Cece wrote:That being said, i recently have had two patients with severe spasticity which I believed were clearly due to demyelinization. To my surprise some improvements occurred after venoplasty. I still cannot figure out why this occurs.
The improvements were immediately after venoplasty?
If you were correct in assessing that the spasticity as being due to demyelinization and yet we also know remyelinization does not occur between the start and end of angioplasty, then restoring the flow must be doing something to restore the function of the demyelinated neurons despite their continued state of demyelinization. (Assuming it is not placebo or an effect of medications such as fentanyl used during the procedure.)
Here we go, this ties into a question asked here two years ago:
and your two-years-ago response:
and a quote from the research linked in the first linkConduction velocity, depressed by 26% with diabetes, was normalized by treatment. These observations support the hypothesis that hyperglycemia-induced blood flow reductions and resultant endoneurial hypoxia are important factors underlying nerve conduction deficits early in the development of diabetic neuropathy.
It could be that when an immediate improvement is seen in spasticity due to demyelinization, the immediate improvement is due to the relief of CNS nerve conduction deficits due to blood-flow reductions and resultant endoneurial hypoxia. This is assuming that the reduced perfusion seen in MS is due to outflow obstructions and that the treatment of outflow obstructions leads to improvement in cerebral perfusion, which would need to be proven.
those are also good hypotheses for reductions in spasticity.
but patients should be realistic that the majority will not see gains in spasticity, at least in the short term