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MS IS A METABOLICALLY DEPENDENT, NEURODEGENERATIVE DISEASE
It is our contention that MS relapses are primarily caused by metabolic changes influencing glial and neuronal function that lead to a breakdown in the blood-brain barrier. Proton MR spectroscopy studies have confirmed that widespread neuronal loss is present even at the earliest clinical stage of the disease and is largely independent of inflammation.13 N-Acetyl aspartate is considered to be a marker of the functional neuronal mass, and a reduced total brain N-acetyl aspartateis an excellent predictor of relapses in patients with MS. Treatments using natalizumab, which are effective in reducing the permeability of the blood-brain barrier,14 may not reduce the disease progression that occurs as a direct result of neuronal loss. This is because immune mechanisms are not responsible for neuronal loss and progressive brain and spinal cord atrophy in MS. Demyelination in MS spares the subcortical U-fibers that are typically involved in oligodendroglial infection and demyelination (progressive multifocal leukoencephalopathy). Symmetry of lesions and sparing of the U-fibers on T2-weighed MR images are compatible with metabolically inherited white matter diseases.15

Relapse-related acute symptoms in patients with MS are caused by physiological blockade of conduction, and even though conduction abnormalities may continue to persist, functional recovery (remission) occurs in the early stage of the disease. There is significant involvement of the gray matter that often manifests early as neurobehavioral, cognitive, and paroxysmal symptoms that are not explained by myelin loss. Pathologically, gray matter involvement is always present in patients with MS where progressive brain atrophy is common in longitudinal MR studies. A recent study16 of the thalamic gray matter of MS patients has confirmed substantial neuronal loss (30%-35% reduction) and concluded that neurodegeneration may make a major contribution to the pathogenesis. There is also evidence from MR spectroscopy that neuronal metabolic dysfunction and neuronal loss is closely associated with disease progression and disability.4 In MS, as axons and their myelin sheaths break down in the metabolically compromised brain, their effective repair and regeneration are blocked by inhibitory factors from astroglia and oligodendrocytes that, in turn, stimulate astroglial proliferation as evidenced by a reduction in the fractional anisotropy of the diffusion tensor MR images.17 Figure 2 summarizes the features that are in keeping with a metabolic regulation of the disease. We know that exposure to sunlight is protective in patients with MS18 and vitamin D levels may be one of the key metabolic regulators in the "at-risk" individuals who carry the MS susceptibility gene or genes.

se1956 wrote:Here
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the EDSS of a woman decreased from 5 to less than 2 after a liver transplant. After 3 years she was symptom free.

I think this may not be the result of the immunosuppression, that is necessary after the transplant, but the result of a "normal" liver metabolism.

R.