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  • Ref Fascial contractility and myofascial trigger points

    The expanded trigger point (TrPt) hypothesis does not sufficiently explain how myofascial TrPts or taut bands are formed, how they create a chronic pain condition, or how the mechanisms of treatments that are used can be explained.

    Several published arguments have been written to question the validity of the TrPt hypothesis. In 1994, Quintner and Cohen published Referred pain of peripheral nerve origin: an alternative to the ‘‘myofascial pain’’ construct. In 2001, Gunn wrote a chapter in Bonica's Management of Pain called Neuropathic Myofascial Pain Syndromes. And in 2004, Pearce published Myofascial Pain, Fibromyalgia or Fibrositis?

    In 2007, Farasyn published "the barrier-dam" theory that offers an alternative explanation for referred muscle pain, but does not address the other components of the TrPt hypothesis.

    If you are aware of any other published sources that question the validity of the TrPt hypothesis, please point me to them.

    Although these authors have done a fine job of debunking the TrPt hypothesis, their explanations for what IS happening are rather general, based on what is known about the nervous system and pain mechanisms. I am trying to present a more specific explanation of what is occurring in the vicinity of these so-called TrPts.

    My main disagreement with the TrPt hypothesis is with the claim that the activating event is muscle damage and that local myofascial pain is due to the release of substances from these damaged muscles. Even though Travell and Simons acknowleged that myofascial pain can occur under several other scenarios (psycho-emotional stress, bacterial and viral infections, and organ disease), none of these scenarios were taken into account in their hypothesis, rather these were seen as perpetuating factors. A broader explanation for local and referred pain is needed, one that accounts for all of the known initiating factors. Only one explanation seems to fit: the brain's response to stressors via autonomic nervous system modulation.

    Before I continue, I want to say that I am not questioning any of the evidence that has been presented to prove that local dysfunction has occurred. This includes the presence of a hyper-irritable spot, a taut muscle band, a change in local chemical milieu, and dysfunctional motor end-plates. I believe, however, that these findings are merely a consequence of autonomic dysregulation.

    My hypothesis examines the role of fascial contractility in the activation of local dysfunction and in the perpetuation of pain. It evolved from clinical observations in a massage therapy practice over the past 10 years. One of the things that I noticed was that whenever taut bands and tender muscles were present, there were 3 other palpatory findings as well.
    1. the skin over the area had restricted mobility
    2. the related articulation had restricted mobility
    3. the entire muscle, not just the taut band, had restricted mobility (it had become 'adhered' to neighboring anatomical structures).
    I further noticed that when the subject was no longer in pain (no matter what the intervention), mobility was restored in all three areas. To my hands, these restrictions felt like the fascia was contracting. I ignored this thought for years because I was taught that fascia did not possess this property. But my hands kept telling me otherwise.

    A little over a year ago, I began looking for explanations by going to Google Scholar and typing in "fascia" and "contract". My head was telling me this was a waste of time, but my hands were doing the typing and they knew better. I learned that certain fascial cells could contract. Myofibroblasts are atypical fibroblasts that combine the ultra-structural features of both fibroblasts and smooth muscle cells. Due to their expression of stress fiber bundles containing alpha smooth muscle actin and due to strengthened adhesion sites on their membrane, these cells possess a much high contractile potential than normal fibroblasts. I continued my search, trying to learn all I could about fascial innervation, both sensory and autonomic. Even though the literature was sparse, there was enough to convince me that this idea was possible.

    The biggest problem I have in providing evidence for my hypothesis is that there is relatively little known about the location and behavior of myofibroblasts. Schleip's histological observations in his laboratory suggest that perimysium is characterized by a high density of myofibroblasts. This fits with my findings and is all I have to build the construct on. Anyway.....here's how I think it works:

    Fascia contracts under autonomic modulation in response to many common stressors:
    • Sudden, prolonged or repetitive tensional demands
    • A real or imagined threat to the organism that activates the fight-or-flight response
    • Structural imbalances and postural strain
    • Psychological and emotional stress
    • Tissue repair and wound healing
    • Viral or bacterial infections
    • Unaccustomed movement
    • Diseases of the organs
    • Becoming chilled
    • Lack of sleep
    If fascial contraction is sustained, this continued tension initiates other biological processes:
    • Intramuscular myofascial force is transmitted along fascial pathways: from endomysium to endotenon, from endomysium to adjacent endomysium, and from endomysium to the basil lamina of sarcolemmas in adjacent muscle fibers
    • Extramuscular myofascial force is transmitted from muscle extra-cellular matrix to compartmental boundaries to neurovascular tracts
    • Fibroblasts proliferate at the site of tension
    • Fibroblasts secrete macromolecules, including the precursor to collagen
    • New collagen fibers cross-bind to existing collagen clusters, aligning along the line of force
    • The local ground substance is structurally altered with an increase in viscoelasticity
    • The local ground substance is chemically altered, becoming more acidic (lower pH)
    • Cytokines, inflamatory signaling compounds, proliferate at the site
    Adjacent nerve fibers are sensitized:
    • Nerve movement is restricted by the increase in fascial tension
    • Changes in the ground substance lower the threshold at which nerves will fire
    • When sufficiently irritated, motor nerves will induce spontaneous electrical activity (SEA) at the neuromuscular junction in one or more of the muscle fibers they innervate
    • Continued SEA develops into contraction knots that are palpable as tender hardenings within the muscle (trigger points)
    • Traversing afferent peripheral nerves become entrapped in the fascial restrictions and sensitized to the changes in the ground substance
    • Pain is perceived at a location distant from the trigger point in the distribution of the sensitized peripheral nerves
    • Central sensitization occurs between the trigger point and the spinal cord, perpetuating the cycle.
    Attached Files

  • #2
    Hi Kim,

    You've given us a lot to consider. The last bullet point caught my attention the most

    Central sensitization occurs between the trigger point and the spinal cord, perpetuating the cycle.


    Can you expand on this? I don't think I'm reading this as it was intended.
    "I did a small amount of web-based research, and what I found is disturbing"--Bob Morris

    Comment


    • #3
      Originally posted by Jon Newman View Post
      Can you expand on this? I don't think I'm reading this as it was intended.
      [/color][/color]
      Great place to start Jon, as the component of central sensitization, which has been implicated in the TrPt theory, is the least clear to me. I included it as a last minute add-on to my poster last year, without full consideration. My first instinct is to just remove it, but first, let's see if there is something to the idea. Here are some of the references that implicate central sensitization in the perpetuation of pain:

      From the expanded TrPt hypothesis:
      "secondary mechanical hyperalgesia is maintained by neuroplastic changes in the central nervous system".

      From the dissertation: FUNDAMENTALS OF MUSCLE PAIN, REFERRED PAIN AND DEEP TISSUE HYPERALGESIA Thomas Graven-Nielsen:
      "Injection procedure and sensitivity assessment by pressure stimulation can cause deep tissue hyperalgesia. However, deep tissue hyperalgesia is not a consistent finding in saline-induced muscle pain indicating that the clinical deep-tissue hyperalgesia is not likely to be explained by the simple peripheral effects after acute muscle pain. In some cases the deep tissue hyperalgesia is correlated to the pain intensity indicating that central summation or sensitisation might be involved."

      and from Giamberardino in Referred muscle pain/hyperalgesia and central sensitisation (2003):
      "Referred pain/hyperalgesia from deep somatic structures is not explained by the mechanism of central sensitisation of convergent neurons in its original form, since there is little convergence from deep tissues in the dorsal horn neurons. It has been proposed that these connections, not present from the beginning, are opened by nociceptive input from skeletal muscle, and that referral to myotomes outside the lesion results from the spread of central sensitisation to adjacent spinal segments."

