Why foot drop is not broken foot nerves

[1eye]

If you have used a walking aid or FES (Functional Electronic Stimulator) you know the drlll. It straps on your leg just below the knee. If it is positioned correctly it feeds an electronic signal from there through a nerve which comes close enough to the skin at that point. That causes eversion, which is a movement of the front of your foot slightly upwards, and outwards, away from the midline of your body. This movement is just enough to get the foot out of the way so it doesn't drag when you are walking. A heel switch may time the eversion with your gait.

The point is, between the box and your foot, the nerve works fine. There is no problem with electrical continuity in that part of the nerve. You may even see toes curl that you have not seen do so in ten years.

My uneducated opinion is that there is no problem with these leg and foot nerves. Rather, the problem is somewhere farther up, perhaps in the brain, where the walking signals are supposed to originate. The evidence against this is that some say walking comes from lower than the brain, which is why chickens walk after their heads are cut off.

So, assuming it is lower, the problem may still be in the Central Nervous System if it is in the spine. If it is inside the skull, it may still be fixed using neuroplasticity, assuming these walking functions are transferred to undamaged parts of the brain. Stroke patients have been able to do this. That is a good reason halting progression must be achieved. Otherwise, the part of the brain that walking has been transferred to may also be affected later on.

[Marc70]

Hi 1eye,

Your question is interesting but I'm not entirely sure what you're trying to get at.

FES helps with footdrop related to spinal cord injuries. I'm a happy FES user and my mobility has remained stable for several years. I can also see the T2 Spinal Lesions causing my walking problems bright and clear in my annual MRI pictures.

In order to improve my situation I would need something to help patch up about 3-4 inches of Myelin and possibly Axoms in my upper back. Don't care how: Stem Cells, jumpstarting my OPC or whatever else may work..

[1eye]

All those other things are iffy. Not sure whether foot drop is a problem below the neck.

See Dr. Zamboni's talk on his new measurements, used in a space station experiment. Astronauts in micro-gravity get something like CCSVI, due to no gravity-assisted venous return. Prevalence of CCSVI in MS is very high.

One stroke patient ended up climbing mountains. I think we need to find out more about fingolimod. No question

[Marc70]

Why is CCSVI the Solution for everything and what does it have to do with Fingolomod?

Isn't it fairly clear by now that MS - like many other chronic diseases - has multiple triggering factors and that each diagnosis will be some individual combination of treatments. (Not the immune system suppressing/moldulating stuff out there now). Blood clotting fixes will definitely be at the table then. Just look at the recent reseach publications on Factor XII. However, you can't exclude either genetic, virological, cell metabolism, or (to some extent) psychological factors here. How big of a role each factor plays will then depend on the individual case.

There is already peer reviewed research on everything written above. It's just that no one wants to put the jigsaw pieces together. Sometimes you get the feeling of being in the early days of cancer research. There will never be one "cure for MS". Only personalized solutions for different subforms where the causes were sufficiently researched and clarified.

[1eye]

CCSVI is not a solution; it's a problem. It has very little to do with fingolimod, except that they both have to do with MS.

[Marc70]

CCSVI is not a solution; it's a problem. It has very little to do with fingolimod, except that they both have to do with MS.

I obviously meant to write "...treatment for CCSVI" not being a solution for everything.

And I still don't understand your interest in some immunomodulating drug like fingolimod.
In the end it's just another way to imped the immunesystem to do what it's supposed to do:
Put out fires where something's burning. All these drugs do is reduce the pressure in the hydrant.
They don't extinguish the fire..

[ElliotB]

"And I still don't understand your interest in some immunomodulating drug like fingolimod"


I believe it is because there have been reports of fingolimod possibly rebuilding mylin, although I don't think there is conclusive evidence of this. Perhaps 1eye can provide details.


CCSVI and CCSVI treatment are not 'proven' as the cause or cure of MS.

[1eye]

Perhaps it depends what you will accept as "proof". I am not as picky as some, and pickier than some others. I am pretty jazzed about the non-operator-dependent objective quantitative measurements that are even good enough evidence for NASA. I think I may do another CCSVI treatment, just for the sake of my heart, because I did have the one mitoxantrone heart attack. Cardiotoxicity is an evil thing. My brain will likely also benefit. My wallet won't. Too bad nobody is working on improving them. Or on more fingolimod evidence. But no use wishing for what we can't have. I just know the odds are not in my favour if I do any of those chemo/radiation/ablation things. Come to think of it, that may be why they won't let us 50+ year olds do them. At least they got that right.

Microgravity inevitably induces disease due to insufficient force propelling venous blood to the heart from whatever is typically above it. When the head is normally above the heart, a missing 1G of force (9.8 meters per second per second) will induce disease after some number of attempted heart beats. This means, for example, that humans orbiting Earth, or traveling towards the Moon or Mars, may eventually succumb to the effect of the low gravitational force.

The problems caused by this missing return flow should not be called CCSVI, because sufficiency is not the problem. It might rather be called Chronic Microgravity-Induced Venous Incompetence (CMVI).

CCSVI is different because the veins are sufficient in normal persons. There is no proof that they are sufficient in people with MS. In fact, one way to attack this problem may be to prove that venous return to the heart from the brain is sufficient in people with MS. "One cannot prove a negative."* If there are any differences between different forms of MS caused by differing manifestations of CCSVI they could be more apparent.

* -Last Call: The Rise and Fall of Prohibition Daniel Okrent. New York: Scribner, 2010 -- http://books.simonandschuster.ca/Last-C ... 0743277044