Prolonged Epileptic Seizures in Primates

TLDR

Cortical damage in baboons was caused by multiple interacting factors, including cerebral epileptic activity. In ten adolescent baboons subjected to 82–299‑minute bicuculline‑induced generalized seizures, widespread ischemic‑type neuronal damage was observed in the neocortex, cerebellum, and hippocampus, originating during the seizure’s second phase and associated with hyperpyrexia, arterial hypotension, hypoxia, acidosis, and occasionally severe hypoglycemia.

Abstract

Neuronal alterations typical of ischemic cell change were seen in the brains of ten adolescent baboons after generalized seizures, lasting 82 to 299 minutes, induced by bicuculline. These changes involved the neocortex (diffusely, in all ten cases, with some accentuation occipitally), the cerebellum (Purkinje and basket cells, predominantly in the arterial boundary zone) and the hippocampus (hi and h_3-5sometimes asymmetrically). The brain damage apparently originated during the second phase of the seizure when hyperpyrexia, mild arterial hypotension, mild systemic hypoxia, and acidosis were characteristically, and severe hypoglycemia occasionally, seen. Cerebellar damage was related to hyperpyrexia and arterial hypotension. Numerous factors (including the cerebral epileptic activity) interacted to produce the cortical damage.