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The Edge of the Spoon

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  • Thinking_Chiro
    replied
    How depressing!

    "I treat dysfunction, NOT pain."
    Substitute dysfunction with subluxation!
    Welcome to my world/nightmare/challenge/favourite blood sport!
    How depressing!
    :angry::vomit:

    Leave a comment:


  • Barrett Dorko
    replied
    The turning of our profession toward the sensibilities of the hairdresser, not there's anything wrong with hairdressers, might have been foreseen.

    I wish I could find the old short story in Omni magazine. It concerned some future in which astronauts from the earth landed on a distant planet and soon had the "aliens" there dressing and trying to look like human beings. Did anyone else read this? Maybe the early
    80s?

    Anyway, the point it made was that cultural changes exceeded the power of all others.

    It haunts me.

    Leave a comment:


  • REKIV
    replied
    I have heard that quote repeatedly in our profession. The problem I see now is that the patient comes to us BECAUSE of the pain, not their dysfunction. Odd to think of it that way- when we say we treat dysfunction, not pain, we are directly opposite of why the patient has come in... so who is most likely wrong? The person whom is experiencing the pain? Or the meatwad sitting across from the patient, trying to prove they are a fountain of knowledge (and trying to prove that they know more about the patient than the patient themselves)?

    Leave a comment:


  • Barrett Dorko
    replied
    Thanks Mikal.

    In post #18 Bas quoted the words of many of our colleagues:

    "I treat dysfunction, NOT pain."
    I was in Atlanta when Paris coined this. At least, he gave no one else credit. It sounded good in '76 because we knew nothing of pain. Certainly not of its complexity.

    Decades later we're still hearing it.

    Leave a comment:


  • Mikal Solstad
    replied
    This thread deserves a bump.

    Leave a comment:


  • Barrett Dorko
    replied
    I thought I'd bump this because something on Facebook generated a lot of interest in it.

    Leave a comment:


  • BB
    replied
    I'm looking, but haven't found much in the literature yet.

    I did find this (SA stands for spontaneous action potential):

    Our finding that type I SA remains after the cell body is pulled away from the ganglion suggests that it is not maintained by chemical factors released from neighboring cells or mechanical stresses on the cell (Rydevik et al., 1989)
    in this full text.

    Leave a comment:


  • Jon Newman
    replied
    Originally posted by Jon Newman View Post
    I think the distinguishing feature of transduction is the conversion of one form of energy into another. Transmission is the journey that new energy form takes. Would it be correct to say that a new round of transduction occurs at each new synapse?

    For more see Diane's post on the Molecular Mechanisms of Nociception
    Consider this article also (free PDF available there also.)

    Leave a comment:


  • Diane
    replied
    So here's a question: What needs to happen for an AIG to get "better"? I mean, what closes the holes that have appeared, making the nervous membrane less like canvas and more like lace?

    Does it heal normally when offered appropriate metabolic economy?
    I don't know if any one knows for certain, but Butler says, blood flow to nerve. This makes perfect sense evolutionarily, thermodynamically, metabolically, physiologically, even mechanically.
    1. Evolutionarily, the two % of the body which is nervous system requires 20% percent of all the O2. (Domisse)
    2. Thermodynamically, life exists to be a gradient reducer. Blood flow moves stuff around reducing gradients of all sorts everywhere at all times. Its role as an O2 provider is consistent with the role of life itself.
    3. Metabolically, if a neuron can't breathe it will die. It makes sense evolutionarily that if it "thinks" or "senses" it can't breathe, it will "think" it might die. I've used anthropomorphic language, but it holds true at the systems level and at a chemical level - the nervi nervorum will report decreased available O2 in the nerve's "environment", and the n. system will be notified/may try to mount a rescue effort/behavioral response at a CNS level. At the neuronal level, various substances such as fractalkine* are produced by/expressed on the membrane of the stressed neuron, which activate microglia in the dorsal horn synapse, which are thought to be involved in upregulating the signal at cord level (bothering the secondary ascending neurons).

    4. Mechanically and 5. physiologically, consider blood flow for a moment, as it is part of a neuron's "environment".
    Blood flow does way more than just deliver O2, although that would be huge for the neuron and the cell that wraps it, Schwann. It's like a river that brings everything good to the neuron and carries everything bad away. It carries away metabolites. It carries away "swelling." (Nerves have no lymph drainage.) These can bother neurons physically, mechanically, on the inside of the axon.
    Once mechanical pressures are relieved (outside and in) and overall pressures (inside and outside) are normal, and the stress metabolites like fractalkine are carried off by the improved circulation, the microglia will de-activate, the signal to the brain stops, the neuron recovers. Physiologically it's a sick, unwell neuron, so it takes a few days. It's membrane must re-regulate.

