Abstracts

Rationale: The baboon provides a natural non-human primate model for photosensitive, idiopathic generalized epilepsy. This study describes an implantation procedure for the placement of subdural grid and strip electrodes for continuous video-EEG monitoring in the epileptic baboon to evaluate the generation and propagation of ictal and interictal epileptic discharges. Methods: Subdural grid, strip and depth electrodes were implanted in six epileptic baboons and one asymptomatic animal (Table 1), targeting brain regions that were activated in functional neuroimaging studies during photoparoxysmal responses (Figure 1). Three epileptic baboons were photosensitive by previous scalp EEG studies. The asymptomatic baboon has a normal scalp EEG prior to implantation. The baboons were monitored with continuous video-EEG monitoring for 2-21 (mean 9) days. Although the animals were tethered, the EEG signal was transmitted wirelessly to optimize their mobility. Spontaneous seizures, interictal epileptic discharges (IEDs), and responses to intermittent light stimulation (ILS) were assessed. Because of cortical injuries related to the electrode implantation and their displacement in earlier studies, the procedure was modified. Histopathological examination of the three last animals monitored (11 to 21 days) determined only to reactive inflammatory changes of the meninges. Results: Habitual myoclonic and generalized tonic-clonic seizures were recorded in four baboons. In three baboons the ictal discharge was triggered multiregionally, usually either by a discharge in the frontal, parietal or occipital cortices. In one baboon, myoclonic seizures were associated with a generalized ictal discharge. IEDs were recorded in all of the epileptic baboons, and similar to the ictal discharges, they were expressed multiregionally (Figure 1) and responsible for triggering most generalized spike-and-wave discharges. Generalized interictal epileptic discharges were suppressed in one baboon with a focal cortical injury due to the subdural electrodes. Generalized photoparoxysmal responses were activated only in one of three photosensitive baboons, while driving responses recorded over the occipital convexity in all three were 2.5 times the stimulus rate. Conclusions: In contrast to previous intracranial investigations in this model, generalized ictal and interictal epileptic discharges were triggered not only by frontal, but also parietal and occipital cortices. Furthermore, targeted visual areas responded differently to ILS in photosensitive than nonphotosensitive baboons, but further studies are required before mechanisms can be implicated for ILS-induced activation of the epileptic networks.