| Literature DB >> 29356971 |
Chien-Min Lin1, Hidetaka Arishima2, Ken-Ichiro Kikuta3, Hironobu Naiki4, Ryuhei Kitai3, Toshiaki Kodera3, Ken Matsuda3, Norichika Hashimoto3, Makoto Isozaki3, Kenzo Tsunetoshi3, Hiroyuki Neishi3, Yoshifumi Higashino3, Ayumi Akazawa3, Hiroshi Arai3, Shinsuke Yamada3.
Abstract
Cerebral amyloid angiopathy (CAA) is a degenerative disorder characterized by amyloid-β (Aβ) deposition in the brain microvessels. CAA is also known to contribute not only to cortical microbleeds but also lobar hemorrhages. This retrospective study examined CAA pathologically in patients who underwent direct surgeries for lobar hemorrhage. Thirty-three patients with lobar hemorrhage underwent open surgery with biopsy from 2007 to 2016 in our hospital. Cortical tissues over hematomas obtained surgically were pathologically examined using hematoxylin, eosin stain, and anti-Aβ antibody to diagnose CAA. We also investigated the advanced degree of CAA and clinical features of each patient with lobar hemorrhage. In the 33 patients, 4 yielded specimens that were insufficient to evaluate CAA pathologically. Twenty-four of the remaining 29 patients (82.8%) were pathologically diagnosed with CAA. The majority of CAA-positive patients had moderate or severe CAA based on a grading scale to estimate the advanced degree of CAA. About half of the CAA-positive patients had hypertension, and four took anticoagulant or antiplatelet agents. In five patients who were not pathologically diagnosed with CAA, one had severe liver function disorder, three had uncontrollable hypertension, and one had no obvious risk factor. Our pathological findings suggest that severe CAA with vasculopathic change markedly contributes to lobar hemorrhage. The coexistence of severe CAA and risk factors such as hypertension, anticoagulants or antiplatelets may readily induce lobar hemorrhage.Entities:
Keywords: Cerebral amyloid angiopathy; Lobar hemorrhages; Pathological examination
Mesh:
Year: 2018 PMID: 29356971 DOI: 10.1007/s00415-018-8740-z
Source DB: PubMed Journal: J Neurol ISSN: 0340-5354 Impact factor: 4.849