The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Review Article
Medical Progress
PreviousPrevious
Volume 330:1797-1810 June 23, 1994 Number 25
NextNext

Myasthenia Gravis
Daniel B. Drachman

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

 Sign up for free e-toc
 

This Article
-Full Text
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
Twenty years ago, the discovery of a deficit of acetylcholine receptors at the neuromuscular junctions of patients with myasthenia gravis1 and the development of an animal model of the disease2 shed new light on a disorder that was first described clinically 300 years earlier by the great physiologist Thomas Willis3. During the past two decades, remarkable progress has been made in our understanding of myasthenia gravis, and the new knowledge has been applied directly to the clinical diagnosis and treatment of this formerly grave disease. Myasthenia gravis is undoubtedly the most thoroughly understood of all human autoimmune diseases and . . . [Full Text of this Article]

Clinical Features

The Neuromuscular Junction in Myasthenia Gravis

The Acetylcholine Receptor

Immunopathogenesis of Myasthenia Gravis

Antibody-Mediated Mechanisms

Accelerated Degradation of Acetylcholine Receptors

Blockade of Acetylcholine Receptors

Damage to Neuromuscular Junctions

Functional Properties of Anti-Acetylcholine-Receptor Antibodies and the Severity of Disease

Properties of Acetylcholine-Receptor Antibodies

"Antibody-Negative" Myasthenia Gravis

Role of Lymphocytes in Myasthenia Gravis

Origin of the Autoimmune Response in Myasthenia Gravis

Diagnosis

Diagnostic Testing

Differential Diagnosis

Search for Associated Conditions

Treatment

Anticholinesterase Agents

Thymectomy

Immunosuppressive Treatment

            Corticosteroids

            Azathioprine

            Cyclosporine

Short-Term Immunotherapies: Plasma Exchange and Intravenous Immune Globulin

Specific Immunotherapy: The Future of Treatment

B-Cell-Directed Approaches

T-Cell-Directed Approaches

Conclusions


Source Information

From the Department of Neurology, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Baltimore, MD 21287-7519, where reprint requests should be addressed to Dr. Drachman.

References


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.