Friday, May 11, 2012

RRMS, SPMS and the lipid hypothesis of multiple sclerosis

From: Blake
I stumbled across your blog while searching for information on Dr. Corthals' hypothesis, and thought you might be a good person to ask this question: to your knowledge, what, if anything, has the lipid theory suggested about the differing courses of MS? I know some in the medical community have doubted whether relapsing and progressive forms of MS are even the same disease, so I'm very interested in how the paradigm shift affects that dynamic.
Any information would be much appreciated!
Before I begin, please remember I'm a novelist, not a physician. For answers you can rely on, talk to your healthcare professional.

Here's a quote from Dr Corthals in the excellent piece about her article:
Eventually, the toxic macrophages are cleared, leading to the emission part of the RRMS (relapsing-remitting MS) cycle. But this detente holds only until the next trigger comes along. Dysfunction of the PPAR is further implicated in MS because it slows the repair mechanism of the central nervous system to a crawl, preventing the efficient renewal and synthesis of myelin.
Secondary progressive (SPMS) is just what happens next. Toxic macrophages don't clear sufficiently and/or for long enough, and myelin renewal ceases due to long-term damage/axonal death. This happens at a greater/faster scale/rate than with RRMS. The increase in both processes also increase the lack of integrity of the blood brain barrier (BBB).

I was initially diagnosed with RRMS and now have SPMS; I feel qualified to at least have an opinion on how they relate to the lipid hypothesis of MS. However, I'll be the first to admit that I don't know enough about the pathophysiology of other forms of MS (primary progressive and progressive relapsing) to feel comfortable even guessing where/how they fit into the hypothesis. If anyone out there does, I'd love to hear from you.
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