      Edit: from Diane's links, I found this mentioned about central sensitization and Fibromyalgia from Ch. 44 from ToP: Myofascial pain and fibromyalgia syndrome (i don't know how to point to other threads). This was written about Fibromyalgia, but it's basically the same thing that has been written about myofascial pain syndrome:
      "The precipitating causes of FMS may vary among individuals, but the painful symptoms may be related to central sensitization of somatosensory pathways leading to an amplified perception of pain. Biological abnormalities that are detected in most patients include dysfunctional sleep by polysomnography; physiological or biochemical evidence for central sensitization"

      My question is: what is the physiological or biochemical evidence for central sensitization?
      Last edited by Kim LeMoon; 14-01-2008, 07:25 PM. Reason: added quote and question about central sensitization

      Comment


      • #4
        Hi Kim,
        Looks like you've been developing your hypothesis from the outside (fascia) in, as I've been developing mine from inside the nervous system out, and we've met at the interstice. Or maybe that should be, interstitial tissue.

        When I did the cutaneous nerve dissection I had to be very careful to sort out what was interstitial tissue from what was tubular skin ligament conveying nerve out to skin. (Nash has a good paper on skin ligaments by the way.) This thread introduces the reader to a book about tunnel syndromes. I reasoned that if large nerves could "hurt", so would small ones, maybe even especially cutaneous nerves since they are so 1.) afferent, and 2.) secretory. Anyway, there they were and I've been thinking about them ever since. This whole forum might be of some use to you, as might this one. In particular, this thread discusses mechanosensation/mechanosensitization. There are several chapters available to read there, and although none of them discuss fascia per se, I think it's safe to say that 1.) contractile elements of whatever type pressing on a nerve/neuron of any size that has afferent capacity, could result in the nerve being distressed. What the brain does about it after that will be up to the brain I suppose. It can ignore signals from tissue very readily when it wants, or it can amplify a signal to the max if it wants.

        I've plowed through quite a bit of info on the peripheral autonomic system as well, should it be of any use to you.
        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


        • #5
          Originally posted by Diane View Post
          Hi Kim,
          Looks like you've been developing your hypothesis from the outside (fascia) in, as I've been developing mine from inside the nervous system out, and we've met at the interstice. Or maybe that should be, interstitial tissue.
          That's a cool way of looking at how we each arrived at our ideas. From the outside in or the inside out - there seems to be many ways to find answers.

          How'd you know that I'd never heard of 'interstice'? You anticipated that and linked to the definition. Thanks.

          I've been reading for hours now, based on the links you posted. Interesting stuff and more than enough to generate tons more questions. It's tempting to keep reading, but I've promised my mind that I will come back to that stuff later. I've got a deadline to meet!

          Some of the information has been very helpful, especially the specifics related to tunnel syndromes with regards to the effects of mechanical tension on peripheral nerves.

          Could you provide me with the complete citation info for the Tunnel Syndrome book? (title, author, year, publisher) There are several quotes that would fit nicely into my paper and you've already posted page #s and the text.

          Another request: do you have a copy of Clifford Wolfe's paper on central sensitization? The link from this thread is dead.
          Last edited by Kim LeMoon; 14-01-2008, 07:58 PM. Reason: another request

          Comment


          • #6
            Hi there Kim,

            I'm very impressed with the depth of your examination.

            Your point regarding the etiology of MTrPs involving muscle damage, and the subsequent disregard of other hypothesised scenarios in the theory, is something I've been uncomfortable with since I was a student, for obvious reasons.

            Your comment, "The biggest problem I have in providing evidence for my hypothesis is that there is relatively little known about the location and behavior of myofibroblasts." is a valid one, and a good place to start. I think it is very important for you to consider the following -
            Klingler W, Schleip R, Zorn A. European Fascia Research Project Report. Structural Integration: Journal of the Rolf Institute; December: 2004.

            Our original hypothesis, as well as that of Prof. Staubesand, was that the contractile cells in fascia would probably have the same physiology and innervation as visceral or vascular SMCs. This hypothesis had a certain appeal to the manual therapists in our team, since its verification would nicely support Prof. Staubesand’s credo of an intimate two-way connection between fascia and the autonomic nervous system. Nevertheless, this hypothesis now appears as unlikely to be substantiated in the light of recent advances in fibroblast research. Here's why: fibroblasts exist in a certain heterogeneity. Those phenotypes which contain smooth muscle-actin stress fibers are often called myofibroblasts (MFB), and many of those have several features in common with smooth muscle cells (SMCs). Yet MFBs have been clearly shown to express different proteins and to use different messenger substances and energy processes for contraction than SMCs. While most SMCs can be easily influenced by input from sympathetic or parasympathetic nerves, contraction of MFBs is regulated by specific cytokines (like TGF, or fibronectin) and by mechanical tension (ref. 14).
            A smaller point in relation to your clinical experience that, "the related articulation had restricted mobility.....(and that) these restrictions felt like the fascia was contracting"-- It remains to be demonstrated that the typical combined contractile force of the SMCs in local fascia is sufficient to cause palpable joint restriction.
            Klingler W, Schleip R, Zorn A. European Fascia Research Project Report. Structural Integration: Journal of the Rolf Institute; December: 2004.

