Citation

Simon RP. Epilepsia 1997; 38(11 Suppl): S35-7.

Affiliation

Department of Neurology, University of Pittsburgh, 3471 Fifth Avenue, Pittsburgh, PA 15213, U.S.A.

Copyright

(Copyright © 1997, John Wiley and Sons)

DOI

10.1111/j.1528-1157.1997.tb06124.x

PMID

19909323

Abstract

The pathologic hallmark of sudden unexpected death in epilepsy (SUDEP) in humans is pulmonary edema. In an animal model of seizures, pulmonary vascular pressure, but not systemic pressure, increases in proportion to seizure duration. The induced pulmonary vascular hypertension drives fluid out of the vascular compartment into the lung parenchyma. Blocking intra-ictal pulmonary vascular pressure elevations prevents changes in the observed doubling of the pulmonary transcapillary fluid flux. In this animal model, the main difference between surviving animals and those that die during the seizure is apnea, with a precipitous fall in the partial pressure of oxygen (pO(2)) and a parallel elevation in the partial pressure of carbon dioxide (pCO(2)) recorded in nonsurvivors. Pulmonary artery and left atrial pressures in animals that die are double those of surviving animals, with a resultant increase in extra-vascular lung water at postmortem examination. The pulmonary edema is due to the combined effects of seizure- and hypoxia-induced pulmonary vascular hypertension. This animal model reproduces both death during epilepsy and pulmonary edema at postmortem examination. The etiology of the pulmonary edema appears to be that of pulmonary vascular hypertension, and the etiology of sudden death appears to be that of centrally induced apnea.

Language: en