[Pathophysiological study of corona radiata infarcts by clinically available diagnostic methods].

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 etiology and pathophysiology using cerebral angiography, single-photon emission computed tomography (SPECT), and tests of hemostatic function including hematocrit, platelet aggregation and adhesiveness. On angiography, 8 of these 18 patients had ulcerative lesions in the common carotid 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, cerebral 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 elevated. A collateral blood supply was visualized in 5 of 7 on cerebral angiography. In these 7 patients, hemodynamic disturbance was considered to contribute 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.(ABSTRACT TRUNCATED AT 250 WORDS)