Observational studyNeurology(R) neuroimmunology & neuroinflammation2025
Iatrogenic Cerebral Amyloid Angiopathy-Related Inflammation: A Multicenter Case Series.
Observational study in Neurology(R) neuroimmunology & neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Early vs Delayed Steroid Treatment in Cerebral Amyloid Angiopathy-Related Inflammation: A Retrospective Cohort Study.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Disease Progression in Iatrogenic Cerebral Amyloid Angiopathy.Neurology · 2026Article
- Positron emission tomography for diagnosing cerebrovascular disorders: a scoping review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Iatrogenic cerebral amyloid angiopathy: neuroinflammation and implications for future therapies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Possible Iatrogenic Cerebral Amyloid Angiopathy Presenting with Recurrent Lobar Hemorrhages: A Case Report.NMC case report journal · 2026Article
- Iatrogenic cerebral amyloid angiopathy 30 years after childhood cadaveric dura mater transplantation: a case report.BMC neurology · 2025Article
- Hiding in Plain Sight: Inflammation in Iatrogenic Cerebral Amyloid Angiopathy.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
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14 authors.
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Abstract
BACKGROUND AND
objectivesVariants of cerebral amyloid angiopathy (CAA) have been increasingly reported. Iatrogenic CAA (iCAA) is a subtype arising in patients with a history of neurosurgery. Current etiopathogenetic hypotheses focus on previous exposure to contaminated materials, such as cadaveric dura, followed by a prion-like mechanism. CAA-related inflammation (CAA-ri) represents the inflammatory variant of CAA, usually with a good response to immunosuppressive therapy. To date, the association between iCAA and CAA-ri has not been clarified yet. This study reports cases of iCAA evolving into CAA-ri, emphasizing the clinical and radiologic overlaps between these conditions.
methodsThis retrospective observational study included patients with clinical and radiologic features of CAA-ri and a history of neurosurgical intervention, observed at 2 Italian neurologic centers. Patients were identified from CAA databases and screened for neurosurgical history before 1990. Eligible cases met diagnostic criteria for CAA-ri. Clinical data were anonymized and included surgical details, evidence of amyloid-β in the CNS (amyloid-PET, CSF biomarkers, genetic screening), and CAA-ri features (symptoms, imaging findings, treatment, and outcomes).
resultsWe identified 6 patients with iCAA who developed clinical and instrumental features of CAA-ri during their follow-up. The mean age at neurosurgery was 17.2 years (range: <1-43) while the onset of CAA-ri occurred at 61.8 years (range: 48-79), with an average latency of 44.7 years (range: 36-59). Despite immunosuppressive treatment, 2 patients experienced a rapid decline in their clinical condition and deceased within a few months from CAA-ri onset. DISCUSSION: This study increases awareness about the potential occurrence of CAA-ri in patients with iCAA, confirming its aggressive nature and highlighting the importance of neuroinflammation in the pathogenesis of the disease. In these patients, CAA-ri seems to be associated with a severe clinical course and a poor response to steroid treatment, often resulting in a fatal outcome in the short term.
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