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Cerebral Amyloid Angiopathy (CAA) is caused by the deposition of a pathological protein (amyloid beta) in the walls of superficial blood vessels of the brain. Such accumulation makes the blood vessel wall weaker predisposing to breakdown and bleeds. Symptomatic bleeds in the superficial parts of the brain, microbleeds and layering of blood right outside of the cortex (superficial siderosis) are the hemorrhagic consequences of this condition. CAA also disturbs the regular blood vessel function and decrease blood flow resulting into "ischemic" (reduced flow related) lesions such as small infarcts (lacunes, microinfarcts) and white matter disease. 

CAA is the prototypical brain disease associated with a fairly high bleeding risk. Patients with CAA have even higher hemorrhage risk if life-long anticoagulant medications are used (such as Coumadin). Good control of blood pressures and avoidance of anticoagulation to the extent possible are important approaches to minimize the risk of bleeding. There are situations where anticoagulants or their alternatives need to be considered (see Atrial Fibrillation part of this website as an example).

Appearance of CAA-related pathologies on brain MRI and PET scans

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