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Thread: Sci Pain

  1. #11
    In my response to you about peripheral nerve damage, I may have misinterpreted Dr. Young's explanation, here's what he said, this should add to what he just wrote.

    Peripheral nerve reconnection and neuropathic pain

    Kilgore and Seneca,
    Wonderful questions. Let me try to provide an answer to these questions... with the hope that others will chime in.

    1. Peripheral nerve regeneration. Kilgore, peripheral nerves provide a better environment for axonal growth than the central nervous system. This has been shown over and over again now in many experiments and in practice. Peripheral nerve surgeons (neurosurgeons, orthopedic, and plastic surgeons) have long reconnected peripheral nerves and find that about 10% of the motor axons in the peripheral nerve will regenerate and reinnervate the muscles and sensory axons will also grow back into the muscle and skin. The motoneurons reside in the gray matter of the spinal cord. The sensory neurons reside in the dorsal root ganglia that are just outside the spinal cord. If the cut to the peripheral nerve is on distal (the term distal always refers to the direction away from the central nervous system and, in the central nervous system, it refers to the direction away from the brain) side of the dorsal root ganglia, you can reconnect a cut or damaged nerve and expect some growth of the axons across the site and down to the peripheral organs. If there is not enough length of the peripheral nerve to reconnect, one can always use another peripheral nerve segment as a bridge. However, if the cut occurs between the dorsal root ganglion and the spinal cord, this causes degeneration of the central sensory axons. The dorsal root ganglion generally will not grow back into the spinal cord or, if they do grow into the spinal cord, they often will not grow up the spinal cord to the brain.

    2. Neuropathic pain and peripheral nerve damage. Deafferentation or loss of sensory input to the brain leads to plastic changes of the brain and spinal cord. These changes are what causes neuropathic pain. So, for example, deafferentation from diabetes, brachial plexus avulsions, nerve root compression, transverse myelitis, multiple sclerosis, limb amputations, or spinal cord injury are all associated with neuropathic pain. The degree of neuropathic pain depends on the degree of deafferentation. Peripheral nerve transections have the highest incidence of neuropathic pain. The degree of neuropathic pain also depends on the response of the spinal cord to the injury. Injury to a peripheral nerve or the spinal cord causes a massive induction of cytokines and neurotrophins in the spinal cord. This response of the spinal cord to the injury causes extensive sprouting of axons, both sensory and motor. The former may lead to aberrant (abnormal) connections of the sensory axons and neuropathic pain. The latter may lead to spasticity.

    There is still much that we do not understand concerning neuropathic pain. For example, Carlstedt from the Royal National Orthopedic Hospital at Stanmore reports that when he inserts a peripheral nerve into the spinal cord and motor axons grow into the nerve and reinnervate with muscles, patients are reporting a lessening of their neuropathic pain. Since he is sticking back the nerves into the spinal cord and presumably the cut end of the nerve is distal to the dorsal root sensory ganglia, this suggests that only motor innervation is occurring without any sensory component. If so, why should the patients be having less pain? Carlstedt suggests the startling idea that neuropathic pain may be somehow related to paralysis. Another possibility is that some sensory neurons in the spinal cord may be sending axons out into the nerves and may be receiving signals from the periphery but this would really be out-of-the-box possibility that nobody had considered before. A third possibility is that when motoneurons are active, they somehow inhibit sensory activity. The last possibility is the most likely and most interesting. It may also explain why electrical stimulation of the spinal cord reduces neuropathic pain in people. The spinal cord never ceases to amaze me with its richness and diversity.


  2. #12
    Senior Member Scorpion's Avatar
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    Jul 2001
    Los Angeles

    I didn't mean to imply quads have it worse. I meant that guys like my friend who is a C-4 quad would tell me to stop bitching, because he'd take the pain if it meant he could be independent, or simply scratch his nose when it itched. It's all relative, and someone's always got it worse than you no matter how bad it seems. I also hope you don't think I was saying it's a matter of ability to cope with the pain. Sure, some people have higher pain thresholds than others, but some people simply hurt more. And they hurt more than others can imagine.

    It just sounds to me like some people are saying 'just deal with your pain' while others are saying 'my pain is so much worse than yours.' Each sentiment is unfounded, because we really have no idea what the other person is feeling.


  3. #13

    After reading your post here on spinal nerve research, I wanted to pass on a link to the newest article on my site, How Pain Nerve Cells Act When *They* Are In Pain.

    I've tried to summarize what happens in sensory nerve cells when there's nerve damage and/or severe chronic pain, including some of the recent research in this field. Considering your post, I thought you might find this of interest.

    David Berg
    PainOnline webmaster

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