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Due to the inability to properly metabolize vitamin B12, white matter lesions are found in all autoimmune diseases.

For instance, in the following study when fifty-eight Sjögren syndrome (SS) patients with neurologic manifestations associated with SS had magnetic resonance imaging (MRI) of the brain, the researchers found that 70% of the patients had white matter lesions and 40% met the radiologic criteria for MS.


Neurologic manifestations in primary Sjögren syndrome: a study of 82 patients.
Delalande, S., J. de Seze, A.L. Fauchais, E. Hachulla, T. Stojkovic, D. Ferriby, S. Dubucquoi, J.P. Pruvo, P. Vermersch, P.Y. Hatron. 2004. Medicine (Baltimore) 83(5):280-91.

“…We retrospectively studied 82 patients (65 women and 17 men) with neurologic manifestations associated with primary SS, as defined by the 2002 American-European criteria…Thirty-three patients had brain involvement and 13 patients had optic neuropathy. The disease mimicked relapsing-remitting multiple sclerosis (MS) in 10 patients
and primary progressive MS in 13 patients…Thirty percent of patients (all with CNS involvement) had oligoclonal bands…Fifty-eight patients had magnetic resonance imaging (MRI) of the brain. Of these, 70% presented white matter lesions and 40% met the radiologic criteria for MS…"

Adding to the fact that MS has multiple factors I really don't believe MS is a single disease. It affects everyone differently and as mentioned earlier medications only work on a percentage of patients. A single statistic hasn't been found across the board with all MS patients. Hormone levels, age, progressive, benign, time to death, all vary from person to person. The link below is to a study that found T cells activated to kill myelin, as you would expect to find with an auto-immune disease. But even there findings were not in ALL patients.

" Approximately one-half of patients with MS have a specific serum IgG autoantibody directed against the inwardly rectifying potassium channel Kir4.1, which is expressed by oligodendrocyte cell bodies and perivascular astrocyte processes in the central nervous system. This finding suggests that Kir4.1 is a target of the immune response involved in MS pathogenesis, at least in a subset of patients with the disease."
http://www.uptodate.com/contents/epidem ... Popup=true

I personally am using Copaxone, supplements, exercise, diet, LDN and whatever else I can think of to try and treat my brand of this illness. Basically carpet bombing to try and hit the pickle barrel.

Below is one of the better overviews of the illness offering many interesting possibilities with references...
http://www.uptodate.com/contents/epidem ... -in-adults

The same underlying pathological process can result in a different constellation of symptoms and therefore result in a range of eventual diagnoses. For instance, the inability to properly metabolize vitamin B12 would affect each individual differently to some respect. I think this is what might be involved with KIR4.1, which is highly expressed in astrocytes.

In the following study the researchers concluded that the damage caused by a vitamin B12 deficiency is manifested as an increase in the number of cells positive for glial fibrillary acidic protein (a protein released by astrocytes during pathological processes in the central nervous system).

Prog Neurobiol. 2009 Jul;88(3):203-20. doi: 10.1016/j.pneurobio.2009.04.004. Epub 2009 Apr 24.
The multi-faceted basis of vitamin B12 (cobalamin) neurotrophism in adult central nervous system: Lessons learned from its deficiency.
Scalabrino G.

“Glial cells, myelin and the interstitium are the structures of the mammalian central nervous system (CNS) mainly affected by vitamin B(12) (cobalamin, Cbl) deficiency. Most of the response to the damage caused by Cbl deficiency seems to come from astrocytes and microglia, and is manifested as an increase in the number of cells positive for glial fibrillary acidic protein…”


Researchers in the following study concluded that patients with MS had increased levels of glial fibrillary acidic protein (GFAP) and that GFAP levels correlated with neurological disablility and disease progression.

J Neurol. 2011 May;258(5):882-8. doi: 10.1007/s00415-010-5863-2. Epub 2011 Jan 1.
Glial fibrillary acidic protein: a potential biomarker for progression in multiple sclerosis.
Axelsson M, Malmeström C, Nilsson S, Haghighi S, Rosengren L, Lycke J.

“The major intermediate cytoskeletal protein of astrocytes, glial fibrillary acidic protein (GFAP)…may…be released into the cerebrospinal fluid (CSF) during pathological processes in the central nervous system (CNS)…MS patients had increased GFAP levels compared with controls…and GFAP levels correlated with neurological disability…and disease progression…GFAP level at the first examination had predictive value for neurological disability 8-10 years later…GFAP, a marker for astrogliosis, is a potential biomarker for MS progression and may have a role in clinical trials for assessing the impact of therapies on MS progression.”

The lack of the enzymes DNase 1 and protease would lead not only to an inflammatory immune response, which would explain the activation of the dendritic cells and the involvement of proinflammatory cytokines, but it would also lead to many other consequences that would be seperate from the immune response (such as the inability to metabolize essential amino acids and vitamin B12), and this would be unique for each individual, even though the underlying pathological process would be the same.

This recently published meta-analysis of CNS disorders shows a higher co-occurrence of brain cancer and MS, but a lower co-occurrence of other kinds of cancer and MS:

http://www.ncbi.nlm.nih.gov/m/pubmed/24458030/