MAGNETIC-RESONANCE-IMAGING ASSESSMENT OF EVOLVING FOCAL CEREBRAL-ISCHEMIA - COMPARISON WITH HISTOPATHOLOGY IN RATS

Background and Purpose This study was performed to document the progre ssion of ischemic brain damage after middle cerebral artery occlusion in the rat using magnetic resonance imaging and histopathologic method s. Methods Cerebral ischemia was induced through permanent tandem occl usion of ipsilateral middle cerebral and common carotid arteries. The evolution of magnetic resonance imaging and histopathologic parameter changes was studied, both short term (1.5 to 8 hours) and long term (2 4 to 168 hours), in five specific brain regions within the middle cere bral artery territory. Results Significant changes in proton nuclear m agnetic resonance spin-lattice and spin-spin relaxation times and the ''apparent'' diffusion coefficient of water could be detected within h ours after the onset of permanent focal cerebral ischemia, whereas sig nificant alterations in proton spin-density ratios were not apparent u ntil approximately 48 hours. Histological changes were evident within 12 hours, with a significant loss of neurons seen in the most severely damaged regions at 7 days. Diffusion-weighted imaging was the most se nsitive technique for visualizing acute ischemic alterations. The wate r diffusion coefficient was the only magnetic resonance imaging parame ter studied to indicate significant alterations within the first 4 hou rs after arterial occlusion in all five brain regions. Conclusions The degree of change for a particular magnetic resonance imaging paramete r appeared to be related to the location and extent of neuronal injury , with the most dramatic changes occurring within the areas displaying the most severe histological damage. These results indicate that comp lete specification of all brain regions affected by ischemic brain inj ury may require a combination of imaging strategies applied over a per iod of days and suggest the possibility of using magnetic resonance im aging to distinguish between permanent and reversible cell damage.