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Multiple Sclerosis
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Article

Spontaneous intracerebral hemorrhage in a patient with multiple sclerosis and tumefactive demyelinating lesion

O Stich1, D Janowitz2, and S Rauer1*

1 Department of Neurology, Albert Ludwigs University Freiburg, Germany
2 Department of Neurology, Hannover Medical School, Germany

* To whom correspondence should be addressed.


  Abstract

In this report, we discuss the occurrence of intracerebral hemorrhage in a patient with multiple sclerosis during treatment with natalizumab, a humanized monoclonal antibody against the {alpha}4{beta}1-integrin. Hemorrhage was located in a previously tumefactive demyelinating lesion. The mechanisms of leukocyte recruitment to the sites of inflammation through interaction of leukocyte {alpha}4{beta}1-integrins and endothelial vascular cell adhesion molecule-1 are well known. However, {alpha}4{beta}1-integrins are also expressed on endothelial cells and CD34+ bone marrow–derived progenitor cells, controlling several key pathways in angiogenesis. Neovascularization may contribute to tissue repair, particularly in large inflammatory cerebral lesions with increased vascular fragility. We discuss possible interaction of natalizumab with angiogenesis during tissue repair.

Key Words: {alpha}4{beta}1-integrin, intracerebral hemorrhage, multiple sclerosis, natalizumab

First published on March 12, 2009, doi:10.1177/1352458508101323

Multiple Sclerosis 2009;15:517.

A more recent version of this article appeared on April 1, 2009

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