Neostigmine Activated Epileptiform Discharge in the Amygdala: Electrographie‐Behavioral Correlations

Abstract

Amygdaloid epileptiform activity was investigated in relation to cholinergic hyperactivity. The physiopathology of psychomotor epilepsy was examined and an experimental model proposed. Neostigmine was injected intracerebrally into the amygdala of the cebus monkey [Cebus apella] with chronically implanted chemitrodes fitted with EEG recording electrodes. The injections were made in the basal amygdaloid nucleus which normally shows very high acetylcholinesterase (AChE) enzymatic activity in histochemical preparations. Neostigmine injection resulted in very high amplitude spike activity in the amygdala only. Other brain areas, including the neighboring temporal cortex, did not show any marked EEG changes. In the 1st day or 2, these EEG changes were associated with myoclonus localized in the ipsilateral muscles of facial expression and also associated with masticatory seizures. Subsequently the animal became aggressive and remained so several months after the injection of neostigmine. The EEG changes continued for approximately 6 wk. Injections i.n. of atropine diminished the amplitude of the epileptiform EEG discharges and modified slightly the animal''s behavior.