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

  1. #1

    The Meaning of Flaccidity and Muscle Atrophy after Spinal Cord Injury

    In the chatroom tonight, I just realized that some people may not understand what flaccidity is and what can cause muscle flaccidity and atrophy. I am just jotting some ideas down here and will later document the statements with references for an article on the main http://carecure.rutgers.edu site.

    Flaccidity means lacking firmness, resilience, or muscle tone. This can result from several causes.

    1. Inhibition. Most people do not know that over 50% of the neurons in the spinal cord are inhibitory, i.e. their role is to reduce motoneuronal activity. Whenever you contract a given muscle, the antagonistic muscle is inhibited. For example, if you extend your leg by activating your quadriceps (either voluntarily or by electrical stimulation), the hamstrings are inhibited. This inhibition is mediated by interneurons in the spinal cord. Many (probably most) of the descending axons from the brain to the spinal cord terminate on inhibitory interneurons rather than on excitatory neurons or motoneurons. Thus, depending on the injury or sprouting of neurons in the spinal cord, you can either tend towards increased muscle tone (spasticity) or reduced muscle tone (flaccidity).

    2. Loss of motoneurons. Injury can of course kill motoneurons. Motoneurons are situated at all levels of the spinal cord but they are most concentrated in the cervical enlargement which innervates the arms and the lumbar enlargement which innervates the legs. The cervical spinal cord above C4 includes the phrenic nucleus which innervates the diaphragm. The thoracic cord (T4-T11) innervates the abdomenal muscles while the sacral spinal cord innervates the pelvic organs include the sex organs, bladder, and anal sphincter. Injury to these areas can kill motoneurons directly. However, it is important to note that one does not need all or even a large proportion of the motoneurons to function. For example, one can destroy close to 90% of the phrenic nuclei and still recover breathing function. Motoneurons that survive can sprout to innervate more muscle fibers than they do normally.

    3. Damage to the spinal roots or peripheral nerves. Motoneurons send their axons out the posterior (the word used for human) or ventral (the word used for animals) spinal roots. They go into the peripheral nerve to the muscles. Therefore, damage to the spinal roots or the peripheral nerves will cause denervation of muscle. Such denervation is frequently associated with severe atrophy of the muscles. For many years, such denervation was thought to be irreversible. The nerves were thought to provide trophic factors that are necessary to maintain the muscles. However, recent studies suggest that this is not the case and that muscle activity (induced by electrical stimulation) alone can maintain the bulk of denervated muscles. Note that motor axons may regenerate in damaged spinal roots but damage to the spinal roots will separate sensory axons from the spinal cord and sensory axons usually will not grow back into the spinal cord.

    Muscle atrophy may occur from two causes: non-use and denervation. For many years, the two were thought to be distinct but recent research suggest that muscles do not necessarily die when they are denervated. Of course, when muscles are denervated, they are deprived of all activity. Damage to peripheral nerves and spinal roots cause the most muscle atrophy because it eliminates all neural activation of the muscle. Of course, spinal cord injury also causes non-use. However, the atrophy associated with spinal cord injury is usually less severe than the atrophy associated with injury to the peripheral nerves or spinal roots.

    A recent study of atrophy of the diaphragm was particularly revealing. When a person with a high cervical injury (C1 to 4) is on a ventilator, the diaphragm which is one of the largest and strongest muscles of the body, rapidly undergoes atrophy. Several studies suggest that 3-4 weeks on a ventilator is sufficient to result in a "floppy" diaphragm. However, microscopic studies of the atrophic diaphragm muscles in animals suggest that the muscle is not dead. Rather, most of the cells die but a thin sheet of muscle fibers remain. More important, cells called myoblasts are present in this sheet. When these cells are stimulated to grow (by activity, exercise, inflammation), they form new muscle fibers. As everybody knows, exercise can produce enlargement of muscles by many times.

    As long as atrophic muscles are moved and stretched, they do not seem to die. However, atrophic muscles, however, do die if they are not moved. When muscles are not moved or stretched, they undergo fibrosis, the myoblasts move out, and the muscle will not be easy to restore. By the way, this does not mean that this is the end of the muscle. In fact, we have been injecting stem cells into denervated muscles and showing that the stem cells will produce new muscle cells in atrophic muscles. Nevertheless, these findings provide a strong rationale for doing physical therapy and passive range of motion to stretch the muscle so that they do not become fibrosed.