            ...questions have been raised as to whether the number of such contractile cells in fascia is sufficient to have any significant effect
            The reference for this last statement is here and suggests that
            The control of the expression of contractile cytoskeletal elements in musculoskeletal connective tissue cells, e.g., fibroblasts, chondrocytes, and osteoblasts, may be found to be of therapeutic benefit in modulating healing and disease processes
            , rather than augmenting muscle function. Also, the fact that
            a wide variety of connective tissue cell types can express the gene for SMA under certain circumstances in vivo and in vitro—and in some cases transiently—raises the question of whether it is necessary to refer to them [MFBs] with the prefix "myo-."
            Last edited by Luke Rickards; 15-01-2008, 01:03 AM.
            Luke Rickards
            Osteopath

            Comment


            • #7
              The Wolfe link worked for me.
              Luke Rickards
              Osteopath

              Comment


              • #8
                The Wolfe link worked for me.
                Perhaps Kim still doesn't have quite full access.. Bernard??

                Could you provide me with the complete citation info for the Tunnel Syndrome book? (title, author, year, publisher)
                What a pain. I thought I'd included this info in the intro thread - sorry. Here's a link.
                It's a great book. Highly recommend it.

                Cary on Kim! :clap2:
                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


                • #9
                  Diane, the link Kim referred to was for another website. Here it is again.
                  Luke Rickards
                  Osteopath

                  Comment


                  • #10
                    Originally posted by Luke Rickards View Post
                    I'm very impressed with the depth of your examination.
                    Thanks. Your comments have been the most helpful I've gotten in the past year. I'm disappointed that Werner Klingler, who is a really nice man and spoke with me in person and has answered email questions about my hypothesis, never pointed me to his own work that would have made me question things like you have. Ah well, it's been good food for thought for the past few hours and has generated several new ideas.

                    A smaller point in relation to your clinical experience that, "the related articulation had restricted mobility.....(and that) these restrictions felt like the fascia was contracting"-- It remains to be demonstrated that the typical combined contractile force of the SMCs in local fascia is sufficient to cause palpable joint restriction.
                    Hmmm...been thinking on this one while I worked with clients all night. Checked and re-checked, and I'm certain that a palpable joint restriction exists pre-treatment and certain that it doesn't when the treatment is effective. If myofibroblast contraction doesn't account for this, what then?

                    So that leads me to open up another can-o-worms. There's something that's been gnawing at me for months and I haven't been able to get a good handle on how it fits in: the local twitch response (LTR). Here's what I've got brewing; maybe you can help me figure out the rest:
                    • The LTR is a confirmatory part of the Travell/Simons TrPt diagnostic criteria and is elicited by snapping palpation of a taut band within a muscle in a lengthened position
                    • Dry needling is most effective if it elicits an LTR (several LTRs actually)
                    • My cross fiber nudging/rolling technique often elicits a weak, but visible/palpable LTR and is done on a muscle in a neutral or shortened position. Additionally, I don't target a taut band, I roll over either the whole muscle or at least a fascicle or two
                    • How come snapping palpation doesn't result in a therapeutic effect, but dry needling and my technique do? Why does the positional change (lengthened vs. neutral/shortened) make a difference?
                    • It has been strongly suggested that the LTR is a spinal reflex - for now, let's assume that is the case
                    • Let's go even further and assume that it is propagated by the muscle spindle
                    Why would the muscle spindle be so darn sensitive? Maybe that's the autonomic piece to this puzzle. Maybe the brain lowers the threshold at the muscle spindle as a protective mechanism and this starts the whole cascade of events that I described in my first post. Would a sensitized muscle spindle create enough tension within the perimysial tunnel to initiate myofibroblast contraction?

