Status epilepticus

I ACCIDENTALLY STUMBLED ON STATUS EPILEPTICUS (SE) in the late '60s when attempting to study inhibition using a protracted stimulation protocol in previously kindled rats. I revisited and described that procedure in 1982 (McIntyre et al.), and continue to study the induction and consequences of the SE in kindled rats.

We have just completed a 10 year series of experiments, which include four different SE forms (non-convulsive, ambulatory, masticatory and generalized) in amygdala kindled rats subjected to the electrical, SE-induction procedure. Here we describe the time course (3, 6, 24 & 72 hr and 5 days) and anatomy of the ensuing brain damage (using rapid silver, TUNEL, Fluoro-Jade and HSP-72); the outcomes profiles of these four different phenotypes are remarkably internally consistent.

We continue to study these four profiles using bilateral microdialysis in an effort to unravel the relationship between amino acid overflow and/or glial release, seizures and the induction of brain damage. For example, in masticatory and generalized SE, there is extensive bilateral, symmetrical brain damage, but in ambulatory SE the damage is unilateral and extensive, while in non-convulsive SE it is unilateral and very restricted. Do the extracellular amino acid responses in those damaged (or spared) areas reflect these pathological outcomes? Importantly, the two less severe SE models suggest that partial SE also is dangerous and has significant and precise neurological sequelae.