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  • CT Origins of nociception

    Jason said:
    http://www.somasimple.com/forums/sho...4&postcount=51
    if we are paying attention to the literature, it seems we have a very large continuum of connective tissue health that is routinely asymptomatic, so finding tissue with health inside this continuum and blaming that for pain is weak reasoning. The health of the nervous tissue is on a much narrower continuum and it is therefore immediately more plausible as a source of persistent nociception.
    Jason, is there some research to support the narrower continuum for nervous tissue health? Or is this inferred from a relative perspective vs the research that demonstrates the large continuum of tissue damage and asymptomatic persons. Just curious.

    Jason also said:
    I've tried so many times to understand this phenomenon of people thinking biomechanics doesn't matter or connective tissue doesn't matter when you understand pain physiology- I've never seen that stated anywhere but it's so pervasive among those struggling to understand the role of neurophysiology in practice that it must be coming from somewhere... ...But I've seen this issue come up enough times in genuinely reflective and intelligent people such as yourself that I have to think its coming from somewhere - I just don't know where.
    I've been facing similar barriers in attempting to introduce pain physiology to my colleagues at work.

    Diane suggested it is pareidolia:
    http://www.somasimple.com/forums/sho...3&postcount=50
    What it is, is pareidolia (virgin mary in a piece of toast, homer simpson's face on Mars, dragons in clouds, etc) that highjack peoples' brains so much that they begin to see the illusions as the only way to see (and thereby reason) anything. Convenient? Yes. A valid science? A good reasoning model for pain?... Um, maybe not so much.
    I think pareidolia accounts for the behavior of those thoughtless Therapists out there. But as Jason points out, there are genuinely thoughtful and reflective minds who get stuck here. What else could be going on? This conversation has been especially relevant for me this weekend, given that I've been laid up for 3 days after buggering my lower back in the gym doing some deep squat/lateral shuffle drills!

    In this http://www.somasimple.com/forums/sho...Starting+point thread we discussed the self signaling capacity of peripheral nerves (relay info back to cns about its internal environment) versus its capacity to relay info back to the cns about the environment external to it (mesoderm). Jason made a similar reference here
    http://www.somasimple.com/forums/sho...0&postcount=54
    Nervous tissue doesn't report the health of the connective tissue, as [some people seem to think]. It reports it's own health
    I don't think this discussion reached a resolution, and I think part of greg's recent posts http://www.somasimple.com/forums/sho...t=12980&page=2 are related to it, at least i think they are to the extent that biomechanists argue that pain follows microtrauma/macrotrauma to the mesoderm (which they argue follows poor biomechanics). Without delving into the problems of defining optimal biomechanics, as I see it the biomechanical model of pain seems to ignore 2 key points;

    1. nociception is neither sufficient or necessary for pain
    2. To the extent that nociception is relevant, they only consider it as it relates to the brain's capacity to detect potential or actual threat to the mesoderm. They do not seem to consider nociception generated from within the nerve (accept of course when the diagnosis is "a pinched nerve". Even then, I doubt that they consider the nociception in terms of hypoxia inside the nerve, but rather "it hurts when a nerve gets compressed").

    To put all this in context, what follows here is only important to the extent that nociception is relevant to pain. I don't want to go down the path of arguing the relative influence of nociception to the overall experience of pain. Rather, to the extent that nociception is relevant, i have some thoughts about the origins of nociception, and how they relate to biomechanical (mesodermal) vs ectodermal explanatory rationales for pain and treatment of it.

    It has been written here that neurons are the only cells in the body that can signal, and that within the context of informing the cns of all things nociceptive, sensory fibers report preferentially on their own wellbeing. My interpretation of this is that those supporting this view are arguing that the nervous system does not have a capacity to detect potential or actual threats to the mesoderm. Or if it does, they are not a priority versus threats to the nervous system itself. I don't understand how this could be the case. I will try to explain why and I look forward to any criticisms anyone may have.

    It seems to me to be a question of the origins of nociception.

