THE ROLE OF HYPOVENTILATION IN A SHEEP MODEL OF EPILEPTIC SUDDEN-DEATH

Citation
Sc. Johnston et al., THE ROLE OF HYPOVENTILATION IN A SHEEP MODEL OF EPILEPTIC SUDDEN-DEATH, Annals of neurology, 37(4), 1995, pp. 531-537
Citations number
33
Categorie Soggetti
Clinical Neurology",Neurosciences
Journal title
ISSN journal
03645134
Volume
37
Issue
4
Year of publication
1995
Pages
531 - 537
Database
ISI
SICI code
0364-5134(1995)37:4<531:TROHIA>2.0.ZU;2-M
Abstract
Unexpected sudden death is a common event in otherwise healthy epilept ics, though its etiology has remained unclear. Many authors have sugge sted cardiac arrhythmias as the cause, and limited data in humans and animal studies have supported this. However, autopsy series in humans have shown pulmonary edema, a phenomenon not compatible with a sudden arrhythmic death, as a possible cause. We developed a model of status epilepticus in unanesthetized, chronically instrumented sheep in which sudden death and pulmonary edema occur. Catecholamine levels and seiz ure type and duration did not differ between animals dying suddenly an d those surviving. Benign arrhythmias were generated in all animals; i n no case did an arrhythmia account for the-death of an animal. Striki ng hypoventilation was demonstrated in the sudden death group but not in the surviving animals. Differences in peak left atrial and pulmonar y artery pressures, and in extravascular lung water were also demonstr ated; pulmonary edema did not account for the demise of the sudden dea th animals. Thus, our model of epileptic sudden death supports a role of central hypoventilation in the etiology of sudden unexpected death and confirms the association with pulmonary edema. The importance of a rrhythmia in its pathogenesis is not confirmed.