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Pathophysiological Study of Corona Radiata Infarcts by Diagnostic Method Clinically Available Fumihito Ohta 1 , Masako Kawahara 1 , Hiroshi Sekimoto 1 , Minoru Fukuda 1 , Mikio Takaya 1 , Toshiki Yamasaki 1 , Kouzo Moritake 1 1Department of Neurosurgery, Shimane Medical University Keyword: corona radiata , watershed infarction , CT , SPECT , cerebral angiography pp.155-161
Published Date 1991/2/1
DOI https://doi.org/10.11477/mf.1406900160
  • Abstract
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The authors evaluated 18 patients who presented with corona radiata infarction, one of the 'water-shed infarctions', on CT and/or MRI to determine its eitology and pathophysiology using cerebral angiography, single-photon emission computedtomography (SPECT), and tests of hemostatic func-tion including hematocrit, platelet aggregation and adhesiveness. On angiography, 8 of these 18 patients had ulcerative lesions in the common car-otid artery bifurcation with or without minimal stenosis and exhibited no or a minimal area of hypoperfusion localized to the corona radiata on SPECT. In these, microembolism from the lesions at the common carotid bifurcation seemed play an important role in the genesis of corona radiata infarction. In 7 of the remaining 10 patients, cere-bral angiography showed occlusive lesions of the internal carotid artery around its origin in 3, more than 90% stenosis of the internal carotid artery in 1, severe stenosis of the M1 segment of the middle cerebral artery in 2, and M1 occlusion in 1. In 5 of these 7, SPECT demonstrated a larger area of hypoperfusion than the corona radiata in the involved hemisphere. In the remaining 2, SPECT demonstrated a hypoperfusion area localized to the corona radiata. In all 7, the hematocrit was ele-vated. A collateral blood supply was visualized in 5 of 7 on cerebral angiography. In these 7 patients, hemodynamic disturbance was considered to con-tribute to the pathogenesis of infarction in the corona radiata. In the final three patients, cerebral angiography showed significant occlusive lesions in the main trunk of the cerebral arteries. In these 3 patients, no hypoperfusion area in the corona radiata was demonstrated on SPECT. All 3 patients had an enhancement of platelet aggregation and/or adhesiveness and an increase in the hematocrit. It appears that in these 3 cases, enhancement of aggre-gation and/or adhesiveness might have caused infarction in the corona radiata. There seem to be various mechanisms, such as microembolism from ulceration of atheromatous lesions in the common carotid bifurcation, hemodynamic disturbance as-sociated with occlusive lesions in the main trunk of the cerebral arteries, increase in hematocrit, and enhancement of platelet aggregation. And they have an important role in the pathogenesis of corona radiata infarction. Therefore, patients with corona radiata infarction must be treated in accor-dance with the pathogenesis of the lesion.


Copyright © 1991, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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