(Stroke. 2000;31:2117.)
© 2000 American Heart Association, Inc.
Original Contributions |
Cerebral Infarction in Adult AIDS Patients
Observations From the Edinburgh HIV Autopsy Cohort
From the Neurology Unit (M.D.C.), Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa; the Department of Pathology (G.A.L.), University of Wales College of Medicine, Cardiff, Wales; and the Department of Pathology (Neuropathology) (J.E.B.), the Department of Clinical Neurosciences (C.P.W.), the Virus Evolution Group, Laboratory for Clinical and Molecular Virology (P.S.), and the Regional Infectious Disease Unit (R.D.B.), University of Edinburgh, Edinburgh, Scotland.
Background and Purpose—Autopsy series of patients with AIDS have found a 4% to 29% prevalence of cerebral infarction. Little is known of the prevalence of cerebral infarction when not associated with non-HIV central nervous system (CNS) infection, lymphoma, or cardioembolic sources. Clinical correlation has seldom been available. We describe the pathological and clinical features of patients from the Edinburgh HIV Cohort Study found to have had cerebral infarcts without evidence of non-HIV CNS infection, CNS lymphoma, or cardioembolic sources at autopsy.
Methods—From 183 autopsy cases, 26 without evidence of opportunistic cerebral infection or lymphoma were selected. These 26 cases went through a second selection process in which the presence of cerebral infarction, in the absence of the conditions mentioned, was verified. Histology and clinical records for the remaining patients were reviewed.
Results—Ten (5.5%) cases fulfilled the inclusion criteria and demonstrated similar hypoxic-ischemic lesions. Small-vessel thickening was seen in all cases, and perivascular space dilatation, rarefaction, and pigment deposition, with vessel wall mineralization and perivascular inflammatory cell infiltrates, were seen in some cases. Vasculitis was not found. One patient had had a transient ischemic attack, and no patient had had a stroke.
Conclusions—Cerebral infarcts in HIV-infected patients are not common in the absence of cerebral non-HIV infection, lymphoma, or embolic sources. We found an HIV-associated vasculopathy with similar features in all risk groups. In AIDS patients presenting with stroke or transient ischemic attack, potentially treatable causes, such as cerebral coinfection or tumor, should be sought.
Key Words: acquired immunodeficiency syndrome • cerebral infarction • pathology
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