(Abst. 3.195 ), 2009
ICTAL HYPOVENTILATION CONTRIBUTES TO CARDIAC ARRHYTHMIA AND SUDEP: REPORT ON TWO DEATHS AND FOUR POTENTIALLY LIFE-THREATENING EVENTS IN VIDEO-EEG MONITORED PATIENTS
Authors: Lisa Bateman, M. Spitz and M. Seyal
Sudden unexplained death in epilepsy (SUDEP) is the most common cause of death in patients with epilepsy with an incidence of 2.2-10 per 1000 patient years. Cardiorespiratory dysfunction and a primary cessation of cerebral function have been proposed as causes of SUDEP. Five cases of monitored SUDEP and three cases of near-SUDEP have previously been reported.
We report two cases of SUDEP and one near-SUDEP in patients undergoing video-EEG telemetry at two centers. Case 1 was a 42 year old woman and Case 2 a 62 year old man. Both had intractable temporal lobe epilepsy (TLE) and were potential surgical candidates. Case 3, a near-SUDEP, was a six-month old girl with Miller-Dieker syndrome. Three other patients with documented ictal/post-ictal hypoxemia and hypercapnia and significant transient post-ictal cardiac arrhythmias are also described.
Both patients with SUDEP had terminal secondarily generalized convulsions, lasting 102 seconds (s) and two minutes (min) respectively. EEG was diffusely suppressed post-ictally. In Case 1, respiratory movements persisted for 12 min and EKG for 18 min, becoming progressively slower and more erratic before ceasing. In Case 2, EKG and respiratory artifacts continued for two min before ceasing. Both patients were prone and it could not be determined whether respiratory efforts resulted in adequate ventilation. EKG tracings revealed ST elevations and peaked T waves, suggesting the presence of hypoxia and acidosis. In Case 3, a 100 s seizure arising from the central vertex was associated with apnea, cyanosis and post-ictal EEG attenuation. The patient was supine. Bradycardia and asystole developed within 15 s of seizure termination. Oxygen saturation (SaO2) during resuscitation, while 100% oxygen was being administered, was 71%. In three other cases, severe ictal/postictal respiratory dysfunction was associated with post-ictal EEG attenuation and cardiac arrhythmia. Case 4, a 34 year-old man with left TLE, had bradycardia and asystole with SaO2 nadir of 60% and peak end-tidal CO2 (ETCO2) of 72 mmHg. Case 5, a 34 year-old man with right TLE, had a ventricular arrhythmia and asystole with SaO2 nadir of 81% and ETCO2 rise to 46mmHg before the sensor was dislodged. Case 6, a 35 year-old woman with suspected frontal lobe epilepsy, had a 17-second run of ventricular ectopy with SaO2 nadir of 81% and peak ETCO2 of 46 mmHg. None of these patients were prone and there was no evidence of upper airway obstruction.
Diffuse post-ictal EEG suppression preceded cardiac arrest in two SUDEP patients and was also seen in a case of near-SUDEP. Three other patients had significant post-ictal cardiac arrhythmias including ventricular ectopy and asystole during periods of postictal hypoxia and hypercapnia. We postulate that ictal and post-ictal hypoventilation may contribute to SUDEP with the resulting hypoxemia, hypercapnia and acidosis leading to failure of recovery of cortical function and eventual cardiac failure.
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