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Updated: Aug 12, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
Published on: March 7, 2019
[Intracerebral hemorrhage related with cerebral amyloid angiopathy]
1Department of Biophysics, Shanghai Medical University.
Insights
Cerebral amyloid angiopathy (CAA) causes intracerebral hemorrhages, often in cerebral lobes. Pathological findings reveal thickened arteries with amyloid deposits and luminal stenosis, confirming CAA as a cause of bleeding in the brain.
Area of Science:
- Neuropathology
- Vascular Neurology
Context:
- Cerebral amyloid angiopathy (CAA) is a significant cause of spontaneous intracerebral hemorrhage (ICH), particularly in the elderly.
- Understanding the pathological hallmarks of CAA-related ICH is crucial for diagnosis and management.
Purpose:
- To report the clinical and neuropathologic findings in 11 patients with intracerebral hemorrhages associated with cerebral amyloid angiopathy.
- To characterize the morphological changes in cerebral vessels in cases of CAA-related ICH.
Summary:
- Eleven cases of intracerebral hemorrhage attributed to CAA were analyzed, with patient ages ranging from 45 to 79 years (average 61.8).
- Hematomas were predominantly located in cerebral lobes, with two cases involving the basal ganglia and thalamus. All hemorrhages ruptured into the ventricles and/or subarachnoid space.
- Neuropathologic examination revealed thickened leptomeningeal and cortical arteries, deposition of homogeneously eosinophilic material, luminal stenosis, and characteristic amyloid birefringence on Congo red staining.
Impact:
- This study highlights the specific neuropathologic features of CAA-related intracerebral hemorrhages.
- Findings contribute to the understanding of the pathogenesis of CAA and its association with cerebrovascular events.
- Provides insights into the vascular changes that predispose to lobar and deep intracerebral bleeds in the context of CAA.
Abstract:
The clinical and neuropathologic findings in 11 cases with intracerebral hemorrhages related to CAA were reported. Their age ranged from 45 to 79 years, the average being 61.8 years. The hematomas were all in cerebral lobes, except two patients whose hematomas were in the basal ganglia and thalamus. These hematomas were in irregular shapes, ruptured into ventricles and/or subarachnoid space in all cases. The vessel's wall of arteries in the leptomeninges, superficial cortex and those adjacent to hemorrhagic foci showed considerable thickness. Hemorrhagic foci showed considerable thickness. Homogeneously eosinophilic structures deposited in these vessel's wall of several small arteries. Some of these vessels showed luminal stenosis. Congo red staining confirmed characteristic amyloid apple-green birefringence under polarizing microscope.
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