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
 
Original Article
Brief Report
PreviousPrevious
Volume 342:21-27 January 6, 2000 Number 1
NextNext

Paraneoplastic Cerebellar Ataxia Due to Autoantibodies against a Glutamate Receptor
Peter Sillevis Smitt, M.D., Ph.D., Ayae Kinoshita, M.D., Ph.D., Bertie De Leeuw, Ph.D., Wiebe Moll, M.D., Ph.D., Michiel Coesmans, M.Sc., Dick Jaarsma, Ph.D., Sonja Henzen-Logmans, M.D., Ph.D., Charles Vecht, M.D., Ph.D., Chris De Zeeuw, Ph.D., Naohiro Sekiyama, Ph.D., Shigetada Nakanishi, M.D., Ph.D., and Ryuichi Shigemoto, M.D., Ph.D.

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
- PDF

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

More Information
-PubMed Citation
There are many types of cerebellar ataxia, including ataxia due to congenital or metabolic disorders and a paraneoplastic form in patients with gynecologic cancer, breast cancer, lung cancer, or Hodgkin's disease.1 This paraneoplastic syndrome is the only type of cerebellar ataxia associated with autoantibodies against neuronal antigens. Often, the neuronal antigens are aberrantly expressed by the tumor cells.2,3,4 The antineuronal autoantibodies are believed to cause cerebellar ataxia, but this is unproved.5,6 In Hodgkin's disease, the lymphoma precedes the ataxia by months to years in 80 percent of patients, and ataxia often occurs during a prolonged complete remission.4 Among patients with . . . [Full Text of this Article]

Case Reports

Patient 1

Patient 2

Methods

Samples

Immunohistochemical Analysis

Cell Labeling and Assay for Inositol Phosphates

Absorption Experiments

Transfer Experiments

Expression of mGluR1 in Tumor Samples

Results

Discussion


Source Information

From the Departments of Neuro-Oncology (P.S.S., B.D.L., W.M., M.C., C.V.) and Pathology (S.H.-L.), Daniel den Hoed Cancer Center, University Hospital Rotterdam, the Netherlands; the Departments of Immunology (B.D.L.) and Anatomy (M.C., D.J., C.D.Z.), Erasmus University Rotterdam, the Netherlands; the Departments of Morphologic Brain Science (A.K., R.S.) and Biologic Sciences (N.S., S.N.), Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan; and the Laboratory of Cerebral Structure, National Institute for Physiologic Sciences, Myodaiji, Okazaki, Japan (A.K., R.S.). Drs. Sillevis Smitt and Kinoshita contributed equally to the article.

Address reprint requests to Dr. Sillevis Smitt at the Department of Neuro-Oncology, Daniel den Hoed Cancer Center, P.O. Box 5201, 3008 AE Rotterdam, the Netherlands, or at sillevis@neuh.azr.nl.

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.