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Thread: The Meaning of Flaccidity and Muscle Atrophy after Spinal Cord Injury

  1. #41
    Thanks Dr. Young for your reply. I have seen a neurosurgeon and he has said that I need untethering of my spinal cord (hope I spelled this right); however he said that there is a very good possiblity that I could be paralyzed waist below and that scares me a lot. That is the reason I have not undergone this surgery since the last time they tried to go in there I was partially paralyzed. My delima is am I making the right decision by not doing this or am I harming myself even more ???

  2. #42
    Senior Member Foolish Old's Avatar
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    Quote Originally Posted by rajurs29
    Thanks Dr. Young for your reply. I have seen a neurosurgeon and he has said that I need untethering of my spinal cord (hope I spelled this right); however he said that there is a very good possiblity that I could be paralyzed waist below and that scares me a lot. That is the reason I have not undergone this surgery since the last time they tried to go in there I was partially paralyzed. My delima is am I making the right decision by not doing this or am I harming myself even more ???
    One man's opinion...

    Quickly search out the very damn best neurosurgeon you can find and get detethered. It is likely that I would be walking today if my tether had been discovered sooner. I know just how scary this is. But what is your prognosis if you do nothing? Time counts.

    Good luck.
    Foolish

    "We have met the enemy and he is us."-POGO.

    "I have great faith in fools; self-confidence my friends call it."~Edgar Allan Poe

    "Dream big, you might never wake up!"- Snoop Dogg

  3. #43
    Quote Originally Posted by rajurs29
    Thanks Dr. Young for your reply. I have seen a neurosurgeon and he has said that I need untethering of my spinal cord (hope I spelled this right); however he said that there is a very good possiblity that I could be paralyzed waist below and that scares me a lot. That is the reason I have not undergone this surgery since the last time they tried to go in there I was partially paralyzed. My delima is am I making the right decision by not doing this or am I harming myself even more ???
    rajurs,

    Common sense tells you that if you are losing function and you don't do anything about it, you will lose more function and the function that is lost will stay lost. So, you need to do something about it and stop stalling. Listen to Foolish Old.

    Wise.

  4. #44
    Could be this(flaccidity and atrophy)a big trouble for the success of future therapies??

    The idea of can recover and not be able to do it because my body are dead(muscles) scares me .
    -Ramps in buildings are necessary, but it would be usefull to have another ones for people (mind/heart).....

    -Hoc non pereo habebo fortior me

  5. #45
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    Can someone explain what parts of the nervous systen have to be in tact for electrostimulation to work on the muscles?

    I'm a t8-t10 and have never been able to get those machines to work on my legs. Sounds like I have spinal root damage. What a bummer.

  6. #46
    Quote Originally Posted by walkanotherday
    Can someone explain what parts of the nervous systen have to be in tact for electrostimulation to work on the muscles?

    I'm a t8-t10 and have never been able to get those machines to work on my legs. Sounds like I have spinal root damage. What a bummer.
    walkanotherday,

    Several factors influence the excitability of the lower spinal cord and much depends on the muscle that you are trying to stimulate.

    • If you are taking fairly high doses of baclofen to suppress spasticity, this reduces the excitabiliy of the muscles to electrical stimulation.
    • If you have have non-use atrophy, this also reduces excitability of the muscles to electrical stimulation.
    • If you have root damage or damage to the motoneurons, you may have a difficult time activating the muscle innervated by those roots or motoneurons.

    When you say you have a T10 level, you are referring to T10 being intact? If so, it means that your injury was lower than T10, i.e. at T11. This is getting close to the lumbar enlargement and damage to the roots may contribute.

    Wise.

  7. #47
    Senior Member MikeC's Avatar
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    Dr Young, I've heard people say that 'e-stim doesn't work on people with lower level injuries.' I thought that there was some cut off where if you were injured below that level it was doubtful (I know that we are all different) that e-stim would work for you. I can move my right big toe and I can move both ankles a little but e-stim does nothing for me (my ankles don't move at all with e-stim alone). Would you say this is because of my level of injury (T-12 but also root damage) or because of the specific roots that are damaged?