    When a sensory pathway 'signals' nociception, it only does so because an action potential threshold has been reached and a wave of depolarization follows. No mesodermal tissues can do this. So I agree that the mesoderm in this sense, can't signal. But what causes an action potential (AP) to be generated? The mesoderm has all manner of dendrites plugged into it. I would think that the very fact that there are receptors embedded in mesoderm and they are attached to dendrites suggests that we evolved this way because the brain wants to know what is going on outside of the nervous system not just what's going on in its internal environment. What are these dendrites informing the brain of when they signal? I see three categories
    1. If the dendrites are plugged into a tendon for example, the APs generated in the dendrites of that neuron could originate from nociceptors embedded in the tenocyte. Noxious chemicals for example in the tenocyte could trigger the AP. The neuron is the signaler but the noxious environment within the tenocyte triggered the signal.
    2. APs are generated from receptors inside the neuron. If the internal environment of the neuron was hypoxic for example, nociceptors would be triggered and an AP could be produced.
    3. If we zoom out from the neuron to a peripheral nerve, Nervi nervorum on the exterior surface of the nerve could generate a nociceptive APs


    So there are three different origins of nociception, two are ectodermal, one is mesodermal.

    Given that a single neuron integrates info from all its dendrites, some facilitatory, some inhibitory, and an impulse is only fired along its axon to the next neuron when a threshold is reached, how would the brain know where the info originated? It couldn't know which of the three origins were involved because the signals from each converge before it even reaches the next neuron! If the brain can't know, how can we ever hope to know as Therapists?

    I think the biomechanists are saying that the entirety of a given nociceptive signal originates from receptors embedded in mesoderm. While an ectodermal approach seems to argue that the entirety of a given signal originates via self signaling mechanisms (if ive misinterpreted the ectodermal perspective, i stand to be corrected). I think both occur, and I don't think we can ever know the relative input of either because by the time it gets to the axon of the first sensory neuron, let alone the spinal cord, I imagine the signal is the product of much convergence. If im right, it seems redundant to separate structures into mesoderm and ectoderm for the purpose of explaining the origins of nociception, because nociception always reflects combined input from both mesoderm and ectoderm.

    I do realize that this whole discussion is bogged down in the world of nociception, which as we know is neither sufficient or necessary for pain. I do realize that most of what it is important about an ectodermal approach lies in the value of acknowledging the brain's role as central to pain production, that reductions in pain from manual therapy occur because a context has been provided to facilitate descending modulation/cortical remapping. Nociception may not even be involved. But I wanted to bring this up, because even though an ectodermal approach to treatment entails a full description of the neuromatrix, the component of treatment that addresses sensory/discriminative factors relies heavily on the self signaling model of nociception, while disregarding/downgrading the potential influence of nociception from receptors embedded in the mesoderm. I don't think it is complete or satisfactory to argue that the self signaling nerve accounts for all of the nociception that contributes to pain.

    Does anyone deny that nociception can originate from receptors embedded in mesoderm? Can anyone suggest how nociception that originates from receptors embedded in mesoderm is any different, or would be received by the brain differently than nociception that originates from receptors embedded on the interior of a peripheral nerve? If not, does this make the distinction between mesodermal and ectodermal approach redundant?

  • #2
    Great thread.

    Pareidolia is so important that I began a couple of courses with those pictures of Homer Simpson on Mercury (I think it was Mercury) in an effort to reach into the current popular culture and demonstrate my coolness despite my age. I also mentioned that we could all remember the word describing the phenomenon by relating it to Homer's must commonly used expletive.

    This went over like a lead balloon.

    Maybe this thread will lead to something more effective.
    Last edited by Barrett Dorko; 14-11-2012, 03:34 PM.
    Barrett L. Dorko

    Comment


    • #3
      As always, well-laid out, Patrick.
      If not, does this make the distinction between mesodermal and ectodermal approach redundant?
      I will think about your other points, but the above remark triggered an immediate reaction.
      The approach, no matter what the origin of the nociception (ecto or meso), should still be on that which we can affect and effect the most - the nervous system and its processes.

      I agree with you that separating the origins of nociception is of academic interest, but not much more.
      We don't see things as they are, we see things as WE are - Anais Nin

      I suppose it's easier to believe something than it is to understand it.
      Cmdr. Chris Hadfield on rise of poor / pseudo science

      Pain is a conscious correlate of the implicit perception of threat to body tissue - Lorimer Moseley

      We don't need a body to feel a body. Ronald Melzack

      Comment


      • #4
        Thanks Bas,
        The approach, no matter what the origin of the nociception (ecto or meso), should still be on that which we can affect and effect the most - the nervous system and its processes.
        I definitely agree with this. I should have said that an ectodermal vs mesodermal approach for describing the origin of nociception is redundant. If it is, I question the value of this statement.
        "Nervous tissue doesn't report the health of the connective tissue, as [some people seem to think]. It reports it's own health. If there is a problem with the connective tissue that only becomes relevant to the organism when it affects the nervous tissue."
        I can't see how this statement can be true. As long as there are receptors in mesoderm that detect noxious chemicals/mechanical stress in the mesoderm such that nociceptive signals are generated and propagated, I can't rule out that the state/health/condition of the mesoderm forms part of the info inherent in nociceptive signals that reach the spinal cord and brain.