    Contractures occur when muscles become atrophic. The muscles not only shrink in terms of thickness but they also shrink in length. This is particularly true if there is spasticity that pulls the limbs into flexion. These are called flexion contractures. It is often quite difficult to stretch the muscles out, especially if the muscles are spastic. When spastic muscles are stretched, they resist the stretching by contracting. There are several ways to change this. One approach is to paralyze the muscle that is being stretched, either with local anesthesia to the nerve or by botulinum toxin (botox) or phenol injections that weaken the nerves going to the muscle (note that botox and phenol work by damaging the nerves). Another approach is to give the person a lot of antispasticity drugs (such as baclofen) which will produce flaccidity in the muscles. A third is to give muscle relaxants, such as valium. Once the muscle is relaxed, it can be stretched but this needs to be done slowly or else the muscle will tear. A common approach is to splint and cast the limbs progressively over a period of several weeks.

    Finally, there is the issue of "learned non-use". This is a relatively recent realization. It seems that non-use not only produces muscle atrophy. There may be "atrophy" of neurons in the spinal cord as well. The good news, however, is that intensive exercise and "forced use" of the motor system can restore the neural circuits necessary for recovery. For example, intensive ambulation training has been reported to restore locomotion to people who have never walked after spinal cord injury for many years. Such ambulation training may restore locomotor reflexes in people who have "complete" spinal cord injury but may not restore voluntary locomotion. Unfortunately, I heard that a recent NIH-funded U.S. study of treadmill training of people with spinal cord injury did not show significant differences between those who had treadmill training and those that did not. This is likely to raise a ruckus because many European studies have reported that weight-supported ambulation training is effective in restoring locomotor function to people.

    In summary, flaccidity does not necessarily mean loss of the neurons that innervate the muscles. It may also mean that the state of excitation of the spinal cord is such that motoneurons are not active. People can develop flaccidity just from having too much inhibition in the spinal cord; this depends on the nature of the injury. However, it can also mean that the spinal nerve roots or peripheral nerve have been damaged. Inactivity causes muscle atrophy. However, if the muscles are moved and kept from fibrosis, they remain ready to be rebuilt with activity and exercise, or even reinnevation if they have been denervated. If the muscles are not moved and allowed to undergo fibrosis, it is more difficult to rebuild the muscles. However, even such cases may not be irreversible. It may be possible to rebuild the muscles by injecting stem cells into them.

    I hope that this is helpful and will stimulate many questions.

    Wise.
    Last edited by Wise Young; 06-17-2006 at 07:20 AM.

  2. #2
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    This is helpful information because I didn't understand flaccidity. I have to do some research of my own to see if the exercise equipment ordered by my nurse caseworker is right for me. I'll study what she ordered then report back.

  3. #3
    Very Helpful, thanks doc.

    Good to know even severe muscle loss may not be irreversible. I had to have most of both my calves removed because of extreme pressure sores caused by ortho boots aimed at preventing footdrop.

    I always thought it would be very ironic if I were cured of sci but could not walk because of no calf muscles

    Also, I always assumed spasticity was as a result of the condition of the cord and not because of all the reasons you provide.

    Thanks again.
    AO.

    -------
    Everyone is entitled to be stupid occasionally, but some people abuse the privilege.

  4. #4
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    Thanks Dr. Young for all the information. I am still having a few questions. As we discussed on a previous thread- My roots looked to have no damage, yet my test showed there was denervation to the muslces. Is this possible to have denervation without showing root damage? Thanks.

  5. #5
    Originally posted by jv:

    Thanks Dr. Young for all the information. I am still having a few questions. As we discussed on a previous thread- My roots looked to have no damage, yet my test showed there was denervation to the muslces. Is this possible to have denervation without showing root damage? Thanks.
    jv, yes, it is possible to have denervation without root damage. I listed several causes of flaccidity or atrophy of muscle. You can have loss of neurons, injury to the root, or injury to the peripheral nerve. I assume that you received an EMG test, showing denervation hypersensitivity of your muscles. This does suggest that you have some denervation of your muscles and, while this does tell you that you are losing some muscles, it does not tell you how much you have left or lost. Looking at the nerve roots can't really tell you whether they are damaged. You may have had damage to motoneurons in the spinal cord at or close to the injury site. So, what tests can one do to distinguish between the various causes of denervation:

    1. Somatosensory evoked potentials (SEP). SEP's are activated by stimulating a peripheral nerve and recording the response in the brain and spinal cord. If one sees a sensory volley heading into the spinal cord through the peripheral nerve in question, it means that the peripheral nerve is intact. Since both motor and sensory fibers travel in the peripheral nerve, the only places where the damage can be is at the ventral root or in the spinal cord.

