Cognitive impairment in patients with cerebrovascular disease: A white paper from the links between stroke ESO Dementia Committee.
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ABSTRACT: Purpose
Many daily-life clinical decisions in patients with cerebrovascular disease and cognitive impairment are complex. Evidence-based information sustaining these decisions is frequently lacking. The aim of this paper is to propose a practical clinical approach to cognitive impairments in patients with known cerebrovascular disease.Methods
The document was produced by the Dementia Committee of the European Stroke Organisation (ESO), based on evidence from the literature where available and on the clinical experience of the Committee members. This paper was endorsed by the ESO.Findings
Many patients with stroke or other cerebrovascular disease have cognitive impairment, but this is often not recognized. With improvement in acute stroke care, and with the ageing of populations, it is expected that more stroke survivors and more patients with cerebrovascular disease will need adequate management of cognitive impairment of vascular etiology. This document was conceived for the use of strokologists and for those clinicians involved in cerebrovascular disease, with specific and practical hints concerning diagnostic tools, cognitive impairment management and decision on some therapeutic options.Discussion and conclusions: It is essential to consider a possible cognitive deterioration in every patient who experiences a stroke. Neuropsychological evaluation should be adapted to the clinical status. Brain imaging is the most informative biomarker concerning prognosis. Treatment should always include adequate secondary prevention.
SUBMITTER: Verdelho A
PROVIDER: S-EPMC7995319 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:PurposePractical suggestions on clinical decisions about vascular disease management in patients with cognitive impairment are proposed.MethodsThe document was produced by the Dementia Committee of the European Stroke Organisation (ESO) based on the evidence from the literature where available and on the clinical experience of the Committee members. This paper was endorsed by the ESO.FindingsVascular risk factors and cerebrovascular disease are frequent in patients with cognitive impairment. While acute stroke treatment has evolved substantially in last decades, evidence of management of cerebrovascular pathology beyond stroke in patients with cognitive impairment and dementia is quite limited. Additionally, trials to test some daily-life clinical decisions are likely to be complex, difficult to undertake and take many years to provide sufficient evidence to produce recommendations. This document was conceived to provide some suggestions until data from field trials are available. It was conceived for the use of clinicians from memory clinics or involved specifically in cognitive disorders, addressing practical aspects on diagnostic tools, vascular risk management and suggestions on some therapeutic options.Discussion and conclusionsThe authors did not aim to do an exhaustive or systematic review or to cover all current evidence. The document approach in a very practical way frequent issues concerning cerebrovascular disease in patients with known cognitive impairment.
| S-EPMC8370070 | biostudies-literature
Project description:With increased numbers of older people a higher burden of neurological disorders worldwide is predicted. Stroke and other cerebrovascular diseases do not necessarily present with different phenotypes in Africa but their incidence is rising in tandem with the demographic change in the population. Age remains the strongest irreversible risk factor for stroke and cognitive impairment. Modifiable factors relating to vascular disease risk, diet, lifestyle, physical activity and psychosocial status play a key role in shaping the current spate of stroke related diseases in Africa. Hypertension is the strongest modifiable risk factor for stroke but is also likely associated with co-inheritance of genetic traits among Africans. Somewhat different from high-income countries, strokes attributed to cerebral small vessel disease (SVD) are higher >30% among sub-Saharan Africans. Raised blood pressure may explain most of the incidence of SVD-related strokes but there are likely other contributing factors including dyslipidaemia and diabetes in some sectors of Africa. However, atherosclerotic and cardioembolic diseases combined also appear to be common subtypes as causes of strokes. Significant proportions of cerebrovascular diseases are ascribed to various forms of infectious disease including complications of human immunodeficiency virus. Cerebral SVD leads to several clinical manifestations including gait disturbance, autonomic dysfunction and depression. Pathological processes are characterized by arteriolosclerosis, lacunar infarcts, perivascular spaces, microinfarcts and diffuse white matter changes, which can now all be detected on neuroimaging. Except for isolated cases of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy or CADASIL, hereditary arteriopathies have so far not been reported in Africa. Prevalence estimates of vascular dementia (2-3%), delayed dementia after stroke (10-20%) and vascular cognitive impairment (30-40%) do not appear to be vastly different from those in other parts of the world. However, given the current demographic transition in both urban and rural settings these figures will likely rise. Wider application of neuroimaging modalities and implementation of stroke care in Africa will enable better estimates of SVD and other subtypes of stroke. Stroke survivors with SVD type pathology are likely to have low mortality and therefore portend increased incidence of dementia.
