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Neurology 2000;54:1155-1160
© 2000 American Academy of Neurology


Articles

A Wallerian degeneration pattern in patients at risk for MS

J. H. Simon, MD, PhD, R. P. Kinkel, MD, L. Jacobs, MD, L. Bub, MD and N. Simonian, MD

From the Neuroradiology/MRI Department (Drs. Simon and Bub), University of Colorado Health Sciences Center, Denver; Mellen Center for MS Treatment and Research (Dr. Kinkel), Cleveland Clinic Foundation, Cleveland, OH; Department of Neurology (Dr. Jacobs), SUNY Buffalo, Buffalo General Hospital, NY; and Biogen Inc. (Dr. Simonian), Cambridge, MA.

Address correspondence and reprint requests to Dr. Jack H. Simon, University of Colorado Health Sciences Center, 4200 E Ninth Avenue Box A034, Neuroradiology/MRI, Denver, CO 80262; e-mail: jack.simon{at}uchsc.edu

BACKGROUND: Demyelination alone may not explain the progressive disability that frequently develops in MS. An alternative explanation for irreversible disability assumes a contribution from axonal injury or loss. In theory, axonal injury may occur in the focal areas characterized by early inflammation, or can be more distant, as in Wallerian degeneration. However, Wallerian degeneration is thought of as a rare or a late finding in MS.

METHODS: Studies showing a classic Wallerian degeneration pattern in the corticospinal tract were selected from a review of MR studies from patients enrolled in a longitudinal treatment trial. Entry was based on first occurrence of an isolated neurologic syndrome consistent with MS and a positive MRI.

RESULTS: This report is based on five cases followed longitudinally who showed development of a classic T2-hyperintense lesion along the ipsilateral corticospinal tract, subsequent to an initial inciting event located in the white matter located in the superior aspect of the corona radiata. Lesions were evident as T2-hyperintensity persisting throughout the 12 to 18 months of observation.

CONCLUSIONS: This series suggests that Wallerian degeneration, implying axonal injury, may occur as a sequela of acute demyelinating lesions in patients presenting with their first symptoms suggestive of MS. This can produce a component of the increasing burden of T2-hyperintense lesions temporally and spatially dissociated from inflammatory or demyelinating activity. Further studies are required to determine if Wallerian degeneration is an important factor contributing to disability progression in MS.

Key words: Wallerian degeneration—MS.




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