Hartings JA, Williams AJ, Tortella FC Exp Neurol 2003;179:139–149 A significant proportion of neurologic patients have electroencephalographic (EEG) seizures in the acute phase after traumatic or ischemic brain injury, including many without overt behavioral manifestations. Although such nonconvulsive seizures may exacerbate neuropathologic processes, they have received limited attention clinically and experimentally. Here we characterize seizure episodes after focal cerebral ischemia in the rat as a model for brain injury–induced seizures. Cortical EEG activity was recorded continuously from both hemispheres up to 72 hours after middle cerebral artery occlusion (MCAo). Seizure discharges appeared in EEG recordings within 1 hour of MCAo in 13 (81%) of 16 animals and consisted predominantly of generalized 1- to 3-Hz rhythmic spiking. During seizures, animals engaged in quiet awake or normal motor behaviors, but exhibited no motor convulsant activity. Animals had a mean of 10.6 seizure episodes within 2 hours, with a mean duration of 60 seconds per episode. On average, seizures ceased at 1 hour 59 minutes after MCAo in permanently occluded animals and did not occur after reperfusion at 2 hours in transiently occluded animals. In addition to seizures, periodic lateralized epileptiform discharges (PLEDs) appeared over penumbral regions in the injured hemisphere, whereas intermittent rhythmic delta activity (IRDA) recurred in the contralateral hemisphere with frontoparietal dominance. PLEDs and IRDA persisted up to 72 hours in permanent MCAo animals, and early onset of the former was predictive of prolonged seizure activity. The presentation of these EEG waveforms, each with characteristic features replicating those in clinical neurologic populations, validates rat MCAo for study of acutely induced brain seizures and other neurophysiologic aspects of brain injury. Karhunen H, Pitkanen A, Virtanen T, Gureviciene I, Pussinen R, Ylinen A, Sivenius J, Nissinen J, Jolkkonen J Epilepsy Res 2003;54:1–10 Poststroke seizures occur in 5% to 20% of patients. Modeling of stroke-induced seizures in animals provides a useful tool for investigating the molecular basis of epileptogenesis and for developing therapies for stroke patients at increased risk for epileptogenesis. The questions addressed in the study were (a) Do rats develop spontaneous seizures after transient occlusion of the middle cerebral artery (MCAO)? (b) Is epileptogenesis associated with impaired hippocampus-dependent spatial learning and memory? (c) Are the functional abnormalities linked to axonal plasticity in the dentate gyrus? (d) Does the sensorimotor impairment induced by MCAO predict the risk of epileptogenesis? Adult male Sprague–Dawley rats were subjected to MCAO for 120 minutes. Development of spontaneous seizures was monitored by 1 week of continuous video-electroencephalographic (EEG) recordings at 3, 7, and 12 months after MCAO. Spontaneous seizures were not detected during 1-year follow-up in ischemic rats. Animals were, however, impaired in the spatial memory task ( P < .001), which was not associated with altered hippocampal long-term potentiation (LTP) or abnormal mossy fiber sprouting (Timm staining). Animals also had a long-lasting sensorimotor deficit ( P < .05). The present study indicates that MCAO causes long-lasting sensorimotor and spatial memory impairment but does not induce epileptogenesis or spontaneous seizures. [ABSTRACT FROM AUTHOR]