Charcot-Bouchard aneurysms revisited: clinicopathologic correlations.


Journal

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
ISSN: 1530-0285
Titre abrégé: Mod Pathol
Pays: United States
ID NLM: 8806605

Informations de publication

Date de publication:
12 2021
Historique:
received: 05 04 2021
accepted: 20 05 2021
revised: 20 05 2021
pubmed: 31 7 2021
medline: 19 3 2022
entrez: 30 7 2021
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 34326486
doi: 10.1038/s41379-021-00847-1
pii: S0893-3952(22)00371-4
pmc: PMC8592842
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2109-2121

Informations de copyright

© 2021. The Author(s).

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Auteurs

Shino Magaki (S)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA. smagaki@mednet.ucla.edu.

Zesheng Chen (Z)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.

Mohammad Haeri (M)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.
Department of Pathology and Laboratory Medicine and Alzheimer Disease Research Center, University of Kansas Medical Center, Kansas City, KS, USA.

Christopher K Williams (CK)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.

Negar Khanlou (N)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.

William H Yong (WH)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.
Department of Pathology and Laboratory Medicine, University of California-Irvine School of Medicine, Irvine, CA, USA.

Harry V Vinters (HV)

Section of Neuropathology, Department of Pathology and Laboratory Medicine, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.
Department of Neurology, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.
Brain Research Institute, Ronald Reagan UCLA Medical Center and David Geffen School of Medicine, Los Angeles, CA, USA.

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