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SVD was manifest largely as concentric lyaline wall thickening; lipothyalinosis and fibrinois necrosis were rarely observed.Thirty-one percent of cases failed to meet stringent clinicopathological criteria for significant prior hypertension.In 9%of cases,patients had been nonelderly, nondiabetic,and normotensive.Five of six cases lacking classic risk factors had systemic conditions known to enhance small-vessel permeability.The nature of SVD appears to have been modified by effective treatment of hypertension.Classic risk factors are often absent.The hypothesis that a variety of conditions that enhance small-vessel permeability may contribute to the pathogenesis of SVD merits consideration. |
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