SPASM AND STIFFNESS AS SPASTICITY

[dania]

what is your case dania, and how long is a long time by your lights?

Not sure what you are asking?

[gibbledygook]

I found capsaicin/chilli in relatively high doses relieves spasticity. It also helps with the bowel.

[sou]

Spasticity is NOT a nutrient deficiency!

It occurs due to loss of communication between the brain and the lower spinal cord, because of damage to the upper motor neurons. Unless this communication is magically restored, spasticity will be present. Some nutrients might help reducing the muscular tone a little, but they are a drop in the Pacific ocean.

Practically nothing can be done for spasticity. You have it, you die with it. Period. Whoever makes promises about it, most possibly wants to make some more money out of your pain. What can be done is prevention of its consequences: back pain, frozen joints, contractures. Nothing else, but this is not treatment of spasticity, it is management of its complications.

If you find this post a little extreme, please tell me about a success story about somebody having spasticity due to permanent upper neuron damage, not inflammation which is temporary, and is now fine. Spasticity treatments and nutrients work for people who wouldn't have spasticity, even if they didn't follow them.

Just my opinion.

[dania]

Sou, I 100% agree with you. Not a nutrient deficiency.
This post is not extreme at all. And I do not believe you can manage any symptoms with diet. Of course if you have a crappy diet and change it to a healthy one you would feel better, That goes for everyone, whether you are 100% healthy or not.

[jimmylegs]

dania you said "not in my case" pls clarify

sou, for you and dania both, plus future readers of this thread, i will post these studies *again*...

The effect of magnesium oral therapy on spasticity in a patient with multiple sclerosis
http://www.ncbi.nlm.nih.gov/pubmed/11136367
The effects of magnesium glycerophosphate oral therapy on spasticity was studied in a 35-year-old woman with severe spastic paraplegia resulting from multiple sclerosis (MS). We found a significant improvement in the spasticity after only 1 week from the onset of the treatment on the modified Ashworth scale, an improvement in the range of motion and in the measures of angles at resting position in lower limbs. No side-effects were reported and there was no weakness in the arms during the treatment.

Painful muscle spasm reversed by magnesium sulphate. A case report.
http://www.ncbi.nlm.nih.gov/pubmed/4035497
A 25-year-old paraplegic man who had sustained a T3/T4 vertebral compression fracture 3 years previously presented with severe, painful spasm of the left hamstring muscle group of 2 hours' duration. This spasm produced extreme knee flexion of a degree which held the left foot posterior to the right buttock. An intravenous injection of 2 g magnesium sulphate produced immediate relief. Possible mechanisms of action of magnesium are discussed

Magnesium concentration in brains from multiple sclerosis patients
Magnesium (Mg) concentrations were studied in the brains of 4 patients with definite multiple sclerosis (MS) and 5 controls. The magnesium contents were determined by inductively coupled plasma emission spectrometry in autopsy samples taken from 26 sites of central nervous system tissues, and visceral organs such as liver, spleen, kidney, heart and lung. The average Mg content in the CNS tissues, as well as visceral organs except for spleen, of MS patients showed a significantly lower value than that seen in control cases. The most marked reduction of Mg content was observed in CNS white matter including demyelinated plaques of MS samples. Whether or not these significantly lower Mg contents found in CNS and visceral organs of MS patients may play an essential role in the demyelinating process remain unclear, requiring further studies on MS pathogenesis from the point of metal metabolism.

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.
http://www.sciencedirect.com/science/ar ... 770091051X
Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 μg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.

QED

[sou]

The effect of magnesium oral therapy on spasticity in a patient with multiple sclerosis
http://www.ncbi.nlm.nih.gov/pubmed/11136367
The effects of magnesium glycerophosphate oral therapy on spasticity was studied in a 35-year-old woman with severe spastic paraplegia resulting from multiple sclerosis (MS). We found a significant improvement in the spasticity after only 1 week from the onset of the treatment on the modified Ashworth scale, an improvement in the range of motion and in the measures of angles at resting position in lower limbs. No side-effects were reported and there was no weakness in the arms during the treatment.

A lucky person with possible magnesium deficiency found a little relief from increased muscle tone. What she would possibly want wouldn't be a painkiller but er ability to walk. This is no success story.

Painful muscle spasm reversed by magnesium sulphate. A case report.
http://www.ncbi.nlm.nih.gov/pubmed/4035497
A 25-year-old paraplegic man who had sustained a T3/T4 vertebral compression fracture 3 years previously presented with severe, painful spasm of the left hamstring muscle group of 2 hours' duration. This spasm produced extreme knee flexion of a degree which held the left foot posterior to the right buttock. An intravenous injection of 2 g magnesium sulphate produced immediate relief. Possible mechanisms of action of magnesium are discussed

No MS, but damaged motor neurons, a single patient. Once more, a fantastic pain killer, but no ability to walk. One might say: "What did you expect? He is a paraplegic!" I would reply that wheelchair bound patients are not subhumans, they do have the right to want to be fine again, no bargain here. But I would consider fantastic a treatment that could do it. So I think about spasticity.