                    For several months, the background picture on my desktop has been a beautiful histologically dyed-red muscle spindle. I look at it every day trying to understand it's place in the mix. It's big, relative to the size of the surrounding muscle fibers and lies in the perimysial tunnel, along with neurovascular bundles. What am I supposed to learn about this structure?

                    Comment


                    • #11
                      Kim

                      I think there is fairly strong evidence that the twitch is reflex mediated at the spinal cord level. Joseph Audette published a strudy on this. I have a video of a twitch response to the contralateral upper trap. If I can figure out how to upload it I will. I cant seem to find the audette paper in PDF but will attach the abstract. I dont believe the muscle spindle hypothesis has stood the test of time, but I don't know that literature well. I think the attached review by Dommerholt is the most recent from the trigger point camp.


                      : Am J Phys Med Rehabil. 2004 May;83(5):368-74, quiz 375-7, 389. Links
                      Bilateral activation of motor unit potentials with unilateral needle stimulation of active myofascial trigger points.

                      Audette JF, Wang F, Smith H.
                      Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts, USA.
                      OBJECTIVE: The objective of this study was to determine if there are electromyographic differences between active and latent myofascial trigger points (MTrPs) during trigger point needling. DESIGN: A total of 21 subjects were recruited prospectively. The experimental group consisted of 13 subjects who had active myofascial pain in the neck for >6 mos. The age-matched, control group consisted of eight subjects without neck pain but with taut bands in the cervical musculature. The active MTrPs (or latent MTrPs in the control group) were identified in the trapezius or levator scapulae muscles, then needle electrodes were inserted ipsilaterally into the muscle with the MTrPs and into the same muscle on the contralateral side. Electromyographic activity was recorded bilaterally with a dual-channel electromyographic machine, and local twitch responses were obtainedusinganacupuncturedryneedlingtechniqueonlyonthesideoftheactiveMTrPs . RESULTS: We demonstrated that in subjects with active MTrPs, bilateral motor unit activation could be obtained with unilateral needle stimulation of the trigger point. In contrast, in all the subjects with latent MTrPs, only unilateral motor unit activation could be obtained in the muscle on the same side of the needle stimulation. The motor unit potentials seen on the electromyograph were similar in morphology to a fasciculation potential but more complex. CONCLUSION: We demonstrated bilateral or mirror-image electromyographic activity associated with unilateral needle stimulation of active MTrPs. We have found no previous mention of this phenomenon in the literature. Our study supports the concept that the perpetuation of pain and muscle dysfunction in active MTrPs may be related to abnormal central nervous system processing of sensory input at the level of the spinal cord.
                      PMID: 15100626 [PubMed - indexed for MEDLINE]
                      Bryan
                      Attached Files

                      Comment


                      • #12
                        Originally posted by Diane
                        Perhaps Kim still doesn't have quite full access.. Bernard??
                        Nope. The thread is located in the Pharos. (accessible to all registered members).
                        Here is the paper ;
                        Attached Files
                        Last edited by bernard; 15-01-2008, 06:51 AM.
                        Simplicity is the ultimate sophistication. L VINCI
                        We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances. I NEWTON

                        Everything should be made as simple as possible, but not a bit simpler.
                        If you can't explain it simply, you don't understand it well enough. Albert Einstein
                        bernard

                        Comment


                        • #13
                          Hi Kim,
                          I'm certain that a palpable joint restriction exists pre-treatment and certain that it doesn't when the treatment is effective. If myofibroblast contraction doesn't account for this, what then?
                          I'm certain of that too. It is very well documented that the pressure of massage has an inhibitory effect on motor neurons. This is easily measured via the Hoffman reflex test. Different intensities and frequencies of pressure have been shown to produce different degrees of tone inhibition.

                          Check out the paper attached.


                          The LTR has been shown to be a particularly unreliable diagnostic characteristic of MTrPs and is no longer considered essential in making the diagnosis. In their recent review, Tough et al. (2007) reported that only 28% of trials on MPS have explicitly used it.

