and sinus arrhythmia.
c. oxygen desaturation.
d. All of the above
e. None of the above
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