January 1992

Cerebral Hemorrhage With Biopsy-Proved Amyloid Angiopathy

Author Affiliations

From the Department of Pathology (Drs Yong, Robert, and Vinters and Ms Secor) and Brain Research Institute (Dr Vinters), UCLA School of Medicine; and Department of Neurology, St Vincent Hospital and Medical Center, Portland, Ore (Dr Kleikamp).

Arch Neurol. 1992;49(1):51-58. doi:10.1001/archneur.1992.00530250055016

• Clinical, radiological, and immunohistochemical findings in brain biopsy specimens from six patients with cerebral amyloid angiopathy—associated intracerebral hemorrhage were reviewed. Acute clinical presentations included headache, nausea and vomiting, loss of consciousness, and focal neurological deficits such as hemiplegia and blindness. Transient schemic attacks experienced by one patient and referable to one hemisphere did not indicate impending hemorrhage in that region. Computed tomographic scans revealed acute, irregular, superficial, lobar hemorrhage with occasional ring enhancement. Immunohistochemical studies were performed on biopsy specimens using primary antibodies against portions of the Alzheimer A4 (β-) peptide or γ-trace peptide (the vascular amyloid protein in patients with hereditary cerebral hemorrhage with amyloidosis—Icelandic type). In all patients, anti-A4 and anti—γ-trace labeled cerebral microvessels. Immunoreactive senile plaques were few compared with the numbers of stained microvessels. Reactive astrocytes in some patients were labeled by both antiserum samples, suggesting uptake or production of these proteins by the astrocytes. This study demonstrates the heterogeneous clinical and radiological features of cerebral amyloid angiopathy—related brain hemorrhage and the value of anti-A4 and anti—γ-trace immunohistochemical study of biopsy material from patients with suspected cerebral amyloid angiopathy—related intraparenchymal bleeding.