THE TRADITIONAL conception that necrosis or dissolution of cerebral tissue in patients having cerebral vascular disease is due solely to vessel obstruction is rapidly being changed. Furthermore, the speed at which so-called "vascular lesions" develop in various areas of the brain is now being considered in terms of inherent tissue vulnerability or resistance to noxae, oxidative processes, tissue-vessel exchange of metabolites, the "systemic factor," and the implicit "vascular factor." *
The prime interest in this communication is to develop the relationship of the lesions described here as "perivascular encephalolysis," and their pathogenesis in terms of (1) structural vascular alterations with special reference to the perivascular space, (2) the effect of systemic diseases upon cerebral metabolism and the accumulation of cellular effete products in the perivascular spaces, and (3) the development of an encephalolytic substance resulting from the influence of these perivascular metabolites upon the tissue enzyme balance presumably residing in the
MOORE MT. PERIVASCULAR ENCEPHALOLYSIS: Histopathology and Pathogenesis. AMA Arch NeurPsych. 1954;71(3):344–357. doi:https://doi.org/10.1001/archneurpsyc.1954.02320390074007
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