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Advanced cerebral amyloid angiopathy (CAA) consists of vascular deposition of amyloid and secondary breakdown of amyloid-laden vessel walls. This chapter focuses on the pathogenesis of CAA, clinical and genetic risk factors, presentations and diagnosis, and prospects for treatment. CAA-related intracerebral hemorrhage (ICH) accounts for a substantial proportion of all spontaneous ICH in the elderly. CAA-related lobar ICH presents similarly to other types of lobar ICH with acute onset of neurological symptoms and the variable presence of headache, seizures, or decreased consciousness according to hemorrhage size and location. CAA-related hemorrhages can also be small and clinically silent. CAA can also present with transient neurological symptoms, another syndrome where diagnosis during life is of particular practical importance. Future treatments for CAA are likely to focus on preventive or protective therapy aimed at decreasing the deposition or toxicity of vascular amyloid.
Vascular malformations constitute an important cause of intracranial hemorrhage especially in younger patients. These malformations may arise from any segment of the different functional units of the brain vasculature, including arteries, arterioles, capillaries, venules, and veins. Among vascular malformations causing intracranial hemorrhage, brain arteriovenous malformations (AVMs) are among the most frequently encountered. Brain AVMs commonly affect distal arterial branches and in roughly half of the cases, the malformation is found in the borderzone region shared by the distal anterior, middle, and/or posterior cerebral arteries. Cerebral angiography may help to differentiate brain AVMs from other types of intracranial anomalies with arterio-venous shunting. Resection of an associated developmental venous anomaly is contraindicated as its occlusion may lead to venous stasis, brain edema, and eventual hemorrhage. A developmental venous anomaly (DVA) is found in up to 30% of cerebral cavernous malformations (CCM) patients.
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