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      Infections and Ischemic Stroke Outcome

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          Abstract

          Background. Infections increase the risk of ischemic stroke (IS) and may worsen IS prognosis. Adverse effects of in-hospital infections on stroke outcome were also reported. We aimed to study the prevalence of pre- and poststroke infections and their impact on IS outcome. Methods. We analysed clinical data of 2066 IS patients to assess the effect of pre-stroke and post-stroke infections on IS severity, as well as short-term (up to 30 days) and long-term (90 days) outcome. The independent impact of infections on poor outcome (death, death/dependency) was investigated by use of logistic regression analysis. The effect of antibiotic therapy during hospitalization on the outcome was also assessed. Results. Pre-stroke infections independently predicted worse short-term outcome. In-hospital infections were associated with worse short-term and long-term IS prognosis. Antibacterial treatment during hospitalization did not improve patients' outcome. Conclusions. Prevention of infections may improve IS prognosis. The role of antibiotic therapy after IS requires further investigations.

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          Inflammation and infections as risk factors for ischemic stroke.

          Armin J Grau, Perttu Lindsberg (2003)
          Inflammatory processes have fundamental roles in stroke in both the etiology of ischemic cerebrovascular disease and the pathophysiology of cerebral ischemia. We summarize clinical data on infection and inflammation as risk or trigger factors for human stroke and investigate current evidence for the hypothesis of a functional interrelation between traditional risk factors, genetic predisposition, and infection/inflammation in stroke pathogenesis. Several traditional vascular risk factors are associated with proinflammatory alterations, including leukocyte activation, and predispose cerebral vasculature to thrombogenesis on inflammatory stimulation. Furthermore, accumulation of inflammatory cells, mainly monocytes/macrophages, within the vascular wall starts early during atherogenesis. During later disease stages, their activation can lead to plaque rupture and thrombus formation, increasing stroke risk. Inflammatory markers (eg, leukocytes, fibrinogen, C-reactive protein) are independent predictors of ischemic stroke. Chronic infections (eg, infection with Chlamydia pneumoniae or Helicobacter pylori) were found to increase the risk of stroke; however, study results are at variance, residual confounding is not excluded, and causality is not established at present. In case-control studies, acute infection within the preceding week was a trigger factor for ischemic stroke. Acute and exacerbating chronic infection may act by activating coagulation and chronic infections and may contribute to atherogenesis. Genetic predisposition of the inflammatory host response may be an important codeterminant for atherogenesis and stroke risk. Inflammation contributes to stroke risk via various interrelated mechanisms. Infectious diseases, traditional risk factors, and genetic susceptibility may cooperate in stimulating inflammatory pathways. Final proof of a causal role of infectious/inflammatory mechanisms in stroke pathogenesis is still lacking and will require interventional studies.
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            Infarct volume is a major determiner of post-stroke immune cell function and susceptibility to infection.

            Andreas Hug, Alexander Dalpke, Nina Wieczorek … (2009)
            Acute ischemic stroke in humans is associated with profound alterations in the immune system. Hallmarks of this stroke-induced immunodepression syndrome are: lymphocytopenia, impairment of T helper cell and monocyte function. We studied which stroke-specific factors predict these immunologic alterations and subsequent infections. Leukocyte/lymphocyte subsets were assessed serially by white blood cell count and fluorescence-activated cell sorter analysis in ischemic stroke patients (n=50) at baseline, day 1, and day 4 after stroke onset and compared to an age-matched control group (n=40). Concomitantly, monocytic human leukocyte antigen-DR expression and the in vitro function of blood monocytes measured by the production of tumor necrosis factor-alpha upon stimulation with lipopolysaccharide were assessed. Associations of these immunologic parameters with stroke specific factors (National Institutes of Health Stroke Scale, infarct size) were explored. Multivariable logistic regression analysis was applied to identify early predictors for poststroke respiratory and urinary tract infections. Infarct volume was the main factor associated with lymphocytopenia on day 1 and day 4 poststroke. Particularly, blood natural killer cell counts were reduced after stroke. Monocyte counts increased after ischemia paralleled by a profound deactivation predominantly after extensive infarcts. Reduced T helper cell counts, monocytic human leukocyte antigen-DR expression, and monocytic in vitro production of tumor necrosis factor-alpha were associated with infections in univariate analyses. However, only stroke volume prevailed as independent early predictor for respiratory infections (OR 1.03; CI 1.01 to 1.04). Infarct volume determines the extent of lymphocytopenia, monocyte dysfunction, and is a main predictor for subsequent infections.
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              Dysphagia following Stroke

              Maurizio Paciaroni, Giovanni Mazzotta, Francesco Corea … (2004)
              Background: Dysphagia is common after stroke. We aimed to study the prognosis of dysphagia (assessed clinically) over the first 3 months after acute stroke and to determine whether specific neurovascular-anatomical sites were associated with swallowing dysfunction. Methods: We prospectively examined consecutive patients with acute first-ever stroke. The assessment of dysphagia was made using standardized clinical methods. The arterial territories involved were determined on CT/MRI. All patients were followed up for 3 months. Results: 34.7% of 406 patients had dysphagia. Dysphagia was more frequent in patients with hemorrhagic stroke (31/63 vs. 110/343; p = 0.01). In patients with ischemic stroke, the involvement of the arterial territory of the total middle cerebral artery was more frequently associated with dysphagia (28.2 vs. 2.2%; p < 0.0001). Multivariate analysis revealed that stroke mortality and disability were independently associated with dysphagia (p < 0.0001). Conclusions: The frequency of dysphagia was relatively high. Regarding anatomical-clinical correlation, the most important factor was the size rather than the location of the lesion. Dysphagia assessed clinically was a significant variable predicting death and disability at 90 days.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neurol Res Int
                Journal ID (publisher-id): NRI
                Title: Neurology Research International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-1852
                ISSN (Electronic): 2090-1860
                Publication date (Print): 2011
                Publication date (Electronic): 28 June 2011
                Volume: 2011
                Electronic Location Identifier: 691348
                Affiliations
                12nd Department of Neurology, Institute of Psychiatry and Neurology, 02-957 Warsaw, Poland
                2Department of Clinical and Experimental Pharmacology, Medical University of Warsaw, 00-927 Warsaw, Poland
                Author notes
                *Katarzyna Grabska: kgrabska@ 123456ipin.edu.pl

                Academic Editor: Alexander Dressel

                Article
                DOI: 10.1155/2011/691348
                PMC ID: 3135130
                PubMed ID: 21766026
                SO-VID: 0013da00-b11d-43e3-8849-1afbd485bc92
                Copyright © Copyright © 2011 Katarzyna Grabska et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 January 2011
                Date accepted : 2 May 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurology
                Data availability:
                ScienceOpen disciplines: Neurology

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