Literature DB >> 29356971

Pathological examination of cerebral amyloid angiopathy in patients who underwent removal of lobar hemorrhages.

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


  38 in total

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Authors:  Marion Apoil; Julien Cogez; Lydie Dubuc; Mathieu Bataille; Vincent de la Sayette; Emmanuel Touzé; Fausto Viader
Journal:  Cerebrovasc Dis       Date:  2013-09-11       Impact factor: 2.762

Review 2.  Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges.

Authors:  Leonardo Pantoni
Journal:  Lancet Neurol       Date:  2010-07       Impact factor: 44.182

3.  Petechial hemorrhages accompanying lobar hemorrhage: detection by gradient-echo MRI.

Authors:  S M Greenberg; S P Finklestein; P W Schaefer
Journal:  Neurology       Date:  1996-06       Impact factor: 9.910

Review 4.  Hypertensive cerebral small vessel disease and stroke.

Authors:  G Alistair Lammie
Journal:  Brain Pathol       Date:  2002-07       Impact factor: 6.508

5.  Ultrastructural morphometry of hypertensive medial damage in lenticulostriate and other arteries.

Authors:  S Takebayashi
Journal:  Stroke       Date:  1985 May-Jun       Impact factor: 7.914

6.  The clinical spectrum of cerebral amyloid angiopathy: presentations without lobar hemorrhage.

Authors:  S M Greenberg; J P Vonsattel; J W Stakes; M Gruber; S P Finklestein
Journal:  Neurology       Date:  1993-10       Impact factor: 9.910

Review 7.  Brain parenchymal and microvascular amyloid in Alzheimer's disease.

Authors:  H V Vinters; Z Z Wang; D L Secor
Journal:  Brain Pathol       Date:  1996-04       Impact factor: 6.508

Review 8.  The development of cerebral amyloid angiopathy in cerebral vessels. A review with illustrations based upon own investigated post mortem cases.

Authors:  T A Mendel; T Wierzba-Bobrowicz; E Lewandowska; T Stępień; G M Szpak
Journal:  Pol J Pathol       Date:  2013-12       Impact factor: 1.072

9.  Development, appraisal, validation and implementation of a consensus protocol for the assessment of cerebral amyloid angiopathy in post-mortem brain tissue.

Authors:  Seth Love; Katy Chalmers; Paul Ince; Margaret Esiri; Johannes Attems; Kurt Jellinger; Masahito Yamada; Mark McCarron; Thais Minett; Fiona Matthews; Steven Greenberg; David Mann; Patrick Gavin Kehoe
Journal:  Am J Neurodegener Dis       Date:  2014-03-28

10.  Change in incidence and aetiology of intracerebral haemorrhage in Oxfordshire, UK, between 1981 and 2006: a population-based study.

Authors:  C E Lovelock; A J Molyneux; P M Rothwell
Journal:  Lancet Neurol       Date:  2007-06       Impact factor: 44.182

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  2 in total

1.  Apolipoprotein E and clusterin inhibit the early phase of amyloid-β aggregation in an in vitro model of cerebral amyloid angiopathy.

Authors:  Yoshinori Endo; Kazuhiro Hasegawa; Ryo Nomura; Hidetaka Arishima; Ken-Ichiro Kikuta; Taro Yamashita; Yasuteru Inoue; Mitsuharu Ueda; Yukio Ando; Mark R Wilson; Tadanori Hamano; Yasunari Nakamoto; Hironobu Naiki
Journal:  Acta Neuropathol Commun       Date:  2019-01-28       Impact factor: 7.801

2.  Mixed-location cerebral microbleeds as a biomarker of neurodegeneration in a memory clinic population.

Authors:  Bibek Gyanwali; Muhammad Amin Shaik; Chuen Seng Tan; Henri Vrooman; Narayanaswamy Venketasubramanian; Christopher Chen; Saima Hilal
Journal:  Aging (Albany NY)       Date:  2019-11-25       Impact factor: 5.682

  2 in total

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