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Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management

Cerebral amyloid angiopathy (CAA) is a common untreatable cause of lobar hemorrhages and cognitive decline in the older population. Subset of patients present with its inflammatory subtype with rapid decline in cognitive functions and neurological deficits. Most commonly the underlying pathophysiolo...

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Autores principales: Singh, Baljinder, Lavezo, Jonathan, Gavito-Higueroa, Jose, Ahmed, Faiza, Narasimhan, Sathya, Brar, Simrandeep, Cruz-Flores, Salvador, Kraus, Jacqueline
Formato: Online Artículo Texto
Lenguaje:English
Publicado: IOS Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9661355/
https://www.ncbi.nlm.nih.gov/pubmed/36447738
http://dx.doi.org/10.3233/ADR-220055
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author Singh, Baljinder
Lavezo, Jonathan
Gavito-Higueroa, Jose
Ahmed, Faiza
Narasimhan, Sathya
Brar, Simrandeep
Cruz-Flores, Salvador
Kraus, Jacqueline
author_facet Singh, Baljinder
Lavezo, Jonathan
Gavito-Higueroa, Jose
Ahmed, Faiza
Narasimhan, Sathya
Brar, Simrandeep
Cruz-Flores, Salvador
Kraus, Jacqueline
author_sort Singh, Baljinder
collection PubMed
description Cerebral amyloid angiopathy (CAA) is a common untreatable cause of lobar hemorrhages and cognitive decline in the older population. Subset of patients present with its inflammatory subtype with rapid decline in cognitive functions and neurological deficits. Most commonly the underlying pathophysiology of this disease is deposition of insoluble amyloid protein into blood vessel walls which results in vessel fragility leading to local neurotoxicity which may eventually leads to lobar hemorrhages and cognitive decline. The term “Amyloid Spell” encompasses transient focal neurological deficits which is commonly misdiagnosed as seizures or transient ischemic attack in the emergency department. Radiologic findings in these patients may reveal microbleeds, cortical superficial siderosis, white matter hyperintensities, and cerebral edema which support the clinical diagnosis which could be otherwise challenging. CAA diagnostic criteria require CT (Edinburgh Criteria) or MRI imaging, or neuropathology. The diagnosis can be suspected without imaging or neuropathology but cannot be confirmed. This review article provides a critical outlook on different types of presentations, updated diagnostic criteria and management of CAA patients illustrating underlying mechanisms associated with neuronal injury secondary to amyloid deposition.
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spelling pubmed-96613552022-11-28 Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management Singh, Baljinder Lavezo, Jonathan Gavito-Higueroa, Jose Ahmed, Faiza Narasimhan, Sathya Brar, Simrandeep Cruz-Flores, Salvador Kraus, Jacqueline J Alzheimers Dis Rep Review Cerebral amyloid angiopathy (CAA) is a common untreatable cause of lobar hemorrhages and cognitive decline in the older population. Subset of patients present with its inflammatory subtype with rapid decline in cognitive functions and neurological deficits. Most commonly the underlying pathophysiology of this disease is deposition of insoluble amyloid protein into blood vessel walls which results in vessel fragility leading to local neurotoxicity which may eventually leads to lobar hemorrhages and cognitive decline. The term “Amyloid Spell” encompasses transient focal neurological deficits which is commonly misdiagnosed as seizures or transient ischemic attack in the emergency department. Radiologic findings in these patients may reveal microbleeds, cortical superficial siderosis, white matter hyperintensities, and cerebral edema which support the clinical diagnosis which could be otherwise challenging. CAA diagnostic criteria require CT (Edinburgh Criteria) or MRI imaging, or neuropathology. The diagnosis can be suspected without imaging or neuropathology but cannot be confirmed. This review article provides a critical outlook on different types of presentations, updated diagnostic criteria and management of CAA patients illustrating underlying mechanisms associated with neuronal injury secondary to amyloid deposition. IOS Press 2022-10-18 /pmc/articles/PMC9661355/ /pubmed/36447738 http://dx.doi.org/10.3233/ADR-220055 Text en © 2022 – The authors. Published by IOS Press https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License (https://creativecommons.org/licenses/by-nc/4.0/) , which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Singh, Baljinder
Lavezo, Jonathan
Gavito-Higueroa, Jose
Ahmed, Faiza
Narasimhan, Sathya
Brar, Simrandeep
Cruz-Flores, Salvador
Kraus, Jacqueline
Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title_full Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title_fullStr Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title_full_unstemmed Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title_short Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management
title_sort updated outlook of cerebral amyloid angiopathy and inflammatory subtypes: pathophysiology, clinical manifestations, diagnosis and management
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9661355/
https://www.ncbi.nlm.nih.gov/pubmed/36447738
http://dx.doi.org/10.3233/ADR-220055
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