| S-EPMC6252289 | biostudies-literature
Project description:White matter abnormalities, related to poor cerebral perfusion, are a core feature of small vessel cerebrovascular disease, and critical determinants of vascular cognitive impairment and dementia. Despite this importance there is a lack of treatment options. Proliferation of microglia producing an expanded, reactive population and associated neuroinflammatory alterations have been implicated in the onset and progression of cerebrovascular white matter disease, in patients and in animal models, suggesting that targeting microglial proliferation may exert protection. Colony-stimulating factor-1 receptor (CSF1R) is a key regulator of microglial proliferation. We found that the expression of CSF1R/Csf1r and other markers indicative of increased microglial abundance are significantly elevated in damaged white matter in human cerebrovascular disease and in a clinically relevant mouse model of chronic cerebral hypoperfusion and vascular cognitive impairment. Using the mouse model, we investigated long-term pharmacological CSF1R inhibition, via GW2580, and demonstrated that the expansion of microglial numbers in chronic hypoperfused white matter is prevented. Transcriptomic analysis of hypoperfused white matter tissue showed enrichment of microglial and inflammatory gene sets, including phagocytic genes that were the predominant expression modules modified by CSF1R inhibition. Further, CSF1R inhibition attenuated hypoperfusion-induced white matter pathology and rescued spatial learning impairments and to a lesser extent cognitive flexibility. Overall, this work suggests that inhibition of CSF1R and microglial proliferation mediates protection against chronic cerebrovascular white matter pathology and cognitive deficits. Our study nominates CSF1R as a target for the treatment of vascular cognitive disorders with broader implications for treatment of other chronic white matter diseases.
| S-EPMC10952452 | biostudies-literature
Project description:The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25-30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood-brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.
| S-EPMC4827373 | biostudies-literature
Project description:Vascular pathology plays an important role in the development of cognitive decline and dementia. In this context, growth differentiation factor-15 (GDF-15) has been suggested to be a biomarker due to its regulatory roles in inflammatory and trophic responses during tissue injury. However, limited data exist on the associations of GDF-15 with either cerebrovascular disease (CeVD) burden or the spectrum of cognitive impairment. Therefore, we aimed to study peripheral levels of GDF-15 incognitive impairment no dementia (CIND) or Alzheimer disease (AD) subjects assessed for CeVD using a case-control cohort design, with cases recruited from memory clinics and controls from memory clinics and the community. All subjects underwent detailed neuropsychological assessment, 3-Tesla magnetic resonance imaging, and venous blood draw. Subjects were classified as CIND or AD based on clinical criteria, while significant CeVD was defined as the presence of cortical infarcts and/or 2 lacunes or more, and/or confluent white matter hyperintensities (WMHs) in 2 or more brain regions. A total of 324 subjects were included in the study, of whom 80 had no cognitive impairment, 144 CIND and 100with AD. Higher GDF-15 levels were significantly associated with disease groups, especially in the presence of CeVD, namely, CIND with CeVD (odds ratios [OR]: 7.21; 95% confidence interval [CI]: 2.14-24.27) and AD with CeVD (OR: 21.87; 95% CI: 2.01-237.43). Among the different CeVD markers, only WMH was associated with higher GDF-15 levels (OR: 3.97; 95% CI: 1.79-8.83). The associations between GDF-15 and cognitive impairment as well as with WMH remained significant after excluding subjects with cardiovascular diseases. In conclusion, we showed that increased GDF-15 may be a biomarker for CIND and AD in subjects with WMH.
| S-EPMC5370808 | biostudies-other
Project description:BackgroundCerebrovascular disease (CVD) may contribute to mild cognitive impairment (MCI). We sought to determine the relation of white matter hyperintensity (WMH) volume and infarcts in brain MRI to MCI in a community-based sample.MethodsA total of 679 elderly persons without dementia underwent brain MRI. WMH and infarcts were quantified using research methods. WMH was adjusted for total cranial volume. The Petersen criteria were used to define MCI. MCI was further subclassified into amnestic and non-amnestic. We used logistic regression to relate WMH and infarcts to prevalent MCI.ResultsWMH were associated with amnestic MCI (odds ratio [OR] = 1.9; 95% confidence interval [CI] 1.1, 3.4) but not non-amnestic MCI (OR = 1.2; 95% CI 0.4, 1.6) after adjusting for age, gender, ethnic group, education, and APOE-epsilon4. Infarcts were more strongly associated with non-amnestic MCI (OR = 2.7; 95% CI 1.5, 4.8) than amnestic MCI (OR = 1.4; 95% CI 0.9, 2.3). In secondary analyses using continuous cognitive scores as outcomes, WMH, but not infarcts, were related to memory, while infarcts were more strongly related with non-amnestic domains.ConclusionWhite matter hyperintensity (WMH) is more strongly related to amnestic mild cognitive impairment (MCI). Infarcts are more strongly related to non-amnestic MCI. The nature of WMH in amnestic MCI requires further study.