    Thanks,
    Mike
    T12 Incomplete - Walking with Crutches, Injured in Oct 2003

  8. #48
    Quote Originally Posted by MikeC
    Dr Young, I've heard people say that 'e-stim doesn't work on people with lower level injuries.' I thought that there was some cut off where if you were injured below that level it was doubtful (I know that we are all different) that e-stim would work for you. I can move my right big toe and I can move both ankles a little but e-stim does nothing for me (my ankles don't move at all with e-stim alone). Would you say this is because of my level of injury (T-12 but also root damage) or because of the specific roots that are damaged?

    Thanks,
    Mike

    MikeC,

    I want to first say that I am not sure that anybody has the whole answer to the question of why flaccidity occurs. I can only say that I don't think that it is necessarily due to loss of motoneurons or damage to roots, as many clinicians are quick to assume. I named at least two circumstances where flaccidity can occur without damage to the motoneurons or roots. One is of course when one takes high doses of anti-spastic drugs such as baclofen. At high doses, these drugs inhibit the spinal cord sufficiently so that the muscles become flaccid. The second is if, for whatever reason, whether due to lack of use (as having the legs in a cast) or anti-spasticity drug, the spinal cord has been inactive for weeks or months. I think that flaccidity can result from this. This is what I call disuse atrophy. Both of these conditions can occur without loss of the motoneurons or damage to the spinal roots.

    Now, even if one does have damage to the motoneurons and the roots, the damage is seldom involves all the muscles of the legs or roots. Motoneurons are distributed over quite length of spinal cord and it is quite difficult to have a cauda equina or other type of injury that damages every or most root. So, when I see somebody who has complete flaccidity of the lower limbs and a T10 injury, I am puzzled and not willing to accept that the condition is due to lower motoneuronal loss or spinal root injuries. By the way, I know several people like that and it has bothered me for a long time.

    There is a condition similar to this in our rat spinal cord injury model. As you may know, the Impactor model of spinal cord injury in the rat that I had developed with John Gruner and Carl Mason at NYU, drops a 10-gram weight onto the T9-10 spinal cord. This is an injury to the thoracic spinal cord just above the lumbar enlargement (where all the lumbar neurons reside). About 10-20% of the rats don't get any muscle tone return. They just drag themselves on their bellies and their legs hang out straight behind them. This tends to occur more in older rats and also when the surgeon is doing the injury for the first time. For this reason, I have long harbored the suspicion that the injury damaged blood vessels in the spinal cord and this caused ischemia of the spinal cord. Please note, that I don't think that damaged all the motoneurons in the lower spinal cord. It just creates a state of low excitability in the lumbar cord and the animals become flaccid. I think that this is a area that needs to be investigated.

    I apologize for this long explanation but a close friend has this and I have spent a lot of time thinking about it and also solutons for the problem.

    Wise.

  9. #49
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    Dr. Young,
    I was on Baclofen for only two weeks but it was for neuropathic pain. It was not effective and I eventually just learned to deal with it.

    I haven't had a single spasm since the injury and my muscles, even before all the atrophy, have always been soft and flaccid.

    T8-T10, is just the area of lesion that shows up on MRIs. (cord appears to be in tact) It's where the spinal cord thins out for me.

    I'm not saying this is my case but is disuse atrophy reversible? Your last post to MikeC is very interesting because while my injury is unknown, the suspicion has always been spinal cord infarct or contusion. I was on blood thinners for quite a long time because of this.

    I guess the real question is: Is there significant research being done on regeneration of spinal roots? or does general SCI injury research cover this? What is the test for spinal root damage?

  10. #50
    Quote Originally Posted by walkanotherday
    Dr. Young,
    I was on Baclofen for only two weeks but it was for neuropathic pain. It was not effective and I eventually just learned to deal with it.

