(Stroke. 2008;39:205.)
© 2008 American Heart Association, Inc.
Original Contributions |
From the Department of Neurosurgery (Y.T., H.I., T.M., C.K., P.S., Y.Y., N.S.), the Institute of Experimental Animal Research (K.K., H.H.), and the Department of Anatomy and Cell Biology (T.A., K.T.), Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Correspondence to Hideaki Imai, MD, PhD, Department of Neurosurgery, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan. E-mail hideimai{at}showa.gunma-u.ac.jp
Background and Purpose— Lacunar infarction accounts for 25% of ischemic strokes, but the pathological characteristics have not been investigated systematically. A new experimental model of lacunar infarction in the miniature pig was developed to investigate the pathophysiological changes in the corticospinal tract from the acute to chronic phases.
Methods— Thirty-five miniature pigs underwent transcranial surgery for permanent anterior choroidal artery occlusion. Animals recovered for 24 hours (n=7), 2 (n=5), 3 (n=2), 4 (n=2), 6 (n=1), 7 (n=7), 8 (n=2), and 9 days (n=1), 2 weeks (n=2), 4 weeks (n=3), and more than 4 weeks (n=3). Neurology, electrophysiology, histology, and MRI were performed. Seven additional miniature pigs underwent transient anterior choroidal artery occlusion to study muscle motor-evoked potentials and evaluate corticospinal tract function during transient anterior choroidal artery occlusion.
Results— The protocol had a 91.4% success rate in induction of internal capsule infarction 286±153 mm3 (mean±SD). Motor-evoked potentials revealed the presence of penumbral tissue in the internal capsule after 6 to 15 minutes anterior choroidal artery occlusion. Total neurological deficit scores of 15.0 (95% CI, 13.5 to 16.4) and 3.4 (0.3 to 6.4) were recorded for permanent anterior choroidal artery occlusion and sham groups, respectively (P<0.001, maximum score 25) with motor deficit scores of 3.4 (95% CI, 2.9 to 4.0) and 0.0 (CI, 0.0 to 0.0), respectively (P<0.001, maximum score 9). Histology revealed that the internal capsule lesion expands gradually from acute to chronic phases.
Conclusions— This new model of lacunar infarction induces a reproducible infarct in subcortical white matter with a measurable functional deficit and evidence of penumbral tissue acutely.
Key Words: axonal damage gyrencephalic brain lacunar infarction penumbra reproducibility
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E. L. Bailey, J. McCulloch, C. Sudlow, and J. M. Wardlaw Potential Animal Models of Lacunar Stroke: A Systematic Review Stroke, June 1, 2009; 40(6): e451 - e458. [Abstract] [Full Text] [PDF] |
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