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Old 04-24-2008, 05:39 PM
Quixotic1 Quixotic1 is offline
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Join Date: Apr 2008
Posts: 61
15 yr Member
Quixotic1 Quixotic1 is offline
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Join Date: Apr 2008
Posts: 61
15 yr Member
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Quote:
Originally Posted by lady_express_44 View Post
What lead me to believe it was a patient was that I noticed his/her sentence:

"He looked at my newest MRI and said,"Well, I don't see a lesion that's causing your face pain. That's good! You don't want a big lesion in your brainstem!" By saying this he was indicating two things. The first is that he knew I had a lesion, but it was invisible. The second was that he believed me when I said I had pain, even though there was no proof on the MRI."

I agree that the author has done a GREAT job of simplifying the complicated . . . but much of what he/she said is based on some old "theories" too. For example, even in the above statement, the author is implying that the problem is that a "lesion" just did not show up on his/her MRI. While I don't doubt that some lesions hide for a short while, I suspect that it may actually be an entirely different part of the disease process going on that has caused his/her facial symptoms . . . not necessarily as a result of yet "unobservable lesions".

(Many of his comments are based on the assumption that lesions are the end-all, be-all to this disease, and that I wouldn't necessarily agree with that either.)

Many of us had symptoms long before we were dx, and some of us can date that back 10+ years. What is going on in our bodies that the lesions aren't always obvious throughout this period; is it that the MRI just didn't pick them up (they are that small?, but causing that much grief?), or is it that something else is going on too and the lesions are just objective EVIDENCE of the bigger picture with this disease?

It seems like there must be more to this because quite often those with PPMS don't have any or many lesions, yet they are often the quickest to become disabled. Same with SPMS, where the "lesion activity" slows down, yet these people continue to PROGRESSIVELY decline.

This authors summary is generalized, fairly accurate, and simple . . . but I just wanted to point out there is probably much more to the story then he/she implies too. From experience, I feel that I could expand on or refine the spinal lesion information, especially with regard to the hidden lesions/the dx process. For example, although spinal lesions might be sneaky, the symptoms from them are pretty cut and dry to the professionals.

Generally speaking though, the information in this article are simple and reasonably accurate, based on some theories.

Cherie
Hi, I don't understand exactly where all of the replies end up here. I hope I am replying to the post about the concept of "lesions.:

Lesions in the most basic medical/physiological (and in MS) sense are defects in the "nerves." Whether they show up on the MRI is irrelevant. When one speaks of "lesions" on the MRI they are, indeed speaking of visible and definable areas of change on the images.

When I write of lesions I speak of damaged oligodendrocyte/axon/myelin units which are more likely to be symptomatic in the spinal cord. They may or may not be symptomatic in the brain, depending on their size and location. The damage may be inflammatory as is seen in the autoimmune and other attack on the myelin or the damage may be degenerative as in direct axonal degeneration and death as is seen (from early in the disease) the areas of "Black holes" seen in the T1-weighted images on MRI. The axonal death is felt to be largely responsible for the accrued disability in MS.

Again, my articles were never meant to be a scientific reference. But, when there are questions about what I was referring to please contact me and I'll answer here. Also, it will help me know where I'm being unclear.

I was a pediatrician for 23 years, but my post-doc work was in Immunology, so I try to NOT mislead. Thanks for your comments.

Quix
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