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Transient ischemic attacks (TIAs) are brief neurological deficits ofcerebrovascular origin that are followed by complete clinical recovery. Although a plethora of animal models exist for ischemic stroke, a verified TIA model is lacking. We aimed to optimize such a model in mice, investigating the impact of varying durations (from 2.5 to 20 minutes) of intraluminal middle cerebral artery occlusion (MCAo). Three conditions were required to mimic clinical TIA reliably: 1) an objective demonstration of occlusion and reperfusion (assessed by laser Doppler flowmetry); 2) no permanent neurological deficit (assessed by sensorimotor neurological evaluation); and 3) no lesion at 24 hours after reperfusion (assessed by magnetic resonance imaging [MRI]). We observed high incidences of MRI lesions with MCAo durations of 15 minutes or longer. In contrast, no permanent neurological deficits or MRI lesions were observed in animals with MCAo below or equal to 10 minutes. Middle cerebral artery occlusion of 12.5 minutes rarely induced MRI lesions, but histopathologic evaluation using routine and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining revealed minute ischemic changes even after 2.5-minute MCAo. Abundance of necrotic and apoptotic changes gradually increased with the duration of ischemia. These results indicate that 10 minutes or shorter focal cerebral ischemia proves a suitable mouse TIA model; in addition, they indicate that MRI-negative microscopic ischemic damage may occur with even a few minutes of arterial occlusion.

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Transient ischemic attack (TIA) has received only little attention in the experimental research field. Recently, we introduced a TIA model for mice, and here we set similar principles for simulating this human condition in Wistar rats. In the model: 1) transient nature of the event is ensured, and 2) 24h after the event animals are free from any sensorimotor deficit and from any detectable lesion by magnetic resonance imaging (MRI). Animals experienced varying durations of ischemia (5, 10, 12.5, 15, 25, and 30min, n=6-8pergroup) by intraluminal middle cerebral artery occlusion (MCAO). Ischemia severity and reperfusion rates were controlled by cerebral blood flow measurements. Sensorimotor neurological evaluations and MRI at 24h differentiated between TIA and ischemic stroke. Hematoxylin and eosin staining and apoptotic cell counts revealed pathological correlates of the event. We found that already 12.5min of ischemia was long enough to induce ischemic stroke in Wistar rats. Ten min or shorter durations induced neither gross neurological deficits nor infarcts visible on MRI, but histologically caused selective neuronal necrosis. A separate group of animals with 10min of ischemia followed up to 1week after reperfusion remained free of infarction and any MRI signal change. Thus, 10min or shorter focal cerebral ischemia induced by intraluminal MCAO in Wistar rats provides a clinically relevant TIA the rat. This model is useful for studying molecular correlates of TIA.

Decompressive craniectomy performed up to 24 hours improved outcome after experimental ICH, with earlier intervention of greater benefit.