    It's crude, but that's my understanding at present.
    Our therapy job is to help with this, from outside the body, by helping the CNS at a cord level on up. Not by banging away on the spine as if it were some sort of magic black box, but by nerves out in the body where they can be handled, especially at a skin level where you can get at them interoceptively AND exteroceptively, and stay out of the way of self-correction meanwhile.

    *(This is supposedly a picture of what fractalkine might look like.)
    * From Nature.com glossary: FRACTALKINE A membrane-bound chemokine that is highly expressed on activated endothelial cells, and is both an adhesion molecule and an attractant for T cells and monocytes.
    Last edited by Diane; 16-09-2008, 09:24 PM.

    Leave a comment:


  • Barrett Dorko
    replied
    So here's a question: What needs to happen for an AIG to get "better"? I mean, what closes the holes that have appeared, making the nervous membrane less like canvas and more like lace?

    Does it heal normally when offered appropriate metabolic economy?

    Leave a comment:


  • BB
    replied
    While it makes sense that an AIG would be more likely to be painful to palpation, all tender spots are not necessarily AIG's. Shacklock's descriptions of neurodynamic quality of neural movements tells us that mechanical strain is imparted to the nerve moreso where they turn a corner, such as at the elbow for the ulnar nerve, or at the "gromitt holes" (as Diane calls them) for cutaneous nerves. Thus, a spot tender to palpation may often be the access point to a mechanosensitive neural tissue in absence of an AIGS.

    Not sure if that adds anything of value or not.

    Leave a comment:


  • Barrett Dorko
    replied
    As always, wonderful help.

    Perhaps we can say (given what Luke especially has provided elsewhere about trigger points) that a change in the nervous tissue that could account for the clinical findings of tenderness and bidirectional, spreading pain has been definitively demonstrated but that a change in the muscular tissue, well, not so much. Perhaps not at all. Is that fair?

    This origin (one of four, remember) of ectopic discharge seems to embody elements of the other three quite readily. I don't look for it, to tell the truth, figuring that addressing the other three that accompany it in various ways will be enough in the clinic. In short, I don't poke people - and that's always a good idea.

    Leave a comment:


  • Diane
    replied
    I think it is worth considering that a peripheral neuron is a continuous sensing cell from cutaneous receptive field (where its ending is buried in amongst all sorts of skin cells in the bottom layers of the epidermis which can secrete neurotransmitters to bother it) to dorsal horn (where it can be bothered by microglia). Anywhere in between it can be bothered by hypoxic conditions secondary to mechanical distortion of its vasa nervorum. It is bi-directional, so it can signal distress up or down from whatever might be a primary bother.

    Lucky for us, we can get on it at least at one end, for sure. Not so much at the other.

    Leave a comment:


  • Jason Silvernail
    replied
    Originally posted by Barrett Dorko View Post
    One question: When considering the origin of ectopic discharge and its management, is it fair to say that this will be manifest quite commonly as a tender spot, painful to palpation, likely to elicit spreading pain and often thought to be a local muscular "lesion" or dysfunction of the spindle? Do we know that it's more likely to be an abnormal impulse generating site (AIG)? Can we say that an accurate deep model includes a nervous membrane that has developed adreno-sensitive ion channels?
    I'm not sure we can necessarily connect the AIG to a tender spot, though we can definitely say with some confidence that an AIG has increased channel density making it more sensitive to stimuli (including normally non-nociceptive chemical irritation and mechanical deformation), and that it is likely to have some adreno-sensitivity as well. So the AIG would be tender if pressed and certainly would be expected to produce local as well as spreading pain sensations when it fires both orthodromically and antidromically.

    Clinically, could we see of the manifestations of adrenosenstivity when the pain experience is magnified by stress or emotional state? Or might that be just as likely a central effect? Short of injecting adrenaline into the area (which is of course how this adreno-sensitivity was discovered), I'm not sure we can know, though its most certainly likely given what we now know.

    The connection from the AIG to the local muscle dysfunction is harder to be sure about, it seems to me the shortest distance there is Wall's instinctive motor response toward resolution.
    Last edited by Jason Silvernail; 14-09-2008, 05:12 PM.

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  • Jon Newman
    replied
    What exactly is the difference between transduction and transmission?--Barrett
    I think the distinguishing feature of transduction is the conversion of one form of energy into another. Transmission is the journey that new energy form takes. Would it be correct to say that a new round of transduction occurs at each new synapse?

    For more see Diane's post on the Molecular Mechanisms of Nociception

    Leave a comment:

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