Brain Advance Access published online on October 17, 2005
Brain, doi:10.1093/brain/awh641
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1 Center for Brain Research, Medical University of Vienna, Vienna, Austria
* To whom correspondence should be addressed. Focal demyelinated plaques in white matter, which are the hallmark of multiple sclerosis pathology, only partially explain the patient's clinical deficits. We thus analysed global brain pathology in multiple sclerosis, focusing on the normal-appearing white matter (NAWM) and the cortex. Autopsy tissue from 52 multiple sclerosis patients (acute, relapsing-remitting, primary and secondary progressive multiple sclerosis) and from 30 controls was analysed using quantitative morphological techniques. New and active focal inflammatory demyelinating lesions in the white matter were mainly present in patients with acute and relapsing multiple sclerosis, while diffuse injury of the NAWM and cortical demyelination were characteristic hallmarks of primary and secondary progressive multiple sclerosis. Cortical demyelination and injury of the NAWM, reflected by diffuse axonal injury with profound microglia activation, occurred on the background of a global inflammatory response in the whole brain and meninges. There was only a marginal correlation between focal lesion load in the white matter and diffuse white matter injury, or cortical pathology, respectively. Our data suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter. With chronicity, diffuse inflammation accumulates throughout the whole brain, and is associated with slowly progressive axonal injury in the NAWM and cortical demyelination.
Received June 15, 2005
Revised August 22, 2005
Accepted August 30, 2005
Article
Cortical demyelination and diffuse white matter injury in multiple sclerosis
2 Department of Neurology, Mayo Clinic, Rochester, MN, USA
3 Department of Neuropathology, University of Göttingen, Germany
4 Department of Neuropathology, University of Göttingen, Germany; Institute for Multiple Sclerosis Research, University of Göttingen and Gemeinnützige Hertie-Stiftung, Germany
5 Department of Neurology, Municipial Hospital Lainz, Vienna, Austria
6 Department of Neuropathology, Zentralkrankenhaus Bremen-Ost, Germany
7 Department of Pathology, Mayo Clinic, Rochester, MN, USA
Hans Lassmann, E-mail: hans.lassmann{at}meduniwien.ac.at
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R. Gold, C. Linington, and H. Lassmann Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research Brain, August 1, 2006; 129(8): 1953 - 1971. [Abstract] [Full Text] [PDF]
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D. Merkler, T. Ernsting, M. Kerschensteiner, W. Bruck, and C. Stadelmann A new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelination Brain, August 1, 2006; 129(8): 1972 - 1983. [Abstract] [Full Text] [PDF]
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G. C. DeLuca, K. Williams, N. Evangelou, G. C. Ebers, and M. M. Esiri The contribution of demyelination to axonal loss in multiple sclerosis Brain, June 1, 2006; 129(6): 1507 - 1516. [Abstract] [Full Text] [PDF]
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A. Compston Making progress on the natural history of multiple sclerosis. Brain, March 1, 2006; 129(Pt 3): 561 - 563. [Full Text] [PDF]
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J. Imitola, T. Chitnis, and S. J. Khoury Insights Into the Molecular Pathogenesis of Progression in Multiple Sclerosis: Potential Implications for Future Therapies Arch Neurol, January 1, 2006; 63(1): 25 - 33. [Abstract] [Full Text] [PDF]
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