Publication / Source: Neurology Central
Authors: Mark Stewart, State University of New York Downstate Medical Center, NY, USA
Sudden death in epilepsy (SUDEP) has received considerable attention in the last decade, resulting in refinements in the definition (“… a non-traumatic, non-drowning death that occurs in benign circumstances in an individual with epilepsy …” See e.g. [1,2]), more detailed calculations of incidence (from approximately one to nine deaths per 1000 patient years) [2–4], and the identification of key cardiopulmonary events that contribute to an overall pattern ending with death .
A wide range of animal models has been used to explore cardiac and/or respiratory derangements due to or associated with seizure activity that may contribute to an individual’s death (for wide-ranging review: ). For example, research employing transgenic mouse models has suggested critical contributions from genetic mutations impacting serotonergic neurotransmission and function in brainstem respiratory centers [2,6–8].
What is known and what is unknown about the circumstances of each human death, however, has been used to raise questions about the appropriateness of particular animal models for the study of SUDEP. As examples, because of data indicating that the majority of deaths occur at night (suggesting a circadian variance in some parameter) and when the individual was in bed (suggesting that, as with some infants, the airway might become obstructed by bedding) (reviewed in ), data from animal models not specifically incorporating these details have been dismissed as incomplete. Identification of clear linkages between the animal model and human pathophysiology has not occurred.
Our rat model and data relevant to SUDEP