• Cats underwent massive microembolization via carotid infusion of 10.5 million microspheres (15 ± 5μ in diameter), resulting in brain death within four hours; 87.4 μ 10.2% of emboli reaching the brain were in the ipsilateral hemisphere; 87.9 μ 4.4% were in the grey matter; and 12.1 μ 4.4% were in the white matter. Evans blue and sodium fluorescein dyes were given intravascularly before and at different times after embolization. Fluorescence microscopy disclosed that embolization initially provoked a hyperemic engorgement of both the embolized and nonembolized hemispheres. Multifocal, blood-brain barrier extravasations occurred throughout the ipsilateral cortex and oral basal ganglia. Severe vasogenic brain edema ensued, with migration of extravasations from cortex into the white matter, which initially showed only minimal injury. Migration and accumulation of edema in white matter, with subsequent uptake and swelling of neuroglia and axons, may be related to secondary white matter damage following cortical embolic lesions. Degenerative foci developed throughout the embolized cortex over the one- to fourhour period of this study. These sites may correspond to those areas in which hyperemia and damage to the blood-brain barrier was present shortly after embolization.
Schuier FJ, Vise WM, Hossmann KA, Zülch KJ. Cerebral MicroembolizationII. Morphological Studies. Arch Neurol. 1978;35(5):264–270. doi:10.1001/archneur.1978.00500290010003
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