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Pathophysiology of Primary Intracerebral Hemorrhage: Insights into Cerebral Small Vessel Disease

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Part of the book series: Stroke Revisited ((STROREV))

Abstract

Spontaneous intracerebral, non-traumatic intracerebral hemorrhage (ICH) results from arterial bleeding and formation of a brain hematoma. While 20% of all ICH cases result from a defined underlying cause (e.g., vascular malformation, coagulopathy, and tumors), the majority of ICHs are related to the rupture of damaged small- and medium-sized arteries of the brain. Pathologies affecting these arteries fall under the broad term cerebral small vessel disease. The two major forms of cerebral small vessel disease that are common in elderly populations are hypertensive small vessel disease (mainly affecting deep perforating arteries supplying the subcortical gray and white matter) and cerebral amyloid angiopathy (CAA) (characterized by the progressive accumulation of β-amyloid in the leptomeningeal and cortical vessels). Pathologic studies suggest that hypertensive small vessel disease can lead to ICH in deep gray nuclei and white matter, thalamus, and pons, while CAA is responsible for a large majority of ICH in lobar areas. In the first part of the chapter, we will discuss the pathophysiology of ICH in relation to these two subtypes of small vessel disease. In the second part, the dynamic processes related to hematoma evolution and mechanisms of primary and secondary brain injury will be explored.

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Pasi, M., Viswanathan, A. (2018). Pathophysiology of Primary Intracerebral Hemorrhage: Insights into Cerebral Small Vessel Disease. In: Lee, SH. (eds) Stroke Revisited: Hemorrhagic Stroke. Stroke Revisited. Springer, Singapore. https://doi.org/10.1007/978-981-10-1427-7_3

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