Vascular cognitive disorder: A new diagnostic category updating vascular cognitive impairment and vascular dementia
ABSTRACT Vascular cognitive impairment (VCI) was proposed as an umbrella term to include subjects affected with any degree of cognitive impairment resulting from cerebrovascular disease (CVD), ranging from mild cognitive impairment (MCI) to vascular dementia. VCI may or may not exclude the host of "focal" circumscribed impairments of specialized functions such as language (aphasia), intentional gesture (apraxia), or categorical recognition (agnosia), among others, that may result from a stroke. Therefore, there are no universally accepted diagnostic criteria for VCI. We conclude that this concept could be more useful if it were to be limited to cases of vascular MCI without dementia, by analogy with the concept of amnestic MCI, currently considered the earliest clinically diagnosable stage of Alzheimer disease (AD). In agreement with our view,the Canadian Study on Health and Aging successfully implemented a restricted definition of VCI, excluding cases of dementia (i.e., vascular cognitive impairment no dementia, VCI-ND). The Canadian definition and diagnostic criteria could be utilized for future studies of VCI. This definition excludes isolated impairments of specialized cognitive functions. Vascular dementia (VaD): The main problem of this diagnostic category stems from the currently accepted definition of dementia that requires memory loss as the sine qua non for the diagnosis. This may result in over-sampling of patients with AD worsened by stroke (AD+CVD). This problem was minimized in controlled clinical trials of VaD by excluding patients with a prior diagnosis of AD, those with pre-existing memory loss before the index stroke, and those with amnestic MCI. We propose a definition of dementia in VaD based on presence of abnormal executive control function, severe enough to interfere with social or occupational functioning. Vascular cognitive disorder (VCD): This term, proposed by Sachdev [P. Sachdev, Vascular cognitive disorder. Int J Geriat Psychiatry 14 (1999)402-403.] would become the global diagnostic category for cognitive impairment of vascular origin, ranging from VCI to VaD. It would include specific disease entities such as post-stroke VCI, post-stroke VaD, CADASIL, Binswanger disease, and AD plus CVD. This category explicitly excludes isolated cognitive dysfunctions such as those mentioned above.
- SourceAvailable from: Xiaomeng Xu
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- "The current study also found a specific association between cerebral perfusion of the frontal lobe and performance on a test of executive function. This is noteworthy , as executive dysfunction is common in older adults with vascular disease (Roman et al. 2004) and may be a result of reduced oxygenation to the highly plastic frontal lobes subsequent to disrupted cerebral hemodynamics . It is also possible that memory deficits in this sample may involve frontal-subcortical dysfunction (e.g., encoding, organizing) given the current association between frontal lobe perfusion and memory (Bonelli and Cummings 2008). "
ABSTRACT: It is well established that aging and vascular processes interact to disrupt cerebral hemodynamics in older adults. However, the independent effects of cerebral perfusion on neurocognitive function among older adults remain poorly understood. We examined the associations among cerebral perfusion, cognitive function, and brain structure in older adults with varying degrees of vascular disease using perfusion magnetic resonance imaging (MRI) arterial spin labeling (ASL). 52 older adults underwent neuroimaging and were administered the Mini Mental State Examination (MMSE), the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), and measures of attention/executive function. ASL and T1-weighted MRI were used to quantify total brain perfusion, total brain volume (TBV), and cortical thickness. Regression analyses showed reduced total brain perfusion was associated with poorer performance on the MMSE, RBANS total index, immediate and delayed memory composites, and Trail Making Test B. Reduced frontal lobe perfusion was associated with worse executive and memory function. A similar pattern emerged between temporal lobe perfusion and immediate memory. Regression analyses revealed that decreased total brain perfusion was associated with smaller TBV and mean cortical thickness. Regional effects of reduced total cerebral perfusion were found on temporal and parietal lobe volumes and frontal and temporal cortical thickness. Reduced cerebral perfusion is independently associated with poorer cognition, smaller TBV, and reduced cortical thickness in older adults. Prospective studies are needed to clarify patterns of cognitive decline and brain atrophy associated with cerebral hypoperfusion.Brain and Behavior 11/2013; 3(6):626-36. DOI:10.1002/brb3.171
