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Article
February 1988

Leuko-Araiosis in Severe Amyloid Angiopathy

Author Affiliations

Service de Neurologie Hôpital Saint-Antoine 184, Rue de Faubourg Saint-Antoine 75571 Paris Cedex 12, France
Hôpital Henri-Mondor Créteil, France
CHU Angers, France

Arch Neurol. 1988;45(2):140-141. doi:10.1001/archneur.1988.00520260026012
Abstract

To the Editor.  —We agree with Dr Hachinski et al1 that "many different causes may underlie the white-matter changes in "leuko-araiosis." In this setting, pathologic data are scarce,2,3 thus we would like to mention our own work on white-matter involvement in cerebral amyloid angiopathy (CAA).4 We observed severe white matter changes in eight of 12 brains selected because of diffuse and severe CAA, associated with small cortical infarcts, multiple petechial hemorrhages, and/or large hematomas. These changes consisted of diffuse or patchy myelin loss involving the centrum semiovale of both hemispheres, sparing the subcortical fibers, corpus callosum, internal capsule, optic radiations, and temporal regions. On microscopic examination, the white matter appeared vacuolated, showing swollen oligodendrocytes, enlargement of perivascular spaces that contained mononuclear cells with hemosiderin-laden macrophages; there was severe myelin loss with partial axonal degeneration, astrocytic proliferation, and the presence of Rosenthal fibers. Senile plaques and neurofibrillary tangles

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