title: Early T1- and T2-weighted MRI signatures of transient and permanent middle cerebral artery occlusion in a murine stroke model studied at 9.4T.
abstract: Early reperfusion following stroke results in reduced tissue injury. Paradoxically, restoration of blood flow under certain conditions may also cause delayed neuronal damage (reperfusion injury). The interrelationship of changes in T1, T2 and diffusion weighted images of tissue water were studied in mouse models of permanent and transient focal cerebral ischemia. A sham surgery or either permanent or transient (30 min) middle cerebral artery occlusion (MCAO) were induced in 14 mice. Magnetic resonance (MR) images of the brain were acquired including: T2 maps, T1 maps and diffusion weighted spin-echo images to produce apparent diffusion coefficient of water apparent diffusion coefficient (ADC) maps. Images were collected on average 90 min after MCAO in both the transient and permanent ischemia groups. Scans were repeated at 24h post-occlusion in mice with transient ischemia. Permanent MCAO resulted in decreases in ADC and no significant change in T2 acutely following MCAO. There were increases in T1 compared to sham controls within the ischemic region in mice following either transient or permanent MCAO (P<0.001). In contrast to permanent MCAO, there were increases in T2 (P<0.001) in the infarct area present in the reperfusion phase within 90 min of transient MCAO. There was considerable infarct growth at 24h (P<0.001). This study demonstrates that following either type of occlusion there are early increases in T1 suggesting an elevated water content in the stroke lesion, while only following transient MCAO are there early increases in T2, indicative of early vasogenic oedema with breakdown of the blood-brain barrier.
authors.affiliation: Department of Clinical Neurosciences, University of Calgary, Institute for Biodiagnostics (West), Room 153, 3330 Hospital Drive, Calgary, Alberta, Canada T2N 4N1. pabarber@ucalgary.ca
authors.forename: Philip A
authors.initials: PA
authors.lastname: Barber
authors.forename: Lisa
authors.initials: L
authors.lastname: Hoyte
authors.forename: David
authors.initials: D
authors.lastname: Kirk
authors.forename: Tad
authors.initials: T
authors.lastname: Foniok
authors.forename: Alastair
authors.initials: A
authors.lastname: Buchan
authors.forename: Ursula
authors.initials: U
authors.lastname: Tuor
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000503:physiopathology; D001834:Body Water / Q000502:physiology; D001929:Brain Edema / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000473:pathology* / Q000503:physiopathology; D004058:Diffusion; D038524:Diffusion Magnetic Resonance Imaging / Q000379:methods*; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016548:Prosencephalon / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology; D020521:Stroke / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors