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© Cambridge University Press 2014. Introduction: Cerebral ischemia is thought to be an important disease mechanism in cerebral small vessel disease (SVD). It has been hypothesized that acute ischemia in the territory of the perforating artery results in lacunar stroke, while chronic ischemia occurring in the distal territories of the perforating arteries results in changes to cerebral white-matter, known as leukoaraiosis. The spatial pattern of leukoaraiosis, with changes first occurring in the brain regions furthest from the origin of the perforating arteries, would be consistent with disease occurring due to hypoperfusion. This has led to the suggestion that cerebral blood flow (CBF) is reduced in SVD, and many studies have been performed to investigate this issue. In addition, cerebral arteriopathy underlying SVD may also impair the ability of small cerebral vessels to vasodilate, leading to problems maintaining perfusion in response to drops in blood pressure and perfusion pressure. Impairments of cerebral reactivity to vasodilatory stimuli [1] and of cerebral autoregulation [2] have been shown in animal models of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a genetic form of SVD. These processes have been investigated in patients with sporadic SVD, as well as with CADASIL. We review the different techniques that can be used to measure CBF, cerebral reactivity, and cerebral autoregulation. We then consider recent studies investigating cerebral hemodynamics in SVD.

Original publication

DOI

10.1017/CBO9781139382694.016

Type

Chapter

Book title

Cerebral Small Vessel Disease

Publication Date

01/01/2011

Pages

180 - 191