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Miliary aneurysms and "fibrinoid" degeneration of cerebral blood vessels
Insights
Intracerebral hemorrhage may stem from fibrinoid degeneration or miliary aneurysms in cerebral arteries, even without hypertension. These findings suggest new insights into the causes of brain bleeds.
Area of Science:
- Neuropathology
- Cerebrovascular Diseases
Background:
- Intracerebral hemorrhage (ICH) is a severe neurological condition.
- The pathogenesis of ICH often involves vascular abnormalities.
Purpose of the Study:
- To describe pathological findings in three cases of ICH.
- To investigate the role of fibrinoid degeneration and miliary aneurysms in ICH.
Main Methods:
- Histopathological examination of cerebral arteries and arterioles.
- Analysis of vascular changes in patients with ICH.
Main Results:
- Observed fibrinoid degeneration and/or miliary aneurysms in cerebral arteries and arterioles.
- Identified sclerosed true aneurysms (fibrous balls).
- Found fibrinoid changes at aneurysm sites, including unusual locations.
Conclusions:
- Fibrinoid degeneration or miliary aneurysms may contribute to vessel rupture and ICH, potentially without hypertension.
- Miliary aneurysms might form without pre-existing fibrinoid changes.
Abstract:
Three cases of intracerebral hemorrhage are described in which there was fibrinoid degeneration of cerebral arteries and arterioles or miliary aneurysms or both. Fibrous balls are shown to be sclerosed true aneurysms. These changes occurred in the absence of malignant hypertension and perhaps in the absence of any hypertension. A further point of interest was the finding of fibrinoid at the site of apparent aneurysm formation in a small artery on the cerebral surface, a location at which miliary aneurysms are not generally thought to form. The presence of intracerebral hemorrhage in all three cases, and the ready demonstration of similar changes in other cases of intracerebral hemorrhage, suggest but do not prove that the fibrinoid degeneration or aneurysm leads to vessel rupture and to hemorrhage itself. Also unsettled is the question of whether miliary aneurysms form only at sites already displaying fibrinoid change. Our data suggest that pre-existing fibrinoid may not be a prerequisite for miliary aneurysm formation.