| S-EPMC2727144 | biostudies-literature
Project description:BackgroundMild cognitive impairment and cognitive impairment, no dementia, are emerging terms that encompass the clinical state between normal cognition and dementia in elderly people. Controversy surrounds their characterization, definition and application in clinical practice. In this article, we provide physicians with practical guidance on the definition, diagnosis and treatment of mild cognitive impairment and cognitive impairment, no dementia, based on recommendations from the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia, held in March 2006.MethodsWe developed evidence-based guidelines using systematic literature searches, with specific criteria for study selection and quality assessment, and a clear and transparent decision-making process. We selected studies published from January 1996 to December 2005 that had mild cognitive impairment or cognitive impairment, no dementia, as the outcome. Subsequent to the conference, we searched for additional articles published between January 2006 and January 2008. We graded the strength of evidence using the criteria of the Canadian Task Force on Preventive Health Care.ResultsWe identified 2483 articles, of which 314 were considered to be relevant and of good or fair quality. From a synthesis of the evidence in these studies, we made 16 recommendations. In brief, family physicians should be aware that most types of dementia are preceded by a recognizable phase of mild cognitive decline. They should be familiar with the concepts of mild cognitive impairment and of cognitive impairment, no dementia. Patients with these conditions should be closely monitored because of their increased risk for dementia. Leisure activities, cognitive stimulation and physical activity could be promoted as part of a healthy lifestyle in elderly people and those with mild cognitive impairment. Vascular risk factors should be treated optimally. No other specific therapies can yet be recommended.InterpretationPhysicians will increasingly see elderly patients with mild memory loss, and learning an approach to diagnosing states such as mild cognitive impairment is now warranted. Close monitoring for progression to dementia, promotion of a healthy lifestyle and treatment of vascular risk factors are recommended for the management of patients with mild cognitive impairment.
| S-EPMC2335177 | biostudies-literature
Project description:Approximately 20,000 people have a transient ischemic attack (TIA) and 23,375 have a minor stroke in England each year. Fatigue, psychological and cognitive impairments are well documented post-stroke. Evidence suggests that TIA and minor stroke patients also experience these impairments; however, they are not routinely offered relevant treatment. This systematic review aims to: (1) establish the prevalence of fatigue, anxiety, depression, post-traumatic stress disorder (PTSD) and cognitive impairment following TIA and minor stroke and to investigate the temporal course of these impairments; (2) explore impact on quality of life (QoL), change in emotions and return to work; (3) identify where further research is required and to potentially inform an intervention study.A systematic review of MEDLINE, EMBASE, PsycINFO, CINAHL, Cochrane libraries and grey literature between January 1993 and April 2013 will be undertaken. Two reviewers will conduct screening search results, study selection, data extraction and quality assessment. Studies of adult TIA and minor stroke participants containing any of the outcomes of interest; fatigue, anxiety, depression, PTSD or cognitive impairment will be included. Studies at any time period after TIA/minor stroke, including those with any length of follow-up, will be included to investigate the temporal course of impairments. QoL, change in emotions and return to work will also be documented. The proportion of TIA or minor stroke participants experiencing each outcome will be reported.If appropriate, a meta-analysis will pool results of individual outcomes. Studies will be grouped and analyzed according to their follow-up timeframe into short-term (< 3 months after TIA/minor stroke), medium-term (3 to 12 months) and long term (> 12 months). Sub-analysis of studies with a suitable control group will be conducted. Exploratory sub-analysis of memory and attention domains of cognitive impairment will be conducted.The current treatment goal for TIA and minor stroke patients is secondary stroke prevention. If these patients do experience fatigue, psychological or cognitive impairments then this treatment alone is unlikely to be sufficient. The results of this comprehensive review will increase understanding of treatment needs for this patient group, identify where further research is required and potentially inform an intervention trial.
| S-EPMC3846122 | biostudies-literature
Project description: Not available
| S-EPMC8142793 | biostudies-literature
Project description:Hypertension and stroke are highly prevalent risk factors for cognitive impairment and dementia. Alzheimer's disease (AD) and vascular dementia (VaD) are the most common forms of dementia, and both conditions are preceded by a stage of cognitive impairment. Stroke is a major risk factor for the development of vascular cognitive impairment (VCI) and VaD; however, stroke may also predispose to AD. Hypertension is a major risk factor for stroke, thus linking hypertension to VCI and VaD, but hypertension is also an important risk factor for AD. Reducing these two major, but modifiable, risk factors-hypertension and stroke-could be a successful strategy for reducing the public health burden of cognitive impairment and dementia. Intake of long-chain omega-3 polyunsaturated fatty acids (LC-n3-FA) and the manipulation of factors involved in the renin-angiotensin system (e.g. angiotensin II or angiotensin-converting enzyme) have been shown to reduce the risk of developing hypertension and stroke, thereby reducing dementia risk. This paper will review the research conducted on the relationship between hypertension, stroke, and dementia and also on the impact of LC-n3-FA or antihypertensive treatments on risk factors for VCI, VaD, and AD.
| S-EPMC3824191 | biostudies-other