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- "Vascular cognitive impairment (VCI) subsumes a wide range of cognitive deficits caused by ischaemic brain lesions.1 White matter hyperintensities (WMHs) on fluid attenuated inversion recovery (FLAIR) and T2 weighted MRI are commonly seen in VCI patients, and the size of the lesions is used to indicate the extent of ischaemia.2–4 However, WMHs are found in a number of neurological disorders and their contribution to VCI symptoms is controversial.5 6 Furthermore, considerable inter-rater variability in the scoring of radiological findings in VCI has been reported7 and, to date, correlations between lesion load and neuropsychological testing results have been shown only for processing speed in one study on cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy.8 "
ABSTRACT: Background White matter hyperintensities (WMHs) are associated with vascular cognitive impairment (VCI) but fail to correlate with neuropsychological measures. As proton MR spectroscopy (1H-MRS) can identify ischaemic tissue, we hypothesised that MRS detectable brain metabolites would be superior to WMHs in predicting performance on neuropsychological tests. Methods 60 patients with suspected VCI underwent clinical, neuropsychological, MRI and CSF studies. They were diagnosed as having subcortical ischaemic vascular disease (SIVD), multiple infarcts, mixed dementia and leukoaraiosis. We measured brain metabolites in a white matter region above the lateral ventricles with 1H-MRS and WMH volume in this region and throughout the brain. Results We found a significant correlation between both total creatine (Cr) and N-acetylaspartyl compounds (NAA) and standardised neuropsychological test scores. Cr levels in white matter correlated significantly with executive function (p=0.001), attention (p=0.03) and overall T score (p=0.007). When lesion volume was added as a covariate, NAA also showed a significant correlation with executive function (p=0.003) and overall T score (p=0.015). Furthermore, while metabolite levels also correlated with total white matter lesion volume, adjusting the Cr levels for lesion volume did not diminish the strength of the association between Cr levels and neuropsychological scores. The lowest metabolite levels and neuropsychological scores were found in the SIVD group. Finally, lesion volume alone did not correlate significantly with any neuropsychological test score. Conclusion These results suggest that estimates of neurometabolite levels provide additional and useful information concerning cognitive function in VCI not obtainable by measurements of lesion load.Journal of neurology, neurosurgery, and psychiatry 02/2013; 84(7). DOI:10.1136/jnnp-2012-303878 · 5.58 Impact Factor
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- "The heterogeneous group of syndromes and diseases characterized by cognitive impairment resulting from a cerebrovascular etiology has been defined recently with the term vascular cognitive disorder (VCD; Sachdev, 1999; Román et al., 2004). The main categories of VCD are vascular cognitive impairment (VCI; i.e., vascular cognitive impairment no dementia and vascular MCI), VaD, and mixed AD plus CVD, previously termed " mixed dementia " (Sachdev, 1999; Román et al., 2004). Drugs currently used for the treatment of AD partially stabilize patients' symptoms without modifying disease progression; and, at present, there is no curative treatment for dementia and AD, nor is there a therapeutical approach to prevent the conversion of MCI to dementia (Giacobini and Becker, 2007; Frisardi et al., 2010a). "
ABSTRACT: Objective: In several longitudinal studies, light-to-moderate drinking of alcoholic beverages has been proposed as being protective against the development of age-related changes in cognitive function, predementia syndromes, and cognitive decline of degenerative (Alzheimer's disease, AD) or vascular origin (vascular dementia). However, contrasting findings also exist. Method: The English literature published in this area before September 2011 was evaluated, and information relating to the various factors that may impact upon the relationship between alcohol consumption and dementia or predementia syndromes is presented in the succeeding texts. Results: Light-to-moderate alcohol consumption may be associated with a reduced risk of incident overall dementia and AD; however, protective benefits afforded to vascular dementia, cognitive decline, and predementia syndromes are less clear. The equivocal findings may relate to many of the studies being limited to cross-sectional designs, restrictions by age or gender, or incomplete ascertainment. Different outcomes, beverages, drinking patterns, and study follow-up periods or possible interactions with other lifestyle-related (e.g., smoking) or genetic factors (e.g., apolipoprotein E gene variation) may all contribute to the variability of findings. Conclusion: Protective effects of moderate alcohol consumption against cognitive decline are suggested to be more likely in the absence of the AD-associated apolipoprotein E ε4 allele and where wine is the beverage. At present, there is no indication that light-to-moderate alcohol drinking would be harmful to cognition and dementia, and attempts to define what might be deemed beneficial levels of alcohol intake in terms of cognitive performance would be highly problematic and contentious. CopyrightInternational Journal of Geriatric Psychiatry 12/2012; 27(12):1218-38. DOI:10.1002/gps.3772 · 3.09 Impact Factor