- "Unexpectedly, after adjusting for sex, age and duration of disease, correlations between total plaque load and axonal loss in both the corticospinal tract and sensory tracts were weak or absent at each level investigated. Since there was little correlation between plaque load and axonal loss, the possibility that demyelination is not the primary determinant of spinal cord axonal loss warrants consideration."
"The degree of atrophy varied in different parts of the cord. Individual lesions played a minor role in local atrophy. Our findings suggest that axonal degeneration, possibly caused by the cumulative number of lesions in the brain and cord, or an alternative atrophic process, is responsible for spinal cord atrophy in multiple sclerosis, rather than tissue loss within individual lesions."
1. In this case we a talking about spinal cord lesions. They differ from WM lesions of brain. From one side, in spinal cord the majority of axons are pretty thick and long, they are myelinated heavier (motor ones more, sensory less, that why patients feel sensory disturbances first during relapse ). More important, the volume of spinal cord WM significantly less compare to brain WM. From other side, they more vulnerable to pressure that always appear during lesion formation, say, very tight quarters. Therefore the degree of axonal loss in spinal cord will depend less on the “plaque load”, it will depend more on localization.
2. It is good to have such imagination, I use knowledge instead.
3. In this forum I will never say directly – use this drug, don’t use that drug. It is not my goal first, second it will depend on your physician and guidelines of MS treatment existed in your country of residence. As I understand people there want to learn more about MS, that’s all, I share. Follow my posts and you find it out.