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Cognitive Impairment in Transient Ischemic Attack Patients: A Systematic Review

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      Abstract

      Background: Although by definition a transient ischemic attack (TIA) lasts less than 24 h, many patients experience cognitive complaints beyond focal symptom resolution. However, their prevalence, causes and profile are unclear. We therefore performed a systematic review on cognitive impairment after TIA. Summary: Medline and Embase were searched for relevant studies. Risk of bias was assessed, and data synthesis was performed according to the severity of cognitive impairment. Thirteen studies were included, with considerable heterogeneity concerning methods and timing of cognitive testing. Confounding, detection bias and attrition were the main causes of a high risk of bias in several studies. The prevalence of post-TIA mild cognitive impairment ranged from 29 to 68%. Severe cognitive impairment was found in 8-22% of patients. Studies using a cognitive screening instrument and those performed shortly after TIA or several years later, reported the highest frequencies of impairment. Patients evaluated with a screening tool were substantially older than those who underwent a full neuropsychological assessment (weighted mean age difference 10.9 years). Based on limited data, the post-TIA cognitive profile showed prominent executive function deficits. Insufficient data refrained us from drawing conclusions on causality. The few studies that reported neuroimaging results found a minor correlation with cognitive impairment. Key Messages: Mild cognitive impairment is present in more than a third of the TIA patients and has a profile comparable with vascular cognitive impairment. Reported rates of post-TIA cognitive impairment are highly variable and higher frequencies are found with cognitive screening tools. Considerable heterogeneity and insufficient data limit further conclusions about potential causative factors.

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      Most cited references 42

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      National Institute of Neurological Disorders and Stroke-Canadian Stroke Network vascular cognitive impairment harmonization standards.

      One in 3 individuals will experience a stroke, dementia or both. Moreover, twice as many individuals will have cognitive impairment short of dementia as either stroke or dementia. The commonly used stroke scales do not measure cognition, while dementia criteria focus on the late stages of cognitive impairment, and are heavily biased toward the diagnosis of Alzheimer disease. No commonly agreed standards exist for identifying and describing individuals with cognitive impairment, particularly in the early stages, and especially with cognitive impairment related to vascular factors, or vascular cognitive impairment. The National Institute for Neurological Disorders and Stroke (NINDS) and the Canadian Stroke Network (CSN) convened researchers in clinical diagnosis, epidemiology, neuropsychology, brain imaging, neuropathology, experimental models, biomarkers, genetics, and clinical trials to recommend minimum, common, clinical and research standards for the description and study of vascular cognitive impairment. The results of these discussions are reported herein. The development of common standards represents a first step in a process of use, validation and refinement. Using the same standards will help identify individuals in the early stages of cognitive impairment, will make studies comparable, and by integrating knowledge, will accelerate the pace of progress.
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        Silent brain infarcts and the risk of dementia and cognitive decline.

        Silent brain infarcts are frequently seen on magnetic resonance imaging (MRI) in healthy elderly people and may be associated with dementia and cognitive decline. We studied the association between silent brain infarcts and the risk of dementia and cognitive decline in 1015 participants of the prospective, population-based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia and stroke at base line. Participants underwent neuropsychological testing and cerebral MRI at base line in 1995 to 1996 and again in 1999 to 2000 and were monitored for dementia throughout the study period. We performed Cox proportional-hazards and multiple linear-regression analyses, adjusted for age, sex, and level of education and for the presence or absence of subcortical atrophy and white-matter lesions. During 3697 person-years of follow-up (mean per person, 3.6 years), dementia developed in 30 of the 1015 participants. The presence of silent brain infarcts at base line more than doubled the risk of dementia (hazard ratio, 2.26; 95 percent confidence interval, 1.09 to 4.70). The presence of silent brain infarcts on the base-line MRI was associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function. Silent thalamic infarcts were associated with a decline in memory performance, and nonthalamic infarcts with a decline in psychomotor speed. When participants with silent brain infarcts at base line were subdivided into those with and those without additional infarcts at follow-up, the decline in cognitive function was restricted to those with additional silent infarcts. Elderly people with silent brain infarcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions. Copyright 2003 Massachusetts Medical Society
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          Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis.

          Reliable data on the prevalence and predictors of post-stroke dementia are needed to inform patients and carers, plan services and clinical trials, ascertain the overall burden of stroke, and understand its causes. However, published data on the prevalence and risk factors for pre-stroke and post-stroke dementia are conflicting. We undertook this systematic review to assess the heterogeneity in the reported rates and to identify risk factors for pre-stroke and post-stroke dementia. Studies published between 1950 and May 1, 2009, were identified from bibliographic databases, reference lists, and journal contents pages. Studies were included if they were on patients with symptomatic stroke, were published in English, reported on a series of consecutive eligible patients or volunteers in prospective cohort studies, included all stroke or all ischaemic stroke, measured dementia by standard criteria, and followed up patients for at least 3 months after stroke. Pooled rates of dementia were stratified by study setting, inclusion or exclusion of pre-stroke dementia, and by first, any, or recurrent stroke. Pooled odds ratios were calculated for factors associated with pre-stroke and post-stroke dementia. We identified 22 hospital-based and eight population-based eligible cohorts (7511 patients) described in 73 papers. The pooled prevalence of pre-stroke dementia was higher (14.4%, 95% CI 12.0-16.8) in hospital-based studies than in population-based studies (9.1%, 6.9-11.3). Although post-stroke (
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            Author and article information

            Affiliations
            Departments of aNeurology and bMedical Psychology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience, Nijmegen, The Netherlands
            Journal
            CED
            Cerebrovasc Dis
            10.1159/issn.1015-9770
            Cerebrovascular Diseases
            Cerebrovasc Dis
            S. Karger AG (Basel, Switzerland karger@123456karger.com http://www.karger.com )
            1015-9770
            1421-9786
            June 2016
            18 February 2016
            : 42
            : 1-2
            : 1-9
            © 2016 The Author(s) Published by S. Karger AG, Basel

            This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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            Figures: 1, Tables: 1, References: 49, Pages: 9
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