    2. H-reflex. This is the test of the monosynaptic reflex in legs. This test stimulates the peripheral nerve which activates action potentials that head proximally and distally. The responses are recorded from the muscle innervated by the stimulated nerve. The action potential that travels distally will activate the muscle, producing a rapid M-response. The action potential that travels proximally will activate motoneurons in the spinal cord which then sends a second and later activation of the muscle, called H-response. If this response is intact, it would strongly indicate that the peripheral nerve, roots, and spinal cord are intact.

    3. Reflexes. An intact reflex can be detected on neurological examination. If, for example, we poke a pin into the hand or foot and the limb withdraws, this means that not only is sensory signal getting into the spinal cord, it is activating appropriate muscle responses.

    Wise.

    [Sorry, I made a small correction]

    [This message was edited by Wise Young on 11-18-03 at 07:24 PM.]

  6. #6
    Originally posted by AO:

    Very Helpful, thanks doc.

    Good to know even severe muscle loss may not be irreversible. I had to have most of both my calves removed because of extreme pressure sores caused by ortho boots aimed at preventing footdrop.

    I always thought it would be very ironic if I were cured of sci but could not walk because of no calf muscles

    Also, I always assumed spasticity was as a result of the condition of the cord and not because of all the reasons you provide.
    AO, sorry, if I gave the impression that spasticity arises from something other than the spinal cord, I did not mean to. Spasticity is very likely to come from the spinal cord. I am referring to flaccidity (the opposite of spasticity).

    Wise.

  7. #7
    Ooops
    My mistake, not yours Doc. You explained it perfectly, I think I read what I was thinking and not what you were writing.

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    Everyone is entitled to be stupid occasionally, but some people abuse the privilege.

  8. #8
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    Wow, thanks for all the info! I did have an EMG done which gave me the numbers of 40% still intact. I also had an SEP done. I was told during the SEP that they were only testing to see if any signals were getting to the brain. I completely failed the SEP. I also believe I had the H-reflex done at the time I had my EMG. I don't know the results of that. I do remember my leg jumped like crazy and I felt some pain(maybe it was just the fact I knew it had to be hurting!). Anyway, I do have reflexes such as my leg pulling away if something sharp hits it. They definitely respond to really cold or really hot water. When doctors check my reflexes at the knees and ankles they do get one, but it is weak. As far as being flacid I don't really know as I have always done a lot of FES that keep my muscles from atrophing. I have a feeling they would atrophy a lot if I didn't do the FES. If you have any additional information after reading this I would love to hear it. Otherwise thank you so much for answering my questions!

  9. #9

  10. #10
    Originally posted by jv:

    Wow, thanks for all the info! I did have an EMG done which gave me the numbers of 40% still intact. I also had an SEP done. I was told during the SEP that they were only testing to see if any signals were getting to the brain. I completely failed the SEP. I also believe I had the H-reflex done at the time I had my EMG. I don't know the results of that. I do remember my leg jumped like crazy and I felt some pain(maybe it was just the fact I knew it had to be hurting!). Anyway, I do have reflexes such as my leg pulling away if something sharp hits it. They definitely respond to really cold or really hot water. When doctors check my reflexes at the knees and ankles they do get one, but it is weak. As far as being flacid I don't really know as I have always done a lot of FES that keep my muscles from atrophing. I have a feeling they would atrophy a lot if I didn't do the FES. If you have any additional information after reading this I would love to hear it. Otherwise thank you so much for answering my questions!
    jv, usually when they do somatosensory evoked potentials on people, they record the responses from scalp electrodes. If they are stimulating a nerve that is below the injury site, the signal may not reach the injury site. Note that they can also try to record the response from an electrode over the electrode where the sensory signal is entering the spinal cord. If they can see a response there, that means that the response is entering the spinal cord. Due to the injury, however, the response may not be travelling up to your brain.

    Wise.

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