Mortality in captive baboons with seizures: A new model for SUDEP?
Szabó CA, Knape KD, Leland MM, Feldman J, McCoy KJM, Hubbard GB, and Williams JT (2009) Mortality in captive baboons with seizures: A new model for SUDEP? Epilepsia 50:8 1995– 8.
Abstract: Because the baboon is a model of primary generalized epilepsy, we were interested in mortality of captive animals with a history of witnessed seizures. Causes of natural death were investigated in 46 seizure baboons (SZ) and 78 nonepileptic controls (CTL), all of which underwent a complete pathologic examination at the Southwest Foundation for Biomedical Research (SFBR) in San Antonio. SZ animals died at a younger age than the control baboons (p < 0.001). Almost all epileptic baboons that died suddenly without an apparent cause (SZ-UKN), had pulmonary congestion or edema without evidence of trauma, systemic illness, or heart disease, compared to nine controls (12%) (p < 0.001), most of which demonstrated evidence of a concurrent illness. Serosanguineous bronchial secretions were found in 15 SZ-UKN baboons (58%), but in only three controls (4%) (p < 0.001). Chronic multifocal fibrotic changes in myocardium were noted in only three (12%) of SZ-UKN baboons and one control baboon. Based upon these results, untreated seizures appear to reduce the life expectancy of captive baboons. Sudden unexpected death in epilepsy (SUDEP) may be a common cause of natural death in epileptic baboons.
Keywords: Papio; Baboon; Mortality; Epilepsy; SUDEP
Context
- Retrospective study of natural history of sudden death in a captive baboon population, comparing animals with and without epilepsy. Most control animals showed evidence of some illness at the time of death while most animals with epilepsy did not; members of the latter group were much more likely to have pulmonary edema/congestion at autopsy. There was also a higher likelihood of finding serosanguineous secretions in the affected animals, which, if blood from tongue bite damage during seizure could be ruled out, suggests pulmonary edema as a primary contributor to the death. This suggests an increase in pulmonary vascular permeability (cf. Theodore and Robin; Theodore and Robin). See Striano and Zara for a comment on this study.