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Vascular cognitive impairment is the second most common cause of dementia after Alzheimer's disease and is expected to grow in prevalence with the aging global population. The purpose of this authoritative book is to give a broad clinical perspective on vascular cognitive impairment and thus create a foundation for the implementation of good dementia care. The book focuses on pathophysiology, diagnosis, treatment and prevention. It demonstrates the underlying causes of the disorder, such as the manner in which vascular risk-factors influence the onset of vascular cognitive impairment. The concept of mixed forms of vascular dementia, Alzheimer's dementia and other vascular diseases is discussed as well as the influence of vascular changes with regard to the onset of Alzheimer's disease. The detailed section on pathophysiology will enhance clinicians' understanding of this complex disorder. Finally there is a section on pharmacological and neuropsychological treatment of cognitive and psychiatric symptoms.


'… this book may be recommended not just for the VaD/VCI cognoscenti, but for all those concerned with the diagnosis and management of dementia syndromes.'

Source: Advances in Clinical Neuroscience and Rehabilitation

'This is a major contribution to the field. It sorts out in clear fashion a very tangled literature. … The excellent organisation and editing of this book, its careful elaboration of complex concepts, and the practical application of this synthesis give rise to a first-rate work. This much-needed book deserves a wide readership.'

David O. Staats MD - University of Oklahoma Health Sciences Center

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  • 9 - Small-vessel diseases of the brain
    pp 118-130
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    Vascular cognitive impairment (VCI) is currently considered the most recent modification of the terminology to reflect the all-encompassing effects of vascular disease or lesions on cognition and incorporates the complex interactions between vascular etiologies, risk factors and cellular changes within the brain and cognition. The recognition of Alzheimer's disease (AD) as the commonest cause of dementia led to the development of operational criteria for the diagnosis of dementia in general. Post-stroke cognitive impairment is frequent, although it has been a neglected consequence of stroke. The main subtypes of vascular dementia (VaD) included in current classifications are cortical VaD or MID, also referred to as post-stroke VaD, subcortical ischemic vascular disease and dementia (SIVD) or small vessel dementia, and strategic infarct dementia. AD with cerebrovascular disease (CVD) can present clinically either as AD with evidence of vascular lesions upon brain imaging, or with clinical features of both AD and VaD.
  • 10 - White matter changes
    pp 131-138
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    This chapter discusses the potential role that vascular risk factors and asymptomatic cerebrovascular disease (CVD) may have on lifetime risk for dementia. It examines evidence regarding the extent and character by which vascular cognitive impairment (VCI) influences cognition and by what mechanism VCI may contribute to incident dementia whether the dementia syndrome results from Alzheimer's disease (AD), vascular dementia (VaD) or a mixed dementia. The chapter reviews the concept of VCI, and also discusses the spectrum and potentially long time course of vascular-related brain injury, and the potentially important role of cerebral white matter in relation to widely distributed cognitive processes such as memory. It addresses cognitive changes associated with aging, and the potential role of asymptomatic vascular brain injury in these processes. The chapter outlines the identification of clinically relevant episodic memory impairment (amnestic mild cognitive impairment (aMCI)) due solely to presumed brain vascular disease.
  • 11 - Hereditary forms of cerebrovascular amyloidosis
    pp 139-154
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    A significant advance in the clinical characterization of vascular dementia (VaD) occurred in the 1970s when V. Hachinski described the term multi-infarct dementia (MID). A number of factors have contributed to difficulty in the development and implementation of diagnostic criteria for VaD. All diagnostic criteria have focused on the two most important issues in VaD: the presence of dementia, and the presence of vascular disease of sufficient severity to cause cognitive deficits. However, there is a great variability in their approach to these two core issues. The most difficult aspect in the diagnosis of VaD is to separate the presence of an ongoing neurodegenerative disease from true VaD. Constitutional and cerebrovascular risk factors and previous strokes have been associated with the presence of VaD. Therefore, detailed clinical, laboratory, neuroimaging, and neuropsychological assessments are necessary for the accurate diagnosis of VaD.
  • 12 - Role of vascular risk factors in dementia
    pp 155-165
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    This chapter focuses on cognitive functioning in multi-infarct dementia (MID) and subcortical (small-vessel disease) vascular dementia (VaD), the most extensively studied subtypes. An important difference in the manifestation of subcortical VaD compared to MID is the effect of a single infarct on cognition. Frontal-executive function and episodic memory are two cognitive domains frequently assessed when trying to discriminate between VaD and other dementia types, and between different VaD subtypes. The chapter describes these domains in more detail, as well as their manifestation in VaD. One of the challenges in clinical practice is to separate between VaD and other dementia types, most often Alzheimer's disease (AD). Future studies should seek to study the whole range of cognitive impairments associated with cerebrovascular disease (CVD), especially the earlier stages when the person still does not fulfill the criteria for dementia. This is where interventions would render the largest benefits.
