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Multiple Sclerosis: Assessment of Disease Progression and Effects of Treatment

Published online by Cambridge University Press:  05 January 2016

D.W. Paty*
Affiliation:
Department of Medicine, Division of Neurology, University of British Columbia
*
Head, UBC Division of Neurology, Vancouver General Hospital, 222 - 2775 Heather Street, Vancouver, B.C., Canada V5Z 3J5
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Abstract:

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MS could well be a two stage disease. The first stage involves the sequential development of multiple small lesions, mostly inflammatory, that accumulate at a given rate. The second stage could be that of consolidation and confluence of lesions that involves not only demyelination but gliosis. MRI now gives us an opportunity to watch the evolution of these processes and also to monitor treatment effects. It is only after the evolution of this process is understood that we can design rational therapies directed toward the prevention of spasticity in MS.

Type
Research Article
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

REFERENCES

1.Ebers, GC, Vinuela, FV, Feasby, T, Bass, B.Multifocal CT enhancement in MS. Neurology 1984; 34: 341346.CrossRefGoogle ScholarPubMed
2.Raine, CS, Scheinberg, LC, Waltz, JM.Multiple sclerosis-oligoden-drocyte survival and proliferation in an active established lesion. Lab Invest 1981; 45: 534536.Google Scholar
3.Prineas, JW.Pathology of the early lesions of multiple sclerosis. Hum Pathol 1975; 6: 531535.CrossRefGoogle Scholar
4.Ludwin, SK.Proliferation of mature oligodendrocytes after trauma to the central nervous system. Nature 1984; 308: 274275.CrossRefGoogle ScholarPubMed
5.Prineas, JW, Kwon, EE, Sharer, LR, Cho, ES.Massive early remyelination in acute multiple sclerosis. Neurology 1987; 37 (Suppl 1): 109.Google Scholar
6.Paty, DW, Isaac, CD, Grochowski, E, et al. Magnetic resonance imaging (MRI) in multiple sclerosis (MS): A serial study in relapsing and remitting patients with quantitative measurements of lesion size. Neurology 1986; 36 (Suppl 1): 177.Google Scholar
7.Willoughby, E, Grochowski, E, Li, D, et al. A prospective study of MRI scanning in multiple sclerosis. Am Ac Neurol, New York 1987. Manuscript in preparation.Google Scholar
8.Palmer, MR, Bergstrom, M, Grochowski, E, et al. Magnetic resonance imaging (MRI) in multiple sclerosis (MS): Quantitative changes in the size of lesions over 6 months in the placebo limb of a therapeutic trial. Can J Neurol Sci 1986; 13: 168.Google Scholar
9.Koopmans, R, Li, DKB, Grochowski, E, et al. Benign and chronic progressive multiple sclerosis: An MRI study. Can J Neurol Sci 1987; 14: 241.Google Scholar
10.Fog, T, Linnemann, F.The course of multiple sclerosis. Acta Neurol Scand 1970; 46 (Suppl 47): 1175.Google Scholar
11.Stewart, WA, Hall, LD, Berry, K, et al. Magnetic resonance imaging (MRI) in multiple sclerosis (MS): Pathological correlation studies in eight cases. Neurology 1986; 36 (Suppl 1): 320.Google Scholar
12.Noseworthy, JH, Seland, TP, Ebers, GC.Therapeutic trials in multiple sclerosis. Can J Neurol Sci 1984; 11: 355362.CrossRefGoogle ScholarPubMed