        The problem is when the Therapist thinks that nociception reflects only the state/condition/health of the mesoderm. And it's an even bigger problem when they think they can change nociception with their hands. But I don't see that it is useful or correct to argue the opposite i.e. That all nociception received by the cns reflects the state/condition/health of the ectoderm. If this were true, there would be no need for receptors in the mesoderm.

        Am I splitting hairs here? Does it really matter when the overall thrust of our explanation is that pain is an output of the brain, and that nociception is not sufficient/necessary for pain? I would argue yes it does matter... as soon as nociception is mentioned (when does it not come up?) during an explanation of an ectodermal treatment approach, it would be remiss of us to only explain nociception as a reflection of the health of neural tissue.

        Comment


        • #5
          Maybe I'm missing something here, but aren't receptors part of the ectoderm?

          Shouldn't there be a distinction between pathology (things that require healing and/or repair) and non-pathologic yet ultimately pain-producing conditions (for which movement is our best bet, and I do mean bet)?
          Barrett L. Dorko

          Comment


          • #6
            Barrett, I agree maybe I'm missing something as well.

            Would not the origin of nociception be when an ion channel on a nociceptor is activated and then a signal is sent through an impulse of the ectodermal tissue.

            Yes the chemical outside the nociceptor coming from the mesoderm, endoderm or skin could eventually make it's way to hit the ion channel causing the event of nociception from a nociceptor. But if that chemical never hits an ion channel or hits ion channels that are not receptive to it then no nociception could ever occur.
            Kory Zimney, PT, DPT

            http://koryzimney.blogspot.com

            "Study principles not methods, a mind that can grasp principles will create its own methods." - Gill

            "All truths are easy to understand once they are discovered; the point is to discover them." - Galileo Galilei

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            • #7
              Thanks Barrett,
              As far as I know receptors that are embedded in mesoderm are part of the ectoderm but I am happy to be corrected. I don't see how this affects my point though, given that the receptor is sampling the environment of the mesoderm... It is sampling the goings on of the mesoderm and reporting back to the cns. While receptors inside the nerve, are sampling the internal environment of the nerve and reporting it back to the cns. True?

              The two different signal origins probably converge, meaning we have to have a guess at the origin of nociception, if we choose to acknowledge it at all. Mechanical deformation of nervous tissue is more likely, I would guess, when there is pain in the absence of obvious trauma.

              Certainly with my current episode of low back pain, movement helps a lot. But can I rule out some damage to the mesoderm in my lumbar spine? I don't think I can. Will I focus on this potential presence of damage while I recover? Definitely not. nor would I spend much time talking about it with a client in pain, accept to the extent that I want them immobilized to facilitate mesodermal healing.

              My point here is really about being as correct as possible in attempts to educate other Therapists as they attempt to cross the chasm (myself included I suppose).

              Barrett, how would you answer a student at your next course who asks the following questions;
              1. If nociception is neither sufficient or necessary for pain, why do you teach a method that has at it's center a nociceptive mechanism for pain (mechanical deformation of nervous tissue)?
              2. Why does the mesoderm have nociceptors embedded in it if sensory nerves only report back to the cns about their own health/condition?

              As I try to teach my colleagues, I am hopeful that they don't ask these questions because I can't think of an answer that doesn't acknowledge the role of mesoderm as an origin nociception. I have to acknowledge the potential influence of mesoderm, even though the whole point is to ectodermalize their treatment approach.

              It seems that some middle ground of understanding is the most correct position

              Comment


              • #8
                In answer to #1 I always say that "Iron bars and concrete walls do not a prison make - but they sure do help."

                Neural tension certainly constitutes a condition that may be a nociceptive driver, and it's what I can deal with with movement, both instinctive and choreographed.

                To #2; If a mesodermal structure is diseased there's not much I can do. If it requires healing and/or repair that is what imaging and specific testing is for. The doctor must help here.