                          How come snapping palpation doesn't result in a therapeutic effect, but dry needling and my technique do?
                          This remains to be demonstrated.
                          Why does the positional change (lengthened vs. neutral/shortened) make a difference?
                          If an LTR can be produced under both conditions, perhaps it doesn't make a difference. Another example of the unreliable nature of this characteristic.
                          Attached Files
                          Luke Rickards
                          Osteopath

                          Comment


                          • #14
                            Bryan, thanks for participating in my musings. This all helps so much.

                            Originally posted by boneill View Post
                            I think there is fairly strong evidence that the twitch is reflex mediated at the spinal cord level.
                            And by what mechanism is the reflex propagated? Some kind of mechanoreceptor is reporting the stimulation - golgi organs? muscle spindles? pacinian corpuscles? I don't know which, but whatever one - it is abnormally sensitive to stimulation. I've found that you don't need to snap hard over a muscle or stick a needle into it to stimulate this mechanoreceptor. Sometimes I barely 'bloop' over the darn thing and it twitches.

                            Joseph Audette published a study on this.
                            Yes, that's the study that I was referring to when I wrote, "strongly suggested that the twitch is a spinal reflex" There are other studies that suggest this too.

                            I dont believe the muscle spindle hypothesis has stood the test of time, but I don't know that literature well.
                            The problem with the previously presented muscle spindle theory is that the researchers tried to prove that the spontaneous electrical activity (SEA) that was recorded at the site of a TrPt was due to muscle spindle activity. I'm suggesting that we might be seeing two different elements within a larger area of dysfunction.

                            Travell and Simons dismissed the muscle spindle hypothesis based on their premise that the contraction knot (TrPt) is running this whole scenario of local dysfunction. They pointed out that the spindle is not in the same location as the contraction knot and that the EMG recordings at the site of the TrPs best match those known for end-plate activity.

                            What if the contraction knot, with its associated dysfunctional end-plate exists, is but a consequence of another governing mechanism, and is not the primary activator? I think we've got two separate, but related phenomenon going on here - 1) a sensitive mechanoreceptor and 2) a contraction knot

                            p.s. I saw your note about contacting Jay Shah from the other TrPt thread. Maybe if you sent him another note mentioning my name (and that I had a poster at the Myopain conference) he might show up. One of his assistants said that he wanted to talk to me at that conference about my hypothesis, but we never got to do so).
                            Last edited by Kim LeMoon; 15-01-2008, 12:18 PM. Reason: added my comment about 'blooping'

                            Comment


                            • #15
                              What if the contraction knot, with its associated dysfunctional end-plate exists, is but a consequence of another governing mechanism, and is not the primary activator? I think we've got two separate, but related phenomenon going on here - 1) a sensitive mechanoreceptor and 2) a contraction knot
                              Interesting.

                              So the next question would have to be; How is the mechanoreceptor sensitivity produced and maintained? The answer must also consider this --
                              Muscle Nerve. 1993 Jul;16(7):693-705.
                              Microneurography and applications to issues of motor control: Fifth Annual Stuart Reiner Memorial Lecture.
                              Hagbarth KE.

                              Among the hypotheses regarding fusimotor functions based on earlier animal experiments some are inconsistent, others are in conformity with microneurographic observations in man. The human data provide evidence against the following two theories: (1) the length follow-up servo theory; and (2) the theory that fusimotor neurons can be selectively activated to produce spindle sensitization and stretch reflex reinforcements. The human data support the theory of alpha-gamma coactivation. In particular, in the early phase of isometric voluntary contractions fusimotor-driven afferent spindle activity assists in autogenetic activation of alpha motoneurons and in reciprocal relaxation of antagonists. As muscle fatigue develops, the autogenetic reflex drive via the fusimotor route declines. The fusimotor bias during contraction provides for maintenance of spindle sensitivity to minute perturbations and for load-compensating reflex adjustments to such perturbations. Reflex overcorrections may lead to uncontrollable oscillations of the type seen in enhanced physiological tremor.
                              Luke Rickards
                              Osteopath

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