This chapter reviews the pathophsyiology and pathology of hypertensive arteriopathy of the brain and its relationship to neuroimaging findings, particularly cerebral microbleeds (CMBs). The prevalence of hypertension is highly age dependent. Hypertension-related cerebral diseases include hypertensive encephalopathy, stroke and vascular cognitive impairment. Although the term arteriopathy includes both arteries and arterioles, the chapter focuses on the intrinsic vascular pathology of arterioles in hypertension. Intracranial atherosclerosis of large arteries is more common in hypertension. The presence of hypertensive arteriolosclerosis must be inferred indirectly. Hypertension is a common age-related disease that is accompanied by loss of vascular integrity, with leakage of red blood cells and perivascular hemosiderin deposition. Cerebral microbleeds caused by hypertensive arteriopathy may be seen in the deep hemispheric regions, brainstem, cerebellum and cerebral lobes; however, the pattern of purely lobar CMBs strongly suggests cerebral amyloid angiopathy (CAA) rather than hypertensive arteriopathy.

This chapter describes the vascular pathologies that underlie cerebral microbleeds (CMBs), concentrating on the two commonest disorders: hypertensive small vessel disease (SVD) and cerebral amyloid angiopathy (CAA). It also describes the process of blood degradation, and the correlation of imaging with histological findings. The chapter concentrates on hypertensive arteriopathy and CAA, which is usually diagnosed following symptomatic lobar intracerebral hemorrhage (ICH). Hypertensive arteriopathy is thought to be caused by a forced dilation of resistance vessels: that is, those vessels that regulate the blood supply volume to the distal capillary bed. The first event in a hemorrhage is the extravasation of all constituents of blood along with plasma. Extravasation may occur by rhexis (rupture of a vessel wall) or by diapedesis affecting arterioles, veins or capillaries. From the perspective of neuroimaging, CMBs are focal deposits of hemosiderin and can be visualized with MRI.