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Cerebral white matter changes in acquired immunodeficiency syndrome dementia: Alterations of the blood‐brain barrier
Author(s) -
Power Christopher,
Kong PeiAnn,
Crawford Thomas O.,
Wesselingh Steven,
Glass Jonathan D.,
McArthur Justin C.,
Trapp Bruce D.
Publication year - 1993
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410340307
Subject(s) - pallor , white matter , pathology , dementia , luxol fast blue stain , myelin , medicine , central nervous system , magnetic resonance imaging , disease , radiology
The cause of acquired immunodeficiency syndrome (AIDS) dementia, which is a frequent late manifestation of human immunodeficiency virus (HIV) infection, is unknown but radiological and pathological studies have implicated alterations in subcortical white matter. To investigate the pathological basis of these white matter abnormalities, we performed an immunocytochemical and histological analysis of subcortical white matter from AIDS patients with and without dementia, from pre‐AIDS patients (asymptomatic HIV‐seropositive patients), and from HIV‐seronegative control subjects. Reduced intensity of Luxol fast blue staining, designated “diffuse myelin pallor,” was detected in 8 of 15 AIDS dementia patients, 3 of 13 AIDS nondemented patients, and none of the pre‐AIDS patients (n = 2) or control subjects (n = 9). In contrast to Luxol fast blue staining, sections stained immunocytochemically for myelin proteins did not show decreased staining intensities in regions of diffuse myelin pallor. In addition, neither demyelinated axons nor active demyelination were detected in light and electron micrographs of subcortical white matter from brains of patients with AIDS dementia. An increase in the number of perivascular macrophages and hypertrophy of astrocytes and microglia occurred in brain sections from HIV‐infected patients. These changes were not specific to dementia or regions of diffuse myelin pallor and they occurred in both gray and white matter. In contrast to the lack of myelin pathology in AIDS dementia brains, significant accumulations of serum proteins in white matter glia were detected in the brains of 12 of 12 patients with AIDS dementia and 6 of 12 AIDS patients without dementia. Serum protein‐immunopositive cortical neurons were detected in the frontal cortex of 11 of 12 patients with AIDS dementia and 3 of 12 nondemented AIDS patients. Seronegative control subjects showed minimal serum protein immunoreactivity in both cortex and white matter. We conclude therefore that alterations in the blood‐brain barrier and not demyelination contribute to the development of AIDS dementia.