title: Diffusion and high resolution MRI of traumatic brain injury in rats: time course and correlation with histology.
abstract: Although widely employed in studies of cerebral ischemia, the use of diffusion-weighted imaging (DWI) for traumatic brain injury (TBI) has been both limited and primarily confined to the first few hours after injury. Therefore, the present study examined the temporal evolution of magnetic resonance imaging (MRI) signal changes from hours to weeks after moderate fluid-percussion TBI in rats. We used isotropic diffusion along three directions and high resolution (HR) spin-echo pulse sequences to visualize DWI and HR MRI changes, respectively. Late changes were compared to histopathological and neurological outcome. A significant decrease (P<0.05) in the apparent diffusion coefficients (ADC) below preinjury levels was found in the left cortex and left hippocampus (ipsilateral to injury) at 1-2 h post-TBI. At 2 weeks post-TBI, ADCs were significantly elevated (P<0.05) above preinjury levels in both cortex and hippocampus. Regions of hypo- and hyperintensity detected in HR MRI scans also showed evidence of tissue damage by histological evaluation. Neurological assessment indicated that such changes were observed at a level of injury which produced moderate impairment 2 weeks after the insult. These results indicate that alterations in DWI and HR MRI signals occur both early (hours) and late (weeks) after lateral fluid-percussion injury. Furthermore, the study showed that DWI was sensitive to MR signal change at 1-2 h post TBI (in select ROIs), whereas HR scans showed MR signal change primarily at later time points (3-4 h and later). Moreover, regions which demonstrate late changes are associated with histological damage and neurological impairment. The study demonstrates the utility of MRI to detect early changes, in some cases, that are predictive of long-lasting damage verified histologically.
authors.affiliation: Georgetown Institute for Cognitive and Computational Sciences, Georgetown University Medical Center, Washington, DC, 20007, USA. Benedict.Albensi@wl.com
authors.forename: B C
authors.initials: BC
authors.lastname: Albensi
authors.forename: S M
authors.initials: SM
authors.lastname: Knoblach
authors.forename: B G
authors.initials: BG
authors.lastname: Chew
authors.forename: M P
authors.initials: MP
authors.lastname: O'Reilly
authors.forename: A I
authors.initials: AI
authors.lastname: Faden
authors.forename: J J
authors.initials: JJ
authors.lastname: Pekar
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D009460:Neurologic Examination; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors