What causes spasticity?

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What causes spasticity?

Postby Lotte » Fri Oct 22, 2010 1:16 pm

I've got it. Baclofen is my favorite drug.

But, what causes spasticity?

I mean, what's going on mechanically? The nerves are doing what? the nerve impulses are doing what?

I've looked all over the internet for an explanation and can't find one.

All my neuro has said is that the "nerves are excited". Ok, but what does that mean? And why are they excited?
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Postby jimmylegs » Fri Oct 22, 2010 1:49 pm

spasticity can be caused by electrolyte imbalance.

magnesium, which is low in MS patients, helps relax muscles.

serum magnesium should be at least 0.91 mmol/L. when i get down under .90 i can feel my muscles tightening.

dietary magnesium comes from sources like dark dark leafy greens. www.whfoods.com is a good resource.

best supplementary form to date is albion-process chelated magnesium glycinate. best absorption, least GI side effects.

some links to earlier discussion on sodium potassium calcium and magnesium wrt muscle and nerve function. includes links to great animated resources.

http://www.thisisms.com/ftopicp-73765.html#73765
body chemistry on sodium and potassium (two very worthwhile animations to check out once you visit the above post)

http://www.thisisms.com/ftopicp-125427.html#125427
the calcium/magnesium connection.

HTH!
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Postby tzootsi » Fri Oct 22, 2010 3:48 pm

I believe the root cause of spasticity in ms is the lack of a good nerve signal to the muscle. When a muscle doesn't get an electrical signal, it tightens up. That's why corpses have stiff muscles. I also agree with Jimmylegs that magnesium helps spasticity.
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Postby jimmylegs » Fri Oct 22, 2010 5:02 pm

correct tzoo, and the nerve signals depend on the correct balance of electrolytes to power the polarization and depolarization cycles that fire nerve and muscle function.
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Postby sou » Sat Oct 23, 2010 12:57 am

A muscle can either tighten or loosen. The brain gives the orders, the spinal cord executes them. The default stance of the human body is that of a fetus and this is what will happen if you completely remove the brain.

In MS, information about the current length of a muscle do not reach the brain, hence information from the brain that says "It 's ok, the muscle is not that long" does not reach the spinal cord. The latter, "afraid" that the muscle is about to be harmed, sends an excitatory signal, ordering it to tighten.

Magnesium helps by making the muscles less tight, thus somehow decreasing the "voice" saying "I am about to be cut! Do something!". Definitely, spasticity is not a deficiency, but can be helped just a little.

Baclofen simulates excitation by the signals that should come from the brain, asking the spinal cord to relax the muscle. But that is a veeeeeeeery stupid drug: It will relax all muscles, all the time. Not just when you need to relax them. It is a fantastic pain killer, but it is more than useless in aiding you walk.

When I was first diagnosed, I was given the impression that we may not be able to cure MS, but we can manage its symptoms. For some reason, I believe that we can't do either. All these years, I haven't taken any drug that worked. I am in serious doubt about applied science. I consider it nothing more than some kids playing the researcher. Research that does not help is useless and should be avoided. I wonder how many drugs would make it if the price were proportional to the therapeutic result, after it happens...
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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Re: What causes spasticity?

Postby NHE » Sat Oct 23, 2010 1:11 am

Hi Tzootsi,

tzootsi wrote:I believe the root cause of spasticity in ms is the lack of a good nerve signal to the muscle. When a muscle doesn't get an electrical signal, it tightens up. That's why corpses have stiff muscles. I also agree with Jimmylegs that magnesium helps spasticity.


Rigor mortis actually has to do with calcium, ATP, and the bonds between actin and myosin (the thin and thick filaments of the muscle).

About wrote:what happens is that the membranes of muscle cells become more permeable to calcium ions. Living muscle cells expend energy to transport calcium ions to the outside of the cells. The calcium ions that flow into the muscle cells promote the cross-bridge attachment between actin and myosin, two types of fibers that work together in muscle contraction. The muscle fibers ratchet shorter and shorter until they are fully contracted or as long as the neurotransmitter acetylcholine and the energy molecule adenosine triphosphate (ATP) are present. However, muscles need ATP in order to release from a contracted state (it is used to pump the calcium out of the cells so the fibers can unlatch from each other). ATP reserves are quickly exhausted from the muscle contraction and other cellular processes. This means that the actin and myosin fibers will remain linked until the muscles themselves start to decompose.


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Postby jimmylegs » Sat Oct 23, 2010 4:49 am

that's really cool NHE! i never studied rigor mortis but it makes so much sense for calcium to be involved.
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