Clinical diagnosis of vascular dementia
Introduction
Vascular dementia (VaD) is the second most common cause of dementia next to Alzheimer's disease (AD). Although there are several diagnostic criteria of VaD, the differential diagnosis between VaD and AD is not so easy because VaD is a heterogeneous clinical entity including various subtypes of cerebrovascular disease (CVD) based on different vascular pathology: lacunar infarction, cortical infarction, subcortical infarction, white matter lesions, cardiogenic emboli, hemodynamic (hypotensive) infarction, hypertensive intracerebral hemorrhage, lobar hemorrhage, and subarachnoid hemorrhage (Fig. 1). In addition, neuropathological studies revealed that vascular and neurodegenerative pathologies coexist, and global neuropsychological scales which are commonly used in the evaluation of dementia are emphasized toward memory deficits and cortical signs, and this may bias the clinical diagnosis of VaD towards concomitant AD pathology in the attempt to exclude pure vascular dementia [1], [2], [3]. Thus it seems difficult to make a firm diagnosis of VaD using current clinical diagnostic criteria [1], [4], [5].
Section snippets
Overview of diagnostic criteria
Current clinical diagnostic criteria of VaD were constructed based on the expert opinion about risk factors, neurological manifestations and pathogenetic mechanisms, and designed to achieve high sensitivity and specificity in contrast to the clinical features of AD (Table 1). They are, however, mostly more than 10 years old and need to be updated.
Those diagnostic criteria were basically designed to differentiate VaD from AD, but the strict dichotomy between VaD and AD is often difficult because
Clinical course and temporal relationship
A temporal relationship between dementia and CVD in post-stroke dementia (VaD) is inferred from the onset of dementia within 3 months following the recent stroke event in NINDS-AIREN criteria. Otherwise, abrupt onset of cognitive dysfunctions, or fluctuating or stepwise deterioration of cognitive deficits is regarded as a characteristic clinical course for VaD. The ADDTC criteria require a clearly documented temporal relationship between onset of dementia and the occurrence of a stroke event by
Subcategories of VaD
Although there are several subtypes of VaD listed in the current diagnostic criteria, no detailed guidelines are given for those subcategories. In the ICD-10 criteria, there are 6 subtypes of VaD with unequal clinical description such as acute onset, multi-infarct, subcortical, mixed cortical and subcortical, other and unspecified.
Case 1 is a right-handed patient with paroxysmal atrial fibrillation who suddenly developed a left unilateral space neglect, anosognosia, inattention, memory deficits
Diagnostic brain imaging
Structural brain imaging techniques such as X-ray CT and MRI have been applied to the discriminative diagnosis of VaD and AD by detecting organic changes including cortical or subcortical infarcts and/or ischemic white matter lesions. Although large infarcts can be easily detected on such structural imaging, mild ischemia may cause partial neuronal loss (incomplete infarction) and consequently result in undetectable structural changes on such brain images.
With regard to the diagnostic
References (29)
- et al.
Vascular cognitive impairment
Lancet Neurol
(2003) - et al.
Discrimination between Alzheimer dementia and controls by automated analysis of multicenter FDG PET
Neuroimage
(2002) - et al.
Analysis of cerebral blood flow of subcortical vascular dementia with single photon emission computed tomography: adaptation of statistical parametric mapping
J Neurol Sci
(2002) - et al.
Relative frequencies of Alzheimer disease, Lewy body, vascular and frontotemporal dementia, and hippocampal sclerosis in the State of Florida Brain Bank
Alzheimer Dis Assoc Disord
(2002) - et al.
Criteria for vascular dementia
Arch Neurol
(2000) - et al.
Current criteria for vascular dementia — a critical appraisal
- et al.
Emerging therapies for vascular dementia and vascular cognitive impairment
Stroke
(2004) Mixed dementia: the most common cause of dementia
Ann N Y Acad Sci
(2002)Diagnostic and statistical manual of mental disorders
(1994)ICD-10 classification of mental and behavioral disorders: diagnostic criteria for research
(1993)
The ICD-10 criteria for vascular dementia
Dementia
Clinical evaluation of the ICD-10 criteria for vascular dementia
Eur Arch Psychiatry Clin Neurosci
Criteria for the diagnosis of ischemic vascular dementia proposed by the State of California Alzheimer's Disease Diagnostic and Treatment Centers
Neurology
Cited by (31)
Cerebral circulation in aging
2016, Ageing Research ReviewsCitation Excerpt :Aging is also associated with alteration in regulation of cerebral circulation, which may reduce cerebral blood flow (CBF) and ultimately affect the cognitive function as a result of brain ischemia and energy failure. Traditional perspectives on the pathophysiology underlying Alzheimer’s disease (AD) and vascular dementia (VaD) have been divergent, and there was a dichotomy between AD and VaD in the clinical diagnosis of dementia (Nagata et al., 2007). AD has been considered to develop as a result of pathological cascade of neurodegeneration triggered by the amyloid deposition (Selkoe, 1991), whereas VaD has been attributed to the accumulation of ischemia or hemorrhagic cerebrovascular lesions (Hossmann, 1994; Gorelick et al., 2011).
Pathophysiological rat model of vascular dementia: Magnetic resonance spectroscopy, microimaging and behavioral study
2014, Brain ResearchCitation Excerpt :Vascular dementia (VaD) is a degenerative illness caused by a variety of vascular lesions resulting in restricting blood supply to different brain regions. It is the second most-common cause of dementia after Alzheimer׳s disease (AD), both referring to a progressive decline in cognitive abilities and memory impairment (Nagata et al., 2007; Querfurth and LaFerla, 2010). Persistent reduction in cerebral blood flow induces hypoxia/ischemia of the brain tissue, deprivation of oxygen and nutrients and can lead to cell death (Bennett et al., 2009).
The need to unify neuropathological assessments of vascular alterations in the ageing brain. Multicentre survey by the BrainNet Europe consortium.
2012, Experimental GerontologyCitation Excerpt :It is well known that vascular alterations are also frequently seen in cognitively unimpaired subjects making the assessment of the significance of lesions problematic (Ferrer, 2010). Thus, the existence of vascular dementia is still debated and the incidences of dementia caused by pure vascular alterations and incidence of dementia caused by vascular alterations in association with other pathologies vary (Barker et al., 2002; Drach et al., 1997; Jellinger, 2008; Kovacs et al., 2008; Nagata et al., 2007). Recently, however, Gorelick et al. (2011) emphasised in a statement for healthcare professionals that vascular contributions to cognitive impairment and dementia are important and should be investigated further.
Chapter 4 Neuroimaging of Cognitive Impairments in Vascular Disease
2009, International Review of NeurobiologyCitation Excerpt :Despite this, its use has been recently growing. It is therefore proposed by Nagata et al. (2007) that the old VaD criteria should be revised especially due to new insight brought by nuclear imaging techniques. Zimny et al. (2007) studied 64 patients with dementia with different degrees of cognitive impairment to assess the relationship between cognitive impairment according to the MMSE and values of CBF, CBV, and MTT obtained in perfusion CT (pCT).
Identification of pure subcortical vascular dementia using <sup>11</sup>C-Pittsburgh compound B
2011, NeurologyCitation Excerpt :We infer that the cognitive disorder in those patients with SVaD without abnormal amyloid imaging is largely ischemic in origin. In the field of dementia, the prevailing view has been that pure vascular dementia is rare and underlying AD is mostly responsible for cognitive decline.18–21 Thus, AD has been considered the predominant pathologic process in the dementia etiology, regardless of the severity of white matter ischemic changes or presence of lacunar infarcts.