Diagnostic and Classification Criteria for the Guillain-Barré Syndrome

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Abstract

Background: Diagnostic criteria for the Guillain-Barré syndrome (GBS) have been available since 1978. Since then, several variants have been described. More recently, a distinction has been made between pure motor forms, severe sensory forms, primary axonal and primary demyelinating varieties. Associations of clinical characteristics, and specific infections and the presence of antiganglioside antibodies have been found. For further studies on GBS, it is therefore necessary to reconsider the available diagnostic criteria and add additional criteria for subclassification. Methods: A panel of (20) experts was formed. The literature representing the recent developments in GBS subclassification was reviewed. Following a consensus protocol, diagnostic and classification criteria were formulated. Results: The diagnosis of GBS can usually be made on clinical characteristics. A schedule for subclassification has been made to cover also the clinical variants in a systematic manner.

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Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barré syndrome.

G Wang, I Nachamkin, Peter Ho … (1999)

Immunopathological studies suggest that the target of immune attack is different in the subtypes of Guillain-Barré syndrome (GBS). In acute motor axonal neuropathy (AMAN), the attack appears directed against the axolemma and nodes of Ranvier. In acute inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed against a component of the Schwann cell. However, the nature of the antigenic targets is still not clear. We prospectively studied 138 Chinese GBS patients and found that IgG anti-GD1a antibodies were closely associated with AMAN but not AIDP. With a cutoff titer of greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti-GD1a antibodies; with a cutoff titer of greater than 1:1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti-GD1a antibodies. In contrast, low levels of IgG anti-GM1 antibodies (> 1:100) were detected in both the AMAN and the AIDP forms (57% vs 35%, NS). High titers of IgG anti-GM1 (>1:1,000) were more common in the AMAN form (24% vs 8%, NS). Serological evidence of recent Campylobacter infection was detected in 81% of AMAN and 50% of AIDP patients, and anti-ganglioside antibodies were common in both Campylobacter-infected and noninfected patients. Our results suggest that IgG anti-GD1a antibodies may be involved in the pathogenesis of AMAN.

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Severe axonal degeneration in acute Guillain-Barré syndrome: evidence of two different mechanisms?

T.E. Feasby, A.F. Hahn, W.F. Brown … (1993)

Four cases of severe acute Guillain-Barré syndrome (GBS) characterized by severe axonal degeneration are presented. All had electrically inexcitable motor nerves as early as 4 days after onset. The disease was rapid in onset and the residual disability was severe. Two different types of pathology were seen. Nerve biopsies in 3 cases showed severe axonal degeneration without inflammation or demyelination. Autopsy in one of these cases showed that the dorsal and ventral roots were also significantly affected. These cases illustrate the primary axonal form of GBS. Nerve biopsy in the fourth case at day 15 showed marked inflammation and demyelination with axonal degeneration. Contralateral nerve biopsy at day 75 showed almost complete loss of axons. This case illustrates another type of axonal degeneration, that which occurs secondary to inflammation and demyelination.

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Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China

G.M. McKhann, D.R. Cornblath, Giang T. T. Ho … (1991)

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Journal

Journal ID (publisher-id): ENE

Journal ID (nlm-ta): Eur Neurol

Journal ID (doi): 10.1159/issn.0014-3022

Title: European Neurology

Publisher: S. Karger AG

ISSN (Print): 0014-3022

ISSN (Electronic): 1421-9913

Publication date Subscription-year: 2001

Publication date (Print): April 2001

Publication date (Electronic): 11 April 2001

Volume: 45

Issue: 3

Pages: 133-139

Affiliations

^aUniversity Hospital and Erasmus University Rotterdam, ^bDutch Neuromuscular Research Support Centre, Baarn, The Netherlands

Article

Publisher ID: 52111 Other ID: Eur Neurol 2001;45:133–139

DOI: 10.1159/000052111

PubMed ID: 11306855

SO-VID: 49512f94-bc31-48ac-9b24-e02bd9abeb37

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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.

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Diagnostic and Classification Criteria for the Guillain-Barré Syndrome

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Abstract

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Karger: Neurology and Neuroscience

Most cited references 4

Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barré syndrome.

Severe axonal degeneration in acute Guillain-Barré syndrome: evidence of two different mechanisms?

Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China

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