Magnesium concentration in brains from multiple sclerosis patients
Magnesium (Mg) concentrations were studied in the brains of 4 patients with definite multiple sclerosis (MS) and 5 controls. The magnesium contents were determined by inductively coupled plasma emission spectrometry in autopsy samples taken from 26 sites of central nervous system tissues, and visceral organs such as liver, spleen, kidney, heart and lung. The average Mg content in the CNS tissues, as well as visceral organs except for spleen, of MS patients showed a significantly lower value than that seen in control cases. The most marked reduction of Mg content was observed in CNS white matter including demyelinated plaques of MS samples. Whether or not these significantly lower Mg contents found in CNS and visceral organs of MS patients may play an essential role in the demyelinating process remain unclear, requiring further studies on MS pathogenesis from the point of metal metabolism.

No spasticity here.

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.
http://www.sciencedirect.com/science/ar ... 770091051X
Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 μg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.

No spasticity here, either.

I don't object that magnesium is an essential nutrient, but it has hardly any efficiency in helping people walk. Like I said, whoever can walk using magnesium would walk even if they didn't use it.

sou

[jimmylegs]

lol! all right then, let's see the science backing *you* up.

i don't have time to post all of the relevant studies out of the thousands of google scholar results on search terms: magnesium spasticity, but here are a couple more at least

Case report Prolonged high-dose intravenous magnesium therapy for severe tetanus in the intensive care unit: a case series[PDF]
... Magnesium infusion has been used to treat spasticity in tetanus, and its effectiveness is supported by several case reports and a recent randomized controlled trial. ... Intravenous magnesium therapy controlled spasticity without the need for additional muscle relaxants.

Magnesium sulfate for control of muscle rigidity and spasms and avoidance of mechanical ventilation in pediatric tetanus
Within 24 hrs of the addition of continuous magnesium infusion, both the severity of spasms and degree of muscular rigidity decreased.

[dania]

Ok , in my case I am not taking high doses of vit D. My spasticity has increase dramatically since having done 2 angios that have now left all 3 veins 100% blocked since over a year. I do take magnesium at night and I do take vit d in the morning. I take magnesium citrate in powder form and the only thing it helps with is constipation. I just had my vit D levels checked and they were in the normal range. I did not have spasticity for 20 years. It only started 2 years ago. But now is on a scale of 1-10, I would put it at 9-9.5. Never changed my diet as it has always been a healthy one.

[jimmylegs]

ok so i'd say maybe some slight modifications might help you..

you can take 100mg elemental magnesium from magnesium glycinate before meals three times a day, but not before bed - stick with citrate for that.

one other thing i could suggest would be to take some magnesium at the same time as d3, as well as before meals and bedtime.

have you ever had a serum test for magnesium? if you are supplementing with citrate but your levels aren't making it into the upper half of the normal range, then perhaps a more absorbable form would be better. spasticity sets in on me when my levels drop into the 0.80s range

fyi, mag citrate is not the most absorbable form.. mag glycinate is better. and glycinate won't have the same laxative effect, so you don't have to worry about spending all day on the toilet!

as for the d3 test result, what was the number/units, if i might inquire? the 'normal' range is so wide, and should be tightened up significantly.

[sou]

Magnesium acts on the muscle itself. In tetanus, it is mostly the muscles surrounding the trauma that suffer from spasticity and magnesium would do great. But how about in loss of control due to damage to upper neurons? All spasticties are different in nature, so we should only be interested in alleviation of MS spasticity.

Even better, not alleviation of spasticity, this is not what we need. If that were so, amputation would cure it completely. We need our ability to walk, without flaccid muscles. Can magnesium do that? Nope...

Again, do we have any success stories (where success is not the reduction of some statistics but a practical result)? I doubt...

[jimmylegs]

no science supporting your argument then sou?

re walking, please feel free to start another thread about ataxia, paraparesis, etc

TGFTM, hope the magnesium works for you!

[lucky125]

Interesting thread. I have been successfully treated for CCSVI 4 times now. So many symptoms improve it is amazing. The one problem I am left with that is very frustrating is spasticity in my left hamstring. It responds to baclofen, but it is so tight that it interferes with my gait.

Today I just had my first dose of Botox in this muscle! I am excited to see what my benefits will be. The neuro who did it predicts that my pain will decrease, and my gait will improve.

I am fortunate that I have this one very obvious muscle that is my main spasticity problem. I have lived with the pain for about 10 years, and I still can't believe that I may finally be getting some relief. If it helps me walk more easily that will be be the icing on the cake!

I am going to keep track of it on my blog. The address is below.

Nicole

[dania]

I am interested in trying Botox.

[dania]

Jimmylegs MS is like having a stroke in slow motion, right?
Check this out.
http://drletitiamuresan.com/Botox-Treat ... P3094.html

[KateCW]

For me it's been like a spinal cord injury in slow motion.