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  • GregLehman
    replied
    Matthew,

    I tried to access them but needed a password. They dont seem to be free anymore

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  • Matthew Danziger
    replied
    Well it looks like I'm talking to myself and some people are watching. That's nothing new from the looks I get in the grocery store...

    I listened to this interview with Phil Plisky last night and it stirred some curiosity: http://www.sportsrehabexpert.com/public/870.cfm Has anyone here looked into the research around the Y-Balance test specifically?

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  • Matthew Danziger
    replied
    I've been following along with most of these, but I thought this interview might be of particular interest to many here. At around 40 minutes into the interview Charlie Weingroff speaks about pain science and how (in his opinion) many are misapplying this information.

    For those more on the sports performance side of things I think the first 40 minutes seem like very interesting and high quality information.

    http://www.sportsrehabexpert.com/public/877.cfm

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  • Mark Hollis
    replied
    Interoception, Exteroception and Proprioception
    While they start from separate peripherally innervated sources at some point they also convergently simultaneously 'share/utilize/contribute to activation or inhibition' of common pathways/regions in the central distributed processing part of the nervous system (brain) (somehows/somewheres they co-ordinate contingently dependant upon the external and internal environment).

    So while talking about them as separate systems is possible (but also a necessary reductionism for thinking/communicating about them) then there has to be considered that there will be parts/areas/pathways of the nervous system that are to do with the relationships between their separate impulses (the relationship being different to the object/system/initiator of impulses peripherally (that which is between you and me is not you or me type thinking/contextualising)).

    John W
    I'm confident in saying that there's a general consensus that people in pain demonstrate less dissociation of movement of body segments during various activities.
    And in some parts also more dissociation of movement? Thinking of Paul Hodges work and also the shifting/lateralisation of motor cortex activity on MRI it would indicate both positive and negative features. I know in his 2010 paper that there was both a change intra and intermuscular which sequentially would change alterations both in an increase and decrease.
    Last edited by Mark Hollis; 30-01-2014, 01:12 AM.

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  • Diane
    replied
    Originally posted by John W View Post
    I think it's plausible that the altered movement patterns observed in patients with persistent pain might contribute to altered neurodynamics, which then might result in more nociception.
    It's also plausible that lack of movement, period, contributes to altered blood flow, which instigates below-awareness-threshold nociception, and maybe guarding by the spinal cord, then maybe a feeling of stiffness, which turns into even less movement, etcetc, leading to altered neurodynamics, leading eventually to pain..

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  • Matthew Danziger
    replied
    For those who are interested in listening, the first interview is up today.

    http://www.sportsrehabexpert.com/public/864.cfm

    Welcome to the first interview of the 2014 teleseminar featuring Ron Hruska.

    In this interview Ron discusses how his life experiences have helped him to develop the Postural Restoration Institute (PRI) systems, as well as looking at the interplay between systems and pattern predictability, polyarticular chains and the importance of inhibiting muscles, PRI treatment goals, squat patterning including thoughts on powering the squat through the respiratory system, and a whole lot more..

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  • zimney3pt
    replied
    Originally posted by Greg Lehman View Post

    Its been suggested that the altered movement contributes to nociception. Just as we don't know if there is nociception (there you go Kory :teeth we don't know if the funky movement contributes to nociception. The altered movement could just be a parallel "dysfunction" with pain and not have any bearing on perpetuating it or creating it.
    That's what I don't get about all these methods that are supposedly correcting dysfunctions that are causing nociception. We don't even know if they are dysfunctional or nociceptive, we assume they are because the patient reports "pain". Don't we believe Lorimer when he stated "nociception is neither sufficient nor necessary to create pain". So how can all these people say they understand neuroscience and pain and still teach what they are teaching?

    We say they are abnormal, heck we don't even have a good measuring tool for what is normal or abnormal for all these things such as strength, muscle balance, posture, biomechanics and everything else that is tested in these methods (I give my biggest hat tip probably to Grey Cook because as far as I can tell at least his measurements seem to be reliable and maybe have some validity at least in some populations at being a predictor of increase injury rate but we need lots of research on this before we get to excited). And even if they were abnormal does that mean they need correcting? Read this article if you haven't already and see the mistakes made in other areas of medicine when we went trying to correct things to normal. And these are areas where we at least have good established normal's with valid and reliable testing methods.
    Last edited by zimney3pt; 19-01-2014, 05:34 AM.

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  • John W
    replied
    Its been suggested that the altered movement contributes to nociception.
    I think it's plausible that the altered movement patterns observed in patients with persistent pain might contribute to altered neurodynamics, which then might result in more nociception. Nerves need to move- often through inherently tight connective tissue confines- in order to maintain their very copious need for blood flow, which imparts an adequate oxygen supply to the very busy nerve cells.

    I think it's important to remember that the neuroplastic changes associated with peripheral and central sensitization occur in order to make the nervous tissue even better at warning the organism of danger. To become better at its baseline functioning, it makes sense that the nervous system's metabolic demand along these pathways would need to increase.

    We know, for instance, that a feature of peripheral sensitization is an increase in Na channel expression, which reduces the threshold for depolarization. In some instances, ectopic firing of the neuron occurs along the axolemma (abnormal impulse generating sites or AIGS). Meanwhile, at the spinal cord, microglia are doing their damnedest to ensure that a vociferous message makes its way to the brain by squirting chemicals in and around the synapse between the first and second order afferent neurons.

    I think we have some good evidence of how this occurs mal-adaptively in a relatively dense tissue where there's quite a bit of movement taking place: tendon- in the condition referred to as tendinopathy or tendinosis. Here we see neo-vascularization. It would make sense that these vascular changes in tendon are mediated by the nervous system's increased oxygen demand to make it better at signaling danger to the brain.

