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Stroke. 1999;30:1043-1046

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(Stroke. 1999;30:1043-1046.)
© 1999 American Heart Association, Inc.


Original Contributions

Novel Brain Ischemic Change on MRI

Delayed Ischemic Hyperintensity on T1-Weighted Images and Selective Neuronal Death in the Caudoputamen of Rats After Brief Focal Ischemia

Masayuki Fujioka, MD; Toshiaki Taoka, MD; Yoshiyuki Matsuo, PhD; Ken-Ichiro Hiramatsu, MD Toshisuke Sakaki, MD

From the Pioneering Brain Research Unit (M.F., T.T., Y.M.), Department of Neurosurgery (M.F.), Nara Emergency Center; Department of Radiology, Nara Prefectural Nara Hospital, Nara; Developmental Research Laboratories, Shionogi & Co, Ltd, Osaka; Department of Neurosurgery, Nabari City Hospital (K.-I.H.), Mie, Japan, and Department of Neurosurgery, Nara Medical University (T.S.), Nara, Japan.

Correspondence to Masayuki Fujioka, MD, Center for the Study of Neurological Disease, The Queen's Medical Center, University Tower, 8th Floor, 1356 Lusitana St, Honolulu, Hawaii 96813. E-mail mfujioka{at}www.cns.queens.org

Background and Purpose—Specific change of persistent hyperintensity/hypointensity on T1-weighted (T1W) and T2-weighted (T2W) MRI, respectively, has been reported to develop in the human basal ganglia after brief hemispheric ischemia. We investigated whether this ischemic change observed in humans could be reproduced experimentally in rats after brief middle cerebral artery (MCA) occlusion (MCAO), and if so, what the neuroradiological change represented histologically.

Methods—The origin of the right MCA of male Wistar rats (n=25) was occluded for 15 minutes by inserting a silicon-coated nylon thread from the external carotid artery into the internal carotid artery. After 15 minutes' MCAO, coronal MR images (T1W, T2W, and T1W with fat saturation pulse) were obtained once at 3-day reperfusion (n=5) and twice at 3- and 7-day reperfusion (n=20). Brain specimens were examined histologically immediately after the last MRI study in all rats.

Results—Neither T1W nor T2W MRI showed marked signal changes 3 days after reperfusion following 15-minute MCAO. However, the ischemic change of hyperintensity and hypointensity on T1W and T2W MRI, respectively, appeared in the striatum following 7-day reperfusion after 15-minute MCAO (n=19/20). Histological examination revealed that the specific lesion in the rat striatum on MRI corresponded to selective neuronal death and proliferation of reactive astrocytes and microglia without infarct, hemorrhage, lipid accumulation, or calcification.

Conclusions—Brief MCAO with reperfusion induces the delayed ischemic changes of hyperintensity and hypointensity on T1W and T2W MRI, respectively, in the rat striatum with high reproducibility. This specific ischemic change on MRI histologically corresponded to selective neuronal death and gliosis with preservation of the macroscopic structure of the brain. A similar MRI pattern reported in patients who have sustained brief ischemia may represent similar histology. We speculate that the ischemic change reflects some biochemical changes affecting the magnetic field as the brain tissue undergoes subtle structural changes.


Key Words: cerebral ischemia, transient • magnetic resonance imaging • middle cerebral artery • neuronal death • rats




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