Vascular cognitive impairment: current concepts and clinical developments. Lancet Neurol 7:246-255

Division of Geriatric Medicine, Halifax, Nova Scotia, Canada.
The Lancet Neurology (Impact Factor: 21.9). 04/2008; 7(3):246-55. DOI: 10.1016/S1474-4422(08)70040-1
Source: PubMed

ABSTRACT Vascular cognitive impairment (VCI) comprises a range of cognitive disorders related to cerebral vessel disease and has generally replaced the term multi-infarct dementia. Despite the heterogeneity of the VCI construct, some clinical patterns can be discerned, which enable subtypes, such as mixed dementia and VCI-no dementia, to be recognised. Diagnostic criteria for vascular dementia do not encompass the full range of the VCI construct, and clinical investigators now recognise the need for harmonised standards to study the many manifestations of VCI seen in daily practice and to inform the development of diagnostic criteria. Although executive dysfunction is a recognised feature of VCI, some data suggest a less exclusive role than was previously proposed. VCI might be preventable, although the evidence for this is not as complete as it is for the prevention of stroke. Future studies into specific therapies for VCI will need to consider the clinical features and outcomes carefully.

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    • "types of lesions are often mixed in MCI which progress to dementia (Moorhouse and 17 Rockwood, 2008). Since cerebrovascular lesions have been consistently found associated "
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    ABSTRACT: Mild cognitive impairment (MCI) is a heterogeneous cognitive status that can be a prodromal stage of Alzheimer's disease (AD). It is particularly relevant to focus on prodromal stages of AD such as MCI, because patho-physiological abnormalities of AD start years before the dementia stage. Medial temporal lobe (MTL) atrophy resulting from AD lesions and cerebrovascular lesions [i.e., white matter lesions (WML), lacunar strokes, and strokes] are often revealed concurrently on magnetic resonance imaging (MRI) in MCI subjects. Personality changes have been reported to be associated with MCI status and early AD. More specifically, an increase in neuroticism and a decrease in conscientiousness have been reported, suggesting that higher and lower scores, respectively, in neuroticism and conscientiousness are associated with an increased risk of developing the disease. However, personality changes have not been studied concomitantly with pathological structural brain alterations detected on MRI in patients suffering from MCI. Therefore, the objective of the present study was to assess the relationship between MTL atrophy, WML, lacunar strokes, and personality traits in such patients. The severity of WML was strongly associated with lower levels of conscientiousness and higher levels of neuroticism. Conversely, no association was detected between personality traits and the presence of lacunar strokes or MTL atrophy. Altogether, these results strongly suggest that personality changes occurring in a MCI population, at high risk of AD, are associated with WML, which can induce executive dysfunctions, rather than with MTL atrophy.
    Frontiers in Aging Neuroscience 07/2014; 6:195. DOI:10.3389/fnagi.2014.00195 · 4.00 Impact Factor
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    • "Vascular cognitive impairment (VCI) consists of a heterogeneous group of cognitive disorders that shares a presumed vascular origin, ranging from mild impairment to dementia [1]. Pathological study indicated that cerebral vascular pathology is very common and about one third of dementia showed multiple vascular changes on autopsy [2]. "
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    ABSTRACT: Our previous study found that cortical gray matter (cGM) volume predicted vascular cognitive impairment independent of age-related white matter changes (WMC). We aimed to investigate predictors for cGM volume in ischemic stroke patients with confluent WMC. One-hundred post-stroke patients with confluent WMC were recruited into the study. All volumetric measures were standardized by intracranial volume as volume ratio. Univariate analyses and multivariate linear regression models were used to test relationship of cGM volume with basic demography, vascular risk factors, APOE status, WMC volume (periventricular and deep WMC), infarct measures (volume, number and location) and microbleed (number, presence and location). After controlling for significant variables in the univariate analyses, multivariate linear regression models found that old age (β=-0.288, p=0.001), low triglyceride (β=0.194, p=0.027), periventricular WMC (PVWMC) (β=-0.392, p<0.001) and presence of thalamic microbleed (β=-0.197, p=0.041) were independently predictive of less cGM volume ratio. Age, PVWMC and left thalamic microbleed predict less cGM volume.
    Journal of the neurological sciences 01/2014; 338(1-2). DOI:10.1016/j.jns.2013.12.044 · 2.47 Impact Factor
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    • "These data should be considered in future studies of ischemia-induced executive dysfunction targeting the MD nucleus. Cognitive impairment has been proposed to arise from several types of vascular lesions including single or multiple infarcts, chronic hypoperfusion and white matter damage, also referred to as leukoaraiosis [30]. While these lesions can affect the prefrontal circuitry including the PFC and MD, they may also damage axon tracts in subcortical structures that were not investigated in the current study. "
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    ABSTRACT: Small (lacunar) infarcts frequently arise in frontal and midline thalamic regions in the absence of major stroke. Damage to these areas often leads to impairment of executive function likely as a result of interrupting connections of the prefrontal cortex. Thus, patients experience frontal-like symptoms such as impaired ability to shift ongoing behavior and attention. In contrast, executive dysfunction has not been demonstrated in rodent models of stroke, thereby limiting the development of potential therapies for human executive dysfunction. Male Sprague-Dawley rats (n=40) underwent either sham surgery or bilateral endothelin-1 injections in the mediodorsal nucleus of the thalamus or in the medial prefrontal cortex. Executive function was assessed using a rodent attention set shifting test that requires animals to shift attention to stimuli in different stimulus dimensions. Medial prefrontal cortex ischemia impaired attention shift performance between different stimulus dimensions while sparing stimulus discrimination and attention shifts within a stimulus dimension, indicating a selective attention set-shift deficit. Rats with mediodorsal thalamic lacunar damage did not exhibit a cognitive impairment relative to sham controls. The selective attention set shift impairment observed in this study is consistent with clinical data demonstrating selective executive disorders following stroke within specific sub-regions of frontal cortex. These data contribute to the development and validation of a preclinical animal model of executive dysfunction, that can be employed to identify potential therapies for ameloriating cognitive deficits following stroke.
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