You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 56 No. 6, June 1999 TABLE OF CONTENTS
  Archives
  •  Online Features
  Neurological Review
 This Article
 •Full text
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (44)
 •Contact me when this article is cited
 Related Content
 •Related article
 •Similar articles in this journal
 Topic Collections
 •Neurology
 •Multiple Sclerosis/ Demyelinating Disease
 •Alert me on articles by topic
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Mechanisms of High-Dose Intravenous Immunoglobulins in Demyelinating Diseases

Martin Stangel, MD; Klaus V. Toyka, MD; Ralf Gold, MD

Arch Neurol. 1999;56:661-663.

Administration of high-dose intravenous immunoglobulins has become one of the most successful new treatment regimens for demyelinating diseases. In a decade of molecular medicine, it came as a surprise that a natural blood product would prove effective in several disorders, including Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and, probably, multiple sclerosis. Many experimental studies, both in vivo and in vitro, have shown that intravenous immunoglobulins can interfere with the immune system at several levels. In addition, intravenous immunoglobulins may promote remyelination in demyelinating disease associated with viral infections. At present, no single mode of action has been identified as the crucial mechanism, which leads us to suggest that multiple effects may act in concert.


From the MRC Centre for Brain Repair, Cambridge University, Cambridge, England (Dr Stangel); and the Department of Neurology and the Clinical Research Group for Multiple Sclerosis and Neuroimmunology, Julius Maximilians Universität, Würzburg, Germany (Drs Toyka and Gold).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

RELATED ARTICLE

Archives of Neurology Reader's Choice: Continuing Medical Education
Arch Neurol. 1999;56(6):762-764.
FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Potential Risk of Progressive Multifocal Leukoencephalopathy With Natalizumab Therapy: Possible Interventions
Stuve et al.
Arch Neurol 2007;64:169-176.
ABSTRACT | FULL TEXT  

Systemic lupus erythematous with recurrent Guillain -Barre-like syndrome treated with intravenous immunoglobulins
Lewis and Gibson
Lupus 2003;12:857-859.
ABSTRACT  

Effect of immunomodulatory drugs on in vitro production of brain-derived neurotrophic factor
Petereit et al.
Mult Scler 2003;9:16-20.
ABSTRACT  

Peripheral neuropathies and anti-glycolipid antibodies
Willison and Yuki
Brain 2002;125:2591-2625.
ABSTRACT | FULL TEXT  

Despair of repair
Stangel and Hartung
J. Neurol. Neurosurg. Psychiatry 2002;72:1-4.
FULL TEXT  

IV immunoglobulin does not reverse established weakness in MS: A double-blind, placebo-controlled trial
Noseworthy et al.
Neurology 2000;55:1135-1143.
ABSTRACT | FULL TEXT  

Human monoclonal antibodies reactive to oligodendrocytes promote remyelination in a model of multiple sclerosis
Warrington et al.
Proc. Natl. Acad. Sci. USA 2000;97:6820-6825.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1999 American Medical Association. All Rights Reserved.