Abstracts

Rationale: Stroke is a major cause of seizures and epilepsy in adult-aging populations, and the pathophysiology behind post-stroke seizures is presently unclear. Experimental studies in animal models are of great value to improve our knowledge in this field. However, systematic investigations of post-stroke seizures/epilepsy in adult animals remain limited. The aim of our present study is to explore whether hypoxic-ischemic (HI) brain injury in adult mice serves a useful model to examine post-stroke seizures. Methods: C57 black mice of 3-9 months were used in the present experiments. Mice received a permanent, unilateral occlusion of right common carotid artery under isoflurane anaesthesia (2%). About one hour later while recovered from anaesthesia, the animals were challenged with global hypoxia via exposing to 8% oxygen for 30 min in an airtight chamber. After the hypoxic episode, the animals underwent continuous video monitoring. Intra-cranial EEG recordings were conducted in some experiments, and the EEG activities of the right hippocampus and left neocortex (ipsilateral and contralateral to carotid occlusion respectively) were monitored during and after HI. The severity of post-HI convulsions was quantified using a generalized seizure score system as per Pohl and Mares (1987) and Veliskova et al. (1990). Sham control mice were similarly operated but without the carotid artery occlusion and global hypoxia. After in vivo experiments, the animals were later sacrificed for histological assessment or for electrophysiological recordings in brain slices. Results: Severe seizures were observed in about 30% of mice examined following the HI insults. These seizures occurred largely within 12-36 hours post-HI and manifested fast running and jumping, barrel rolling, falling with the loss of righting reflex. Histological examination revealed that the hippocampus and temporal cortex ipsilateral to the carotid artery occlusion were grossly damaged. In contrast, such ipsilateral brain damage was absent in mice that did not exhibit severe behavioural seizures. Conclusions: It appears to be a notable correlation between the severity of HI-induced ipsilateral brain injury and the occurrence of post-HI seizures. Works are in progress to characterize EEG activities in post-HI mice and to examine the effects of anticonvulsive agents on post-HI seizures.