ArticleCureus2025
Cerebral Amyloid Angiopathy: A Case Report.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral amyloid angiopathy (CAA) is a cerebrovascular condition characterized by the buildup of beta-amyloid protein within the walls of small and medium-sized blood vessels in the brain's cortex and leptomeninges. Clinically, it can present with a range of neurological symptoms, including recurrent headaches, cognitive disturbances, seizures, and focal deficits. A key feature of CAA is the tendency for lobar brain hemorrhages, though its clinical and radiological profile can overlap with other neurological disorders such as Alzheimer's disease, demyelinating conditions, vascular syndromes, and neoplasms. CAA pathology is frequently observed in individuals with Alzheimer's disease, with a subset showing significant vascular involvement. Although histopathological confirmation remains definitive, advanced imaging, particularly MRI, has become central to diagnosis, often identifying features such as cortical microbleeds, superficial siderosis, and non-deep (lobar) hemorrhages. In some presentations, especially inflammatory variants, patients may benefit from immunosuppressive treatment such as corticosteroids, making early diagnosis critical. Recognizing the distinction between CAA-related hemorrhages and other causes of cerebral bleeding is vital for timely and appropriate management. We present a case of an elderly male who had multiple hospital presentations with unexplained self-resolving expressive dysphasia, seizure, and gradually increasing confusion with the possibility of underlying dementia that responded well to high-dose steroids. This case underscores the need to consider inflammatory cerebral amyloid angiopathy (iCAA) as a differential in patients with recurrent, unexplained neurological symptoms with CT evidence of micro- and macro-hemorrhages and a dramatic response to steroids for symptomatic improvement. Improved awareness of atypical presentations and the utility of MRI can support earlier intervention. Further investigation is needed to refine diagnostic tools, identify reliable biomarkers, and explore therapeutic strategies targeting the underlying vascular and inflammatory mechanisms of the disease.
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