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Axonal Damage in Multiple Sclerosis Patients with High versus Low Expanded Disability Status Scale Score

Published online by Cambridge University Press:  16 February 2016

Steven D. Brass ,
Sridar Narayanan ,
Jack P. Antel ,
Yves Lapierre ,
Louis Collins  and
Douglas L. Arnold
Steven D. Brass
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
Sridar Narayanan
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
Jack P. Antel
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
Yves Lapierre
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
Louis Collins
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
Douglas L. Arnold*
Affiliation:
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, Montreal, Quebec, Canada
*
Montreal Neurological Hospital, Department of Neurology and Neurosurgery, 3801 University Street, Montreal, Quebec H3A2B4, Canada
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Abstract

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Background:

The pathophysiological basis for differences in disability in patients with multiple sclerosis is unclear.

Methods:

We used magnetic resonance imaging to examine whether differences in disability in cohorts of multiple sclerosis patients with similar T2-weighted lesion volume and disease duration were associated with a more destructive disease process in the more disabled patients.

Results:

The benign and severely disabled groups had similar brain atrophy metrics and similar decreases of the neuronal marker, N-acetylaspartate, in the normal appearing white matter of the cerebrum on magnetic resonance spectroscopy examination in vivo. The severely disabled cohort had more spinal cord atrophy.

Conclusion:

The dissociation of spinal cord atrophy and cerebral atrophy between these two groups suggests that the difference between the more benign and more disabled groups cannot be explained by a more aggressive pathological process that is affecting the entire neuroaxis in a homogeneous fashion.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 31 , Issue 2 , May 2004 , pp. 225 - 228
Copyright
Copyright © The Canadian Journal of Neurological 2004

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