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Etienne Roullet, MD
Service de Neurologie Hôpital Saint-Antoine 184, Rue de Faubourg Saint-Antoine 75571 Paris Cedex 12, France

F. Françoise Gray, MD
Hôpital Henri-Mondor Créteil, France

Frédéric Dubas, MD
CHU Angers, France

Arch Neurol. 1988;45(2):140-141.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

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