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Multiple Sclerosis
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case-report

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

O Stich

Department of Neurology, Albert Ludwigs University Freiburg, Germany

D Janowitz

Department of Neurology, Hannover Medical School, Germany

S Rauer

Department of Neurology, Albert Ludwigs University Freiburg, Germany sebastian.rauer{at}uniklinik-freiburg.de

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}4β1-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}4β1-integrins and endothelial vascular cell adhesion molecule-1 are well known. However, {alpha}4β1-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}4β1-integrin • intracerebral hemorrhage • multiple sclerosis • natalizumab

This version was published on April 1, 2009

Multiple Sclerosis, Vol. 15, No. 4, 517-519 (2009)
DOI: 10.1177/1352458508101323
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