DIFFUSION-WEIGHTED AND T-2-WEIGHTED INCREASES IN MAGNETIC-RESONANCE IMAGES OF IMMATURE BRAIN DURING HYPOXIA-ISCHEMIA - TRANSIENT REVERSAL POSTHYPOXIA

Citation
Ui. Tuor et al., DIFFUSION-WEIGHTED AND T-2-WEIGHTED INCREASES IN MAGNETIC-RESONANCE IMAGES OF IMMATURE BRAIN DURING HYPOXIA-ISCHEMIA - TRANSIENT REVERSAL POSTHYPOXIA, Experimental neurology, 150(2), 1998, pp. 321-328
Citations number
33
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
150
Issue
2
Year of publication
1998
Pages
321 - 328
Database
ISI
SICI code
0014-4886(1998)150:2<321:DATIIM>2.0.ZU;2-H
Abstract
Hypoxic-ischemic changes in brain are detected earlier with diffusion- weighted (DW) than with T-2-weighted magnetic resonance (MR) imaging t echniques in adults, whereas the response in immature brain is not kno wn. We investigated MR imaging changes prior to, during, and/or after 2 h of hypoxia-ischemia (right carotid artery occlusion + 2 h of hypox ia) in 7-day-old rats anesthetized with isoflurane. In general, within the first 45 min of hypoxia-ischemia there were no changes in the DW or T-2-weighted images. By the second hour of hypoxia-ischemia there w ere marked areas of increased intensity in both the T-2 and the DW ima ges, with cortex and striatum being affected prior to thalamus and hip pocampus. The area of DW exceeded that of T-2 hyperintensities. In the first hour after hypoxia-ischemia there was a transient recovery of h yperintensities on both T-2 and DW images. Between 24 and 72 h the hyp erintense area on DW images decreased, whereas that on T-2-weighted im ages increased. The distribution of pathological damage assessed histo logically correlated with the areas of hyperintensity on the MR images . In contrast to adult brain, early hypoxic-ischemic injury in immatur e brain is detected as an increase in intensity in both diffusion- and T-2-weighted images, indicating a unique alteration in brain water dy namics in this neonatal model of hypoxia-ischemia. These imaging chang es and alterations in brain water can rapidly but transiently reverse upon the start of normoxia and reperfusion, suggestive of secondary en ergy failure or delayed neuronal death.