                Not all of this can be ascertained without some brief, trial treatment - and by brief I mean 3-4 visits.
                Barrett L. Dorko

                Comment


                • #9
                  Kory said:
                  Yes the chemical outside the nociceptor coming from the mesoderm, endoderm or skin could eventually make it's way to hit the ion channel causing the event of nociception from a nociceptor.
                  Hi kory,
                  What other purpose would the nociceptor (in your example a chemoreceptor) serve other than being receptive to the concentration of noxious chemicals in the environment in which it 'lives'? To say that the receptor binds to a noxious chemical as a matter of chance is to imply, to my thinking, that this is not the receptor's primary function. But my understanding is that all chemoreception occurs by chance collisions of molecule and receptor, the higher the concentration, the higher the chance of a 'lock and key' fit. That's what the receptor is there for!

                  So I think you're correct in saying that nociception begins at the receptor, which is ectoderm(?), but nociception cannot happen unless there is an action potential generated.

                  I don't understand the resistance (I think I see here) in acknowledging the role of the mesoderm in triggering nociceptors, when it is exactly the same process that occurs inside a peripheral nerve when it's internal environment triggers nociception. E.g. Hypoxia of internal environment of peripheral nerve.

                  Comment


                  • #10
                    Nociceptors trigger themselves!
                    It's not what they're plugged into that's as irrelevant as much as the fact that nociception is not related in any predictable manner to pain perception.

                    However, if you want to tie an operator model to nociception, if you really really do, then it makes more sense, likely, to tie it to mesoderm inside ectodermal structures, i.e., neural structures. The mesoderm inside ectodermal structure is from neural crest, at least, somewhat more closely related to ectoderm than mesoderm proper, the stuff that makes the "stuffing" structures of the body.
                    Diane
                    www.dermoneuromodulation.com
                    SensibleSolutionsPhysiotherapy
                    HumanAntiGravitySuit blog
                    Neurotonics PT Teamblog
                    Canadian Physiotherapy Pain Science Division (Archived newsletters, paincasts)
                    Canadian Physiotherapy Association Pain Science Division Facebook page
                    @PainPhysiosCan
                    WCPT PhysiotherapyPainNetwork on Facebook
                    @WCPTPTPN
                    Neuroscience and Pain Science for Manual PTs Facebook page

                    @dfjpt
                    SomaSimple on Facebook
                    @somasimple

                    "Rene Descartes was very very smart, but as it turned out, he was wrong." ~Lorimer Moseley

                    “Comment is free, but the facts are sacred.” ~Charles Prestwich Scott, nephew of founder and editor (1872-1929) of The Guardian , in a 1921 Centenary editorial

                    “If you make people think they're thinking, they'll love you, but if you really make them think, they'll hate you." ~Don Marquis

                    "In times of change, learners inherit the earth, while the learned find themselves beautifully equipped to deal with a world that no longer exists" ~Roland Barth

                    "Doubt is not a pleasant mental state, but certainty is a ridiculous one."~Voltaire

                    Comment


                    • #11
                      Patrick, at the risk of exposing my misunderstanding of your points, I'd like to suggest out the following:
                      I don't understand the resistance (I think I see here) in acknowledging the role of the mesoderm in triggering nociceptors
                      I do not think there is resistance to the possibility that mesoderm can trigger nociception.
                      Sure it is a possibility.

                      But how do we tell?
                      Why do we want to know?
                      And if we do find out, what are we going to do with that info? What good does it do us and the patient?

                      And if we acknowledge that most of the time we simply do not know - why sweat it so much?
                      We don't see things as they are, we see things as WE are - Anais Nin

                      I suppose it's easier to believe something than it is to understand it.
                      Cmdr. Chris Hadfield on rise of poor / pseudo science

                      Pain is a conscious correlate of the implicit perception of threat to body tissue - Lorimer Moseley

                      We don't need a body to feel a body. Ronald Melzack

                      Comment


                      • #12
                        Hi Diane!
                        Thanks for weighing in.
                        It's not what they're plugged into that's as irrelevant as much as the fact that nociception is not related in any predictable manner to pain perception.
                        I did start this thread by commenting that this line of thinking is only important to the extent that nociception is important in pain output. Perhaps the whole thread is a waste of time.

