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      Influenza‐like illness as a trigger for ischemic stroke

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          Abstract

          Objective

          We hypothesized that ILI is associated with risk of incident stroke, and that the risk would be highest closest in time to the event.

          Methods

          This case‐crossover analysis utilized data obtained from the California State Inpatient Database of the Healthcare Cost and Utilization Project ( HCUP). The outcome of interest was ischemic stroke. Exposure was defined as a visit to the emergency department or hospitalization for influenza‐like illness ( ILI) 365, 180, 90, 30, or 15 days before stroke (risk period) or similar time intervals exactly 1 or 2 years before stroke (control period). Conditional logistic regression was used to calculate the odds ratio and 95% confidence interval ( OR, 95% CI).

          Results

          In 2009, 36,975 hospitalized ischemic strokes met inclusion criteria, and of these strokes, 554 (1.5%) had at least 1 episode of ILI in the 365‐day risk period prior to their stroke. Using non‐overlapping time intervals from ILI to stroke, the odds of ischemic stroke was greatest in the first 15 days post ILI ( OR: 2.88, 95% CI: 1.86–4.47). The strength of the relationship decreased as the time from ILI increased, and was no longer significant after 60 days. There was a significant interaction ( P = 0.017) with age and ILI; the odds of stroke associated increased 7% with each 10‐year decrease in age ( OR per 10‐year age decrease 1.07, 95% CI: 1.03–1.35).

          Interpretation

          We found that ILI increases short‐term risk of stroke, particularly in people under the age of 45, and therefore may be considered to act as a trigger for stroke.

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          Most cited references16

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          Analysis of 1008 consecutive patients aged 15 to 49 with first-ever ischemic stroke: the Helsinki young stroke registry.

          To analyze trends in occurrence, risk factors, etiology, and neuroimaging features of ischemic stroke in young adults in a large cohort. We evaluated all 1008 consecutive ischemic stroke patients aged 15 to 49 admitted to Helsinki University Central Hospital, 1994 to 2007. Etiology was classified by Trial of Org 10172 in Acute Stroke Treatment criteria. Comparisons were done between groups stratified by gender and age. Estimated annual occurrence was 10.8/100,000 (range 8.4 to 13.0), increasing exponentially with aging. Of our 628 male and 380 female (ratio 1.7:1) patients, females were preponderant among those 44 clearly had more risk factors. Cardioembolism (20%) and cervicocerebral artery dissection (15%) were the most frequent etiologic subgroups. Proportions of large-artery atherosclerosis (8%) and small-vessel disease (14%) began to enlarge at age 35, whereas frequency of undetermined etiology (33%) decreased along aging. Posterior circulation infarcts were more common among patients <45 years of age. Left hemisphere infarcts were more frequent in general. There were 235 (23%) patients with multiple and 126 (13%) with silent infarcts, and 55 (5%) patients had leukoaraiosis. The frequency of ischemic stroke increases sharply at age 40. Etiology and risk factors start resembling those seen in the elderly in early midlife but causes defined in younger patients still are frequent in those aged 45 to 49. Subclinical infarcts were surprisingly common in the young.
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            Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment.

            Vasculopathies caused by varicella zoster virus (VZV) are indicative of a productive virus infection in cerebral arteries after either reactivation of VZV (shingles) or primary infection (chickenpox). VZV vasculopathy can cause ischaemic infarction of the brain and spinal cord, as well as aneurysm, subarachnoid and cerebral haemorrhage, carotid dissection, and, rarely, peripheral arterial disease. VZV vasculopathy in immunocompetent or immunocompromised individuals can be unifocal or multifocal with deep-seated and superficial infarctions. Lesions at the grey-white matter junction on brain imaging are a clue to diagnosis. Involvement of both large and small arteries is more common than that of either alone. Most patients have a mononuclear cerebrospinal fluid pleocytosis, often with red blood cells. Cerebrospinal fluid pleocytosis and rash are absent in about a third of cases. Anti-VZV IgG antibody in the cerebrospinal fluid is found more frequently than VZV DNA. In recent years, the number of recognised VZV vasculopathies has grown, and accurate diagnosis is important for the effective treatment of these disorders.
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              Long-term outcomes following development of new-onset atrial fibrillation during sepsis.

              New-onset atrial fibrillation (AF) is associated with adverse outcomes during a sepsis hospitalization; however, long-term outcomes following hospitalization with sepsis-associated new-onset AF are unclear.
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                Author and article information

                Contributors
                akb2188@cumc.columbia.edu
                Journal
                Ann Clin Transl Neurol
                Ann Clin Transl Neurol
                10.1002/(ISSN)2328-9503
                ACN3
                Annals of Clinical and Translational Neurology
                John Wiley and Sons Inc. (Hoboken )
                2328-9503
                14 March 2018
                April 2018
                : 5
                : 4 ( doiID: 10.1002/acn3.2018.5.issue-4 )
                : 456-463
                Affiliations
                [ 1 ] Department of Neurology College of Physicians and Surgeons Columbia University New York New York 10032
                [ 2 ] Department of Epidemiology Mailman School of Public Health Columbia University New York New York 10032
                [ 3 ] Department of Neurology Weill Cornell Medicine Cornell University New York New York 10065
                Author notes
                [*] [* ] Correspondence

                Amelia K. Boehme, Gertrude Sergievsky Center, Department of Neurology and Epidemiology, Columbia University, 710 W 168th Street, Room 612, New York, NY 10032. Tel: 212 305 0395; Fax: 212‐305‐1658; E‐mail: akb2188@ 123456cumc.columbia.edu

                Article
                ACN3545
                10.1002/acn3.545
                5899905
                29687022
                6c5d59e6-e39d-4c9e-bea9-5a83c7724663
                © 2018 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 27 December 2017
                : 17 January 2018
                : 31 January 2018
                Page count
                Figures: 2, Tables: 4, Pages: 8, Words: 5582
                Funding
                Funded by: National Institute of Neurological Disorders and Stroke
                Award ID: L30 NS093600
                Award ID: T32 NS007153‐31
                Funded by: National Institute of Minority Health and Health Disparities
                Award ID: R21 MD012451
                This work was funded by National Institute of Neurological Disorders and Stroke grants L30 NS093600 and T32 NS007153‐31; National Institute of Minority Health and Health Disparities grant R21 MD012451.
                Categories
                Research Article
                Research Articles
                Custom metadata
                2.0
                acn3545
                April 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.4 mode:remove_FC converted:15.04.2018

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