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      Etiologic and Clinical Characterization of Patients with Recurrent Spontaneous Intracerebral Hemorrhage

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          Abstract

          Background: The impact of recurrent stroke has been extensively addressed with regard to ischemic stroke, revealing potentially different etiologies of recurrent events in the individual patient. In contrast, data on recurrent intracerebral hemorrhage (ICH) are scarce, especially considering etiologic characterization. We aimed to determine the etiology of recurrent ICH at each event to identify potential etiologic changes. Patients and Methods: We analyzed the data of patients admitted to our stroke unit with recurrent ICH between 1998 and 2014 with regard to clinical characteristics and etiology. Results: Thirty-three patients (2.6%) with recurrent ICH were identified. Mean age (mean ± SD) at the initial event was 69 ± 9 and 72 ± 9 years at recurrence. Median interval between events was 18 months. Mean National Institutes of Health Stroke Scale (first/second event) was 4/9 at admission and 2/8 at discharge. Over 30% of patients developed symptomatic epilepsy. Etiologic distribution was (first/second event) the following: probable cerebral amyloid angiopathy (CAA) (12/20), possible CAA (3/0), hypertensive (5/4), anticoagulation (4/3), vascular malformation (2/4), ischemia with secondary hemorrhage (4/0), vasculitis (0/1), undetermined (4/0). Conclusions: Recurrent ICH is rare, CAA being its most common etiology. Etiology of ICH may differ between the first/second event in about 10%. The findings indicate the need of a complete and distinct work-up including MRI in every instance of ICH recurrence.

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          Most cited references14

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          The ABCs of measuring intracerebral hemorrhage volumes.

          Hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). We compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis. The formula ABC/2 was used, where A is the greatest hemorrhage diameter by CT, B is the diameter 90 degrees to A, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness. The ICH volumes for 118 patients were evaluated in a mean of 38 seconds and correlated with planimetric measurements (R2 = 9.6). Interrater and intrarater reliability were excellent, with an intraclass correlation of .99 for both. We conclude that ICH volume can be accurately estimated in less than 1 minute with the simple formula ABC/2.
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            Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study.

            To identify those factors associated with cerebral hemorrhage among brains with cerebral amyloid angiopathy (CAA), we undertook a comparative postmortem histopathological study of amyloid-containing vessels in the brains of patients with and without hemorrhage. Those without hemorrhage were represented by the following two groups: (1) elderly patients from a large general hospital (n = 66; age range, 75-107 years) and (2) patients with various neuropsychiatric disorders (n = 70; age range, 27-96 years). CAA was found in 45% of the first group and in 54% of the second group. The findings in these patients were compared with those in 17 brains in which both CAA and cerebral hemorrhage were present. We found that CAA was more severe in the brains with cerebral hemorrhage than in those without, and that fibrinoid necrosis was seen only in the brains with cerebral hemorrhage (12 of the 17 brains). Microaneurysms occurred only in the presence of severe, rather than moderate or mild, CAA. Serial sections in 2 brains of patients with cerebral hemorrhage showed fibrinoid necrosis, microaneurysms, and vascular rupture in close association with the hemorrhage. In 2 patients, hemorrhage was precipitated by trauma, and in 1, it was secondary to metastatic carcinoma. The features of brains from patients with CAA that are most consistently related to cerebral hemorrhage are (1) a severe degree of CAA and (2) the presence of fibrinoid necrosis, with or without microaneurysms.
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              Cause of stroke recurrence is multifactorial: patterns, risk factors, and outcomes of stroke recurrence in the South London Stroke Register.

              This article examines stroke recurrence and whether the subtype of the initial stroke influences the risk and subtypes of further strokes. The proportion of recurrences attributable to conventional risk factors is quantified. From January 1995 to August 2000, all first-in-a-lifetime strokes (n=1626) were identified and prospectively followed up in a defined multiethnic inner city population of 234 533. Twelve overlapping referral sources and face-to-face follow-up at 3 months and 1 and 3 years were used to attain complete registration of stroke recurrence. Index and recurrent stroke were classified according to the Oxford Community Stroke Project classification. In 2744 person-years of follow-up, 153 recurrences were observed. At 5 years, the cumulative risk of first stroke recurrence was 16.6% (95% CI, 13.5 to 20.4), and the combined risk of death or stroke recurrence was 65.3% (95% CI, 61.9 to 68.6). Ethnicity and subtype of index stroke were not associated with stroke recurrence. A change in subtype between index and recurrent stroke occurred in 45.5% (95% CI, 35.8 to 55.2) of cases and was most frequent among index lacunar strokes and primary intracerebral hemorrhages. In multivariable analyses, diabetes mellitus and atrial fibrillation were associated with both stroke recurrence and recurrence-free survival. In the stroke population, 9.1% (95% CI, -2.0 to 20.2) of recurrences were attributable to diabetes and 4.9% (95% CI, -7.3 to 17.2) to atrial fibrillation during the first year after the index stroke. The cause of stroke recurrence is multifactorial, and the subtypes of index and recurrent strokes are often not identical. Most recurrences remain unexplained by conventional risk factors.
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                Author and article information

                Journal
                ENE
                Eur Neurol
                10.1159/issn.0014-3022
                European Neurology
                Eur Neurol
                S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                0014-3022
                1421-9913
                November 2016
                03 November 2016
                : 76
                : 5-6
                : 295-301
                Affiliations
                Department of Neurology, Universitätsmedizin Mannheim, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
                Author notes
                *Marc E. Wolf, Department of Neurology, Universitätsmedizin Mannheim, Theodor-Kutzer-Ufer 1-3, DE-68167 Mannheim (Germany), E-Mail wolf@neuro.ma.uni-heidelberg.de
                Article
                452659 Eur Neurol 2016;76:295-301
                10.1159/000452659
                27806359
                5c42266c-6e3c-4816-8b68-1a9e5c900786
                © 2016 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 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.

                History
                : 08 September 2016
                : 14 October 2016
                Page count
                Figures: 2, Tables: 2, References: 19, Pages: 7
                Categories
                Original Paper

                Medicine,General social science
                Cerebral amyloid angiopathy,Intracerebral hemorrhage,Recurrence,Etiology

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