Hypoxic-isehemic encephalopathy (HIE) is a significant cause of infant morbidity for both term and premature babies. Non-invasive evaluation of neonatal HIE can stage treatment of injury in the postnatal phase. A brain injury model in neonatal rabbits of common carotid artery occlusion combined with hypoxia was studied. DWI and PWI methods similar to those of our perfusion and diffusion programs for clinical stroke were used. Methods and Results A navigated DWI and PWI technique was used and were repeated every 30 - 40 minutes. ischemic changes were noted in the diffusion weighted images, hypoxia was discontinued. observations were made for up to 2 hours after the return to normoxia. Hypoxia alone caused no change in either ADC or perfusion until 4 hours. ADC decrease was then dramatic, bilateral, and accompanied by globally decreased perfusion. Reversal of hypoxia within 30 min of diffusion changes dramatically led to rapid normalization of both diffusion and perfusion scans. Figure 26 shows in vivo diffusion- weighted images. The first diffusion image is normal, even after ischemia. After 50 minutes (second image), a bright area appeared in the hemisphere ipsilateral to the carotid occlusion, indicative of metabolic disturbances and brain injury. When oxygen returned to normal, the brain returned to normal state and no evidence of injury was apparent. Images taken 24 hours later showed no areas of increased signal intensity. In this case, perfusion MRI showed impaired blood flow to the ischemic area, which resolved upon the return to normoxia. Discussion These early results suggest that focal metabolic changes may be detected before the onset of permanent neurologic injury in carotid artery ligation combined with hypoxia. These injuries are accompanied, and possibly preceded, by corresponding perfusion deficits. This suggests that neurons tolerate hypoxia reasonably well as long as there is adequate perfusion.
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