    I haven't had a single spasm since the injury and my muscles, even before all the atrophy, have always been soft and flaccid.

    T8-T10, is just the area of lesion that shows up on MRIs. (cord appears to be in tact) It's where the spinal cord thins out for me.

    I'm not saying this is my case but is disuse atrophy reversible? Your last post to MikeC is very interesting because while my injury is unknown, the suspicion has always been spinal cord infarct or contusion. I was on blood thinners for quite a long time because of this.

    I guess the real question is: Is there significant research being done on regeneration of spinal roots? or does general SCI injury research cover this? What is the test for spinal root damage?
    Walk,

    In your case, where you may have had ischemia (loss of blood flow) or tranverse myelitis (unknown cause or inflammation-mediated cause), there may be damage to neurons in the lower spinal cord. Careful neurological and neurophysiological tests (especially early after injury) should provide some insights into what happened. For example, it would be important to know whether you had reflexes. This should be tested both neurologically (deep tendon reflex) and also neurophysiologically (H-reflex and M-reflex). If there was damage to the spinal roots, needle recordings from the muscles should show hypersensitivity as the needle is inserted into the muscle. However, these studies need to be carried out while it was happening. Once the muscles become flaccid, it is hard to find out why.

    I did not discuss one phenomenon because it is controversial: spinal shock. This is something that was described by Sir Charles Sherrington at the turn of the century. He reported that when he cut the spinal cord of monkeys, the monkeys would lose all reflexes for a period of time. Since he cut the spinal cord above the lumbar enlargement and did not damage that part of the spinal cord directly, he hypothesized that there was a remote effect of the injury and called this spinal shock. Unfortunately, spinal shock does not always occur, especially in other animals such as rats and cats. In humans, careful study of the spinal cord suggest that not all reflexes are lost and different reflexes return at different rates and at different times. However, due to mechanisms that are not well-understood, some people have spinal shock where various spinal reflexes are completely or partly suppressed for days, weeks, or even months.

    There is some evidence that flaccidity is reversible. For many years, there was deep pessimim amongst physical therapists and rehabiitation doctors that flaccidity can be reversed. They base this pessimism on the inability of surface stimulation to activate flaccid muscles. The reason why surface stimulation cannot activate flaccid muscle is because the current does not penetrate into the muscle. Most such stimulation is simply activating nerve fibers at the surface of the muscle and the nerves then activate the muscle. In order to stimulate the muscle direclty, one needs much higher current levels. As discussed in previous topics, there is a Swiss group that has shown that very high current stimulators can prevent or even reverse muscle atrophy after cutting of the peripheral nerves. Note that such stimulation just maintains the muscle but does not improve voluntary control of the muscle.

    So, in summary, careful neurological and neurophysiological study should be able to determine the distribution and the reason for your flaccidity. Let's assume that you have no deep tendon reflexes. In such a cases, neurophysiological testing by stimulating the peripheral nerve should be done to see whether this would activate the muscle. If such stimulation produce little or no muscle activation, this suggest that there has been loss of muscle or loss of peripheral nerve. If peripheral nerve stimulation produce no activation of sensory responses in the spinal cord, this would suggest strongly that you have had spinal root damage. This test should be done nerve by nerve.

    Finally, you need to get high-resolution MRI scans of your spinal cord. In China, many of the hospitals have 3 Tesla MRI scanners that can do a test called diffusion tensor analysis (DTA). This test shows oriented fibers in the spinal roots and white matter of the spinal cord. Such scans may show whether there is disruption of fibers in the spinal roots. Such scans should be carefully read by somebody who is familiar with the technology. Unfortunately, there are not that many hospitals in the United States that have the right instrumentation and experienced doctors to do and interpet these kinds of tests. I have been thinking that we need to establish a center that can carry out these types of tests and provide definitive information to people concerning the cause of their symptoms.

    Wise.

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