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Charcot–Bouchard aneurysms revisited: clinicopathologic correlations
Intracerebral hemorrhage (ICH) is a significant cause of morbidity and mortality worldwide. Hypertension and cerebral amyloid angiopathy (CAA) are the most common causes of primary ICH, but the mechanism of hemorrhage in both conditions is unclear. Although fibrinoid necrosis and Charcot–Bouchard an...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group US
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8592842/ https://www.ncbi.nlm.nih.gov/pubmed/34326486 http://dx.doi.org/10.1038/s41379-021-00847-1 |
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author | Magaki, Shino Chen, Zesheng Haeri, Mohammad Williams, Christopher K. Khanlou, Negar Yong, William H. Vinters, Harry V. |
author_facet | Magaki, Shino Chen, Zesheng Haeri, Mohammad Williams, Christopher K. Khanlou, Negar Yong, William H. Vinters, Harry V. |
author_sort | Magaki, Shino |
collection | PubMed |
description | Intracerebral hemorrhage (ICH) is a significant cause of morbidity and mortality worldwide. Hypertension and cerebral amyloid angiopathy (CAA) are the most common causes of primary ICH, but the mechanism of hemorrhage in both conditions is unclear. Although fibrinoid necrosis and Charcot–Bouchard aneurysms (CBAs) have been postulated to underlie vessel rupture in ICH, the role and significance of CBAs in ICH has been controversial. First described as the source of bleeding in hypertensive hemorrhage, they are also one of the CAA-associated microangiopathies along with fibrinoid necrosis, fibrosis and “lumen within a lumen appearance.” We describe clinicopathologic findings of CBAs found in 12 patients out of over 2700 routine autopsies at a tertiary academic medical center. CBAs were rare and predominantly seen in elderly individuals, many of whom had multiple systemic and cerebrovascular comorbidities including hypertension, myocardial and cerebral infarcts, and CAA. Only one of the 12 subjects with CBAs had a large ICH, and the etiology underlying the hemorrhage was likely multifactorial. Two CBAs in the basal ganglia demonstrated associated microhemorrhages, while three demonstrated infarcts in the vicinity. CBAs may not be a significant cause of ICH but are a manifestation of severe cerebral small vessel disease including both hypertensive arteriopathy and CAA. |
format | Online Article Text |
id | pubmed-8592842 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group US |
record_format | MEDLINE/PubMed |
spelling | pubmed-85928422021-11-23 Charcot–Bouchard aneurysms revisited: clinicopathologic correlations Magaki, Shino Chen, Zesheng Haeri, Mohammad Williams, Christopher K. Khanlou, Negar Yong, William H. Vinters, Harry V. Mod Pathol Article Intracerebral hemorrhage (ICH) is a significant cause of morbidity and mortality worldwide. Hypertension and cerebral amyloid angiopathy (CAA) are the most common causes of primary ICH, but the mechanism of hemorrhage in both conditions is unclear. Although fibrinoid necrosis and Charcot–Bouchard aneurysms (CBAs) have been postulated to underlie vessel rupture in ICH, the role and significance of CBAs in ICH has been controversial. First described as the source of bleeding in hypertensive hemorrhage, they are also one of the CAA-associated microangiopathies along with fibrinoid necrosis, fibrosis and “lumen within a lumen appearance.” We describe clinicopathologic findings of CBAs found in 12 patients out of over 2700 routine autopsies at a tertiary academic medical center. CBAs were rare and predominantly seen in elderly individuals, many of whom had multiple systemic and cerebrovascular comorbidities including hypertension, myocardial and cerebral infarcts, and CAA. Only one of the 12 subjects with CBAs had a large ICH, and the etiology underlying the hemorrhage was likely multifactorial. Two CBAs in the basal ganglia demonstrated associated microhemorrhages, while three demonstrated infarcts in the vicinity. CBAs may not be a significant cause of ICH but are a manifestation of severe cerebral small vessel disease including both hypertensive arteriopathy and CAA. Nature Publishing Group US 2021-06-14 2021 /pmc/articles/PMC8592842/ /pubmed/34326486 http://dx.doi.org/10.1038/s41379-021-00847-1 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Magaki, Shino Chen, Zesheng Haeri, Mohammad Williams, Christopher K. Khanlou, Negar Yong, William H. Vinters, Harry V. Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title | Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title_full | Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title_fullStr | Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title_full_unstemmed | Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title_short | Charcot–Bouchard aneurysms revisited: clinicopathologic correlations |
title_sort | charcot–bouchard aneurysms revisited: clinicopathologic correlations |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8592842/ https://www.ncbi.nlm.nih.gov/pubmed/34326486 http://dx.doi.org/10.1038/s41379-021-00847-1 |
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