  • 13 - Cardiovascular disease, cognitive decline, and dementia
    pp 166-177
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    This chapter describes brain abnormalities that can be observed on magnetic resonance imaging (MRI) in patients with vascular dementia (VaD). It presents an overview of MRI abnormalities indicative of cerebrovascular disease. Computed tomography (CT) is sufficient to rule out causes of cognitive decline other than VaD or neurodegenerative types of dementia. In addition, infarcts can be observed on CT, and small-vessel disease and atrophy are appreciable to some extent. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoaraiosis (CADASIL) is a hereditary form of VaD, presenting in young patients in the absence of vascular risk factors. On imaging, diffuse white matter hyperintensities involving the U-fibers are characteristically observed, mainly in the temporal, temporopolar, and frontal regions. Quantitative methods such as diffusion tensor imaging (DTI) and magnetization transfer imaging (MTI) provide valuable new ways to assess the integrity of white matter in more detail.
  • 14 - Vascular factors in Alzheimer’s disease
    pp 178-192
  • from diagnostic dichotomy to integrative etiology
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    The purpose of functional imaging in clinical practice is to increase diagnostic accuracy when differentiating between dementia disorders. The techniques most often used are imaging of regional cerebral blood flow (rCBF), using single photon emission computed tomography (SPECT), and imaging of glucose metabolism using positron emission tomography (PET). rCBF assessed with SPECT has been used to study vascular reactivity and to evaluate the effect of dementia treatment. It has also been studied in CADASIL, a hereditary form of vascular dementia (VaD). PET shows the same disease pattern as SPECT when ligands are used for investigating rCBF. It is also used to study regional glucose metabolism using Fluoro-Deoxy-D-Glucose (FDG), oxygen metabolic extraction rate and cerebral oxygen metabolic rate. According to the meta review by Dougall and his group, it is clear that the clinical usefulness of SPECT in differentiating VaD from Alzheimer's disease is limited.
  • 15 - Treatment of cognitive changes
    pp 195-199
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    This chapter summarizes the data of some biomarkers that are associated with the presence of vascular disease, and potential markers of different brain pathologies relevant to vascular dementia (VaD) and for differential diagnosis. Many prospective population-based studies have reported an association between increased plasma levels of inflammation markers and an increased risk of atherosclerotic vascular diseases and dementia. Accumulation of extracellular neuritic plaques with a core of fibrillar β-amyloid protein (Aβ) is a characteristic feature of Alzheimer's disease (AD). The main pool of plasma Aβ seems to originate from platelets although a proportion of it originates from cerebrospinal fluid (CSF) and brain. The endothelial cells of the brain capillaries are sealed together by continuous tight junctions and there are few channels running through the cells. These restrictive characteristics constitute the basis of the blood-brain barrier (BBB). The presence of BBB damage supports the diagnosis of VaD.
  • 17 - Treatment of behavioral symptoms in vascular dementia
    pp 206-219
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    This chapter outlines some characteristics of vascular dementia (VaD) related to large-vessel diseases in terms of pathology, pathogenesis, and clinical aspects. Large-vessel VaD is characterized by a step-wise cognitive deterioration, focal signs and symptoms which are the result of repeated ischemic strokes. The chapter reviews some of large-vessel diseases such as atherosclerosis, arterial dissection, angiitis, moyamoya disease, and intracranial arterial dolichoectasia. The pathogenesis of large-vessel VaD is complex and to some extent remains a matter of investigation. Efforts in defining diagnostic criteria are made in order to characterize patterns of brain infarction from which it is reliable to deduce the presence of dementia. Some of the most important pathophysiological mechanisms and factors implicated in large-vessel VaD are volume of lesions, number of lesions, location of lesions, and coexistence of other brain pathologies, particularly Alzheimer's disease (AD).
  • 18 - Control of vascular risk factors
    pp 220-234
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    Small-vessel disease related to subcortical dementia is one of the main subtypes of the vascular dementia (VaD) syndrome. The early cognitive features of subcortical vascular dementia (SVD) are characterized by a dysexecutive syndrome with slowed information processing, usually mild memory deficit and behavioral symptoms. SVD incorporates two entities "the lacunar state" and "Binswanger's disease". Cerebral amyloid angiopathy (CAA) falls into the category of small-vessel diseases and contributes to the SVD syndrome. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common form of hereditary small-vessel diseases leading to cognitive decline and dementia. Small-vessel diseases of the brain may also manifest in progressive visual impairment. Hereditary endotheliopathy with retinopathy, nephropathy and stroke (HERNS), cerebroretinal vasculopathy (CRV) and hereditary vascular retinopathy (HVR) were reported independently, but are different phenotypes in the same disease spectrum.


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