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Correspondence: When an article is eligible for submission of Correspondence, a link to the response form is available within the full-text article. You must be a current subscriber who has activated the online portion of your subscription in order to send a Correspondence. Any reader can read published Correspondence.

Correspondence to:

ARTICLES:
Fred D. Lublin, Monika Baier, and Gary Cutter
Effect of relapses on development of residual deficit in multiple sclerosis
Neurology 2003; 61: 1528-1532 [Abstract] [Full text] [PDF]
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Correspondence published:

[Read Correspondence] Effect of relapses on development of residual deficit in multiple sclerosis
Dale A Menard   (4 February 2004)
[Read Correspondence] Reply to Menard
Fred D. Lublin, MD   (4 February 2004)

Effect of relapses on development of residual deficit in multiple sclerosis 4 February 2004
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Dale A Menard,
Neurology Associates
581 11th Ave Cir NW, Hickory, NC 28601

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Re: Effect of relapses on development of residual deficit in multiple sclerosis

dalemenard{at}aol.com Dale A Menard

We read with interest the article by Dr. Lublin et al. [1]. However, the conclusions may be too broad. The data collection is performed comprehensively, including placebo groups from multiple trials. Their data shows that untreated patients who suffer relapses will have progression of their disability. The decision should not be whether or not to place an individual patient on disease-modifying therapy, but which therapy to choose.

With the choice of disease-modifying therapy comes the debate regarding possible effect of agents, especially glatiramer acetate, on the natural progression of enhancing and T2 lesions. In addition, there is the question of the likelihood of progression to T1 black holes which is invariant. Another consideration is whether an agent may have a lesser effect on relapses and still slow progression to disability.

My concern is that pharmaceutical companies will only focus on the conclusion that "MS exacerbations produce a measurable and sustained effect on disability," without recognizing that this effect has only been confirmed in placebo cohorts. The data as presented exclude treated patients from the data set.

A better conclusion is "MS exacerbations in untreated patients produce a measurable and sustained effect on disability." This still leaves the possibility that some disease-modifying therapies may slow progression to disability at a greater rate than their effect on relapse rate may indicate.

References

1. Lublin,FR, Baier,M, and Cutter,G. Effect of relapses on development of residual deficit in multiple sclerosis. Neurology 2003;61:1528-32.

Reply to Menard 4 February 2004
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Fred D. Lublin, MD,
Mount Sinai Medical Center
5 East 98th Street, Box 1138, New York, NY 10029-6574

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Re: Reply to Menard

fred.lublin{at}mssm.edu Fred D. Lublin, MD

Dr. Menard raises interesting issues which are not, by design, addressed in our manuscript, as we only had access to placebo treated patients. Therefore the issue of what to treat with is not germane to this report. We hope to be able to assess the effect of the therapeutic agents on the degree of recovery from an exacerbation when that data is available to us. However, this does not alter our conclusion about the benefit of reducing the number of exacerbations.


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