**Cerebral Amyloid Angiopathy**

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Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/58461

#### **1. Introduction**

Cerebral amyloid angiopathy (CAA) is an important but under-recognized cause of sponta‐ neous intracranial hemorrhage (ICH) in the normotensive individuals. [1] Both sporadic and hereditary forms may occur. Hereditary form of CAA is seen at a younger age, as early as the third decade; in contrast, the sporadic form is more common in elderly and increases in both prevalence and severity with increasing age. CAA results from deposition of β-amyloid protein in small and medium sized cortical, subcortical, and leptomeningeal vessels. This deposition is responsible for the wide spectrum of clinical symptoms and neuroimaging findings. [1,2] CAA is not associated with the presence of systemic amyloidosis. [3] Majority of cases of CAA are asymptomatic. However, symptomatic patient may present with sudden neurological deficit due to transient ischemic attack, progressive cognitive decline, or potentially devastat‐ ing intracranial hemorrhage. [3,4] Computed tomography is the imaging modality of choice for evaluation of suspected acute intracranial hemorrhage. Magnetic resonance imaging is a sensitive technique for identifying microhemorrhages, microangiopathy-related ischemic changes and assessment of disease progression. The early and accurate diagnosis of CAA is important because of the likely implication it has on future management targeted to reduce the risk of recurrent hemorrhage. In this chapter our emphasis will be on the complex patho‐ physiology, important clinical and radiological features and the role of imaging in secondary prevention of CAA related ICH. [1,3,4]

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
