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INTRODUCTION

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Vascular cognitive impairment and vascular dementia (VCI-VaD) denote deficits in cognition and behavior, along a spectrum of severity, that are associated with cerebrovascular disease (CVD). A dementia syndrome results when CVD is severe enough to cause significant deficits in occupational, social, or functional abilities. VaD is among the most common causes of dementia in the elderly, although its prevalence is disputed. Vascular disease can disrupt structural cognitive networks with lesions such as microinfarcts, microbleeds, macroinfarcts, large hemorrhages, and chronic progressive white matter degeneration, as well as altered cerebral hemodynamics, such as hypoperfusion, disrupted cerebrovascular autoregulation (Chap. 301) neurovascular decoupling (loss of normal hemodynamic responses to neural activity), and blood brain barrier dysfunction. The pathophysiological underpinnings of VCI-VaD remain an active area of research.

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Age remains the strongest risk factor for CVD and stroke. By the age of 70, 70% of the population has white matter disease and lesions on neuroimaging, with small infarcts (lacunar infarcts) found in 11–24% of the population. In addition to genetic predisposition, risk factors that directly contribute to CVD include chronic hypertension, hyperlipidemia, diabetes, and smoking. Cardiac disease, such as atrial fibrillation or heart failure, can also cause cognitive impairment via embolic infarcts and hypoxemia due to inadequate cerebral blood flow.

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A review of data from across the globe indicates good evidence for variability in CVD and stroke risk. Intracranial atherosclerosis, for example, is higher in Asians, Hispanics, and American blacks than it is in European and American whites, while whites may have more extracranial disease. The causes of these disparities remain under investigation, but likely include genetics, lifestyle, and access to health care.

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VaD is strongly associated with hemorrhagic and ischemic strokes, with an estimated one-third of stroke survivors affected by post-stroke dementia or cognitive impairment. Hemorrhages, including subdural, intracerebral and subarachnoid bleeds, account for roughly 20% of all strokes. The disruption of cerebral networks caused by hemorrhage depends to a certain extent on size and location. Subarachnoid hemorrhage (SAH) has a more intricate relation with cognitive deficits. For instance, a history of SAH can triple the lifetime risk of developing a dementia syndrome; the molecular underpinnings of this observation are being actively studied. Of note, hemorrhagic strokes may occur as a result of vessel wall damage and inflammation associated with cerebral amyloid angiopathy (CAA). The build-up of β-amyloid protein in cerebral blood vessels that increases their susceptibility to rupture. Although CAA is frequently present in patients with Alzheimer’s disease (AD) (Chap. 423), it can also be found in the absence of neocortical amyloid plaques or in individuals with specific genetic predispositions and lead to cognitive impairment in the absence of AD.

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Ischemic strokes compose 80% of all strokes. Large vessel and small vessel disease (SVD) can lead to dementia, although the mechanisms and clinical presentation vary. In a cross-sectional study of 706 VaD cases, large vessel disease, often referred to as multi-infarct dementia, ...

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