This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Neurology 1997;48(Suppl 5):S64-S69
Myasthenia gravis (MG) is the prototypic autoimmune disease for a number of reasons. (a) The antigen, the acetylcholine receptor (AChR), is known. (b) Antibodies against the AChRs can be detected and measured in patients' serum. (c) The patients' IgG binds to the AChRs at the postsynaptic region and, by fixing complement or crosslinking, results in internalization or degradation of the AChRs and simplification of the postsynaptic junctional folds. (d) The IgG antibodies are pathogenic because they transmit the disease to experimental animals and cause destruction of the AChRs in cultured myotubes. (e) Immunization of healthy animals with AChRs leads to MG that can be subsequently passed to other animals with purified IgG. (f) Removal of the pathogenic autoantibodies results in clinical improvement. [1-4]
Although MG is no longer "gravis" because it responds fairly well to the available therapies, we still do not have a cure for the disease. Treatment begins with anticholinesterases, which are helpful early in the disease, followed by thymectomy, performed in patients above puberty and below the age of 60 years. Therapy continues as needed and for long periods with the administration of steroids or various immunosuppressive therapies including azathioprine, cyclosporine and, periodically, plasmapheresis. [1-4] Given the chronicity of the disease, the long-term use of these therapeutic modalities needs to be curtailed because of their cumulative adverse side effects. The need for another effective immunomodulating therapy without long-term side effects has prompted experimentation with high-dose IVIg, an immunomodulating drug that is expensive but relatively safe compared to the other therapies. Considering the multiple mechanisms of action of IVIg in modifying the immune response, as discussed later, this drug may be a promising modality in the treatment of certain patients with MG at a given state of their illness.
I review here the present knowledge …
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