                        But I think it's worth discussing, not because I want to tie an operator model to nociception, I'm not sure how you leapt to that. but rather because I want to be able to effectively argue against the next therapist who wants to argue that mesoderm contributes to nociception when I talk about neurophysiology. I still don't see that I can say the mesoderm is irrelevant. If it is irrelevant, nociception from the internal environment of the nerve must be equally irrelevant. I don't see that we can disregard nociception from receptors plugged in the mesoderm, while acknowledging nociception from receptors plugged into the ectoderm. And I think my reasoning is sensible. Do you disagree with it?

                        Comment


                        • #13
                          If it is irrelevant, nociception from the internal environment of the nerve must be equally irrelevant.
                          Yes, I think it actually is. Irrelevant.
                          So (you might wonder, as any reasonable person might..), what is? Relevant?
                          Not the nociception, but handling the person in a way that convinces their brain on every level to turn it down. The un-nocicepting of a patient, if you will. The de-pain-ification process.
                          ...And, in the process, not creating any MORE of it, by inadvertently leaning in on them too hard because of some vain, misguided attempt to get to some deep bit of supposedly nocicepting mesoderm, with some cockeyed idea that wiggling it or jiggling it or needling it is going to be useful or helpful in some manner taught to one by some guru type who was taught by someone else and so on, backwards all the way to Descartes.
                          Diane
                          www.dermoneuromodulation.com
                          SensibleSolutionsPhysiotherapy
                          HumanAntiGravitySuit blog
                          Neurotonics PT Teamblog
                          Canadian Physiotherapy Pain Science Division (Archived newsletters, paincasts)
                          Canadian Physiotherapy Association Pain Science Division Facebook page
                          @PainPhysiosCan
                          WCPT PhysiotherapyPainNetwork on Facebook
                          @WCPTPTPN
                          Neuroscience and Pain Science for Manual PTs Facebook page

                          @dfjpt
                          SomaSimple on Facebook
                          @somasimple

                          "Rene Descartes was very very smart, but as it turned out, he was wrong." ~Lorimer Moseley

                          “Comment is free, but the facts are sacred.” ~Charles Prestwich Scott, nephew of founder and editor (1872-1929) of The Guardian , in a 1921 Centenary editorial

                          “If you make people think they're thinking, they'll love you, but if you really make them think, they'll hate you." ~Don Marquis

                          "In times of change, learners inherit the earth, while the learned find themselves beautifully equipped to deal with a world that no longer exists" ~Roland Barth

                          "Doubt is not a pleasant mental state, but certainty is a ridiculous one."~Voltaire

                          Comment


                          • #14
                            Thanks Bas,
                            I do not think there is resistance to the possibility that mesoderm can trigger nociception.
                            I think this qualifies as resistance
                            Jason said:
                            "Nervous tissue doesn't report the health of the connective tissue, as [some people seem to think]. It reports it's own health. If there is a problem with the connective tissue that only becomes relevant to the organism when it affects the nervous tissue."
                            This is what sparked this thread.
                            But how do we tell?
                            Why do we want to know?
                            And if we do find out, what are we going to do with that info? What good does it do us and the patient?
                            I would answer to each if these,
                            1. we can't
                            2. Because I think asking why is always important
                            3. It probably wouldn't change my treatment of my clients

                            So why bother then? Because I think that if the goal is to spread the word and change the profession, any loopholes that provide a learner with an opportunity to say "you're biased by your beliefs" need to be identified and clarified. I think the statement above from Jason, as I interpret it, is one such loophole.

                            Does that make sense?

                            Comment


                            • #15
                              I do not see that statement from Jason anything other than a careful distinction:
                              If there is a problem with the connective tissue that only becomes relevant to the organism when it affects the nervous tissue."
                              Is this not a clear message that when tissue damage/excessive stress affects the nervous system - there can be nociception? The chemicals from pathology are stressful to the nerve receptors and can trigger nociception. IOW, the nerve reports on its OWN distress from chemical (or mechanical) stresses.

                              I do not see this as a resistance - more an elegant refinement.
                              We don't see things as they are, we see things as WE are - Anais Nin

                              I suppose it's easier to believe something than it is to understand it.
                              Cmdr. Chris Hadfield on rise of poor / pseudo science

                              Pain is a conscious correlate of the implicit perception of threat to body tissue - Lorimer Moseley

                              We don't need a body to feel a body. Ronald Melzack

                              Comment

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