    It makes sense to me, then, that the relative stiffness between body segments that have been routinely observed in patients with persistent pain problems reflects an interruption in the motor output that normally follows from a normal/adaptive response to inputs from all three dimension of the neuromatrix, including sensory-discriminative input, which includes nociception.

    It seems reasonable as well that that response is instinctual and therefore subject to interruption from cultural dictates.

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  • Greg Lehman
    replied
    Thanks John,

    You wrote:

    If you go to Pubmed and type in keywords like "low back pain", "motion analysis", "gait" "motor control", you'll get a bunch of hits. That there's altered motor patterns in individuals with pain is not a contentious subject, as far as I know. I'm confident in saying that there's a general consensus that people in pain demonstrate less dissociation of movement of body segments during various activities. I think there's some data out there in the lifting literature as well. I think its reasonable to conclude from this that increased isometric muscular contractions across body segments is associated with this.
    If you do that you'll even come across some of my own publications on the topic. I never denied an association. I just questioned the relevance

    Its been suggested that the altered movement contributes to nociception. Just as we don't know if there is nociception (there you go Kory :teeth we don't know if the funky movement contributes to nociception. The altered movement could just be a parallel "dysfunction" with pain and not have any bearing on perpetuating it or creating it.

    I know Lorimer talks about "facilitating protective neurotags'. - I just don't know how we can say they are protective. It seems we are putting a value (e.g. protection) onto the observation of altered movement, motor control or changes in muscle activation. They might just be secondary casualties of pain.

    P.S read Gandevia - nothing about interoception there. Also read a paper by Bud Craig on Interoception. He never mentioned proprioception. Sherrington seems to list Interoception, Exteroception and Proprioception as separate.

    Leave a comment:


  • John W
    replied
    Greg,
    I'm not sure if that reference is even in this thread- it may be in that other thread that talks about this thoracic ringy thingy.

    If you go to Pubmed and type in keywords like "low back pain", "motion analysis", "gait" "motor control", you'll get a bunch of hits. That there's altered motor patterns in individuals with pain is not a contentious subject, as far as I know. I'm confident in saying that there's a general consensus that people in pain demonstrate less dissociation of movement of body segments during various activities. I think there's some data out there in the lifting literature as well. I think its reasonable to conclude from this that increased isometric muscular contractions across body segments is associated with this.

    You might need to acquaint yourself with the "Advanced Search" features here to find a specific post from a specific person. :angel:

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  • zimney3pt
    replied
    Greg or others, how do we know something is nociceptive? Clinical how do we measure nociception?

    Sent from my VS840 4G using Tapatalk
    Last edited by zimney3pt; 19-01-2014, 05:13 AM.

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  • docjohn
    replied
    So this is all attributed to "pain" sensation only. Is that correct? Not other sensations of "tingling", "burning", "numbness", "coldness", etc? Just persistent pain (dull achy, sharp debilitating, all types?).

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  • GregLehman
    replied
    PS: what post number did you cite a study. I looked back over the past 50 and didn't see it

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  • GregLehman
    replied
    Hi John,

    Well written explanation. I agree with it. But I'm not sure how you got to this thought:

    Greg, you seem to be reasoning from the periphery and trying to deduce your way up to the spinal cord and then I guess to the brain. It's not a linear process.
    Not at all. I recognize all of the other factors in neuromatrix. I'm not viewing the brain as a projector of the periphery. I recognize it can be both a creator and modulator of an abnormal neurodynamic.

    What I was discussing was the common explanation given for the persistence of nociception. I never meant to imply that nociception should be mistaken for pain. Or nociception viewed completely in isolation.


    You had even previously written:

    The compression/tension of blood vessels description isn't quite consistent with the concept of an abnormal neurodynamic. The tension/compression is of the nervous tissue itself, which results in altered motor output/isometric muscular behavior, which then leads to vascular compromise of the nervous tissue in the region.
    Obviously, this isn't a linear process but it seems to hold some weight on SS being a possible factor/contributor to pain. It certainly seems to be significant part of what DNM hopes to address. (along with numerous other things)


    In regards to "altered motor output/isometric muscular behaviour, which then leads to vascular compromise of the nervous tissue" I agree that there might be a few studies showing that people occasionally move differently from people without pain however, this is very inconsistent. The EMG studies don't support a consistent change. Those studies showing kinematic changes only report on the joints that showed differences. No one ever highlights all the joints that showed no kinematic differences.

    Further, you call these inconsistent differences Defects. While I think that might occur some time I don't know why those movement differences or motor control differences would actually create hypoxia to a nerve. If those differences exist, they are only that, Differences. There is nothing inherently aberrant about the motor control. Slightly more motor activity? Who cares, there is a huge variation across people and why would more cause a problem?

    Last, those differences could just as easily be viewed as Red Herrings instead of Defects. We see this when the pain resolves and the abberant motor control persists.

    I hope this makes sense. I'm not ignoring the brain. I'm just questioning this nociceptive story that seems so prevalent.

    Why can't the nerves just be sensitized? Why does there even have to be tension/compression or ischemia? I was under the impression that Butler was moving in this direction anyway. Away from altered tension and more into the neurodynamic being a window into nervous system sensitivity. Please correct if I'm off here.

    Thanks,

    Greg

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  • John W
    replied
    By the way, there is tons of evidence of defensive motor output in persistent pain states. I cited a recent study earlier in this thread. There are dozens of studies like that. If you look more closely and critically analyze most of the motion analysis literature in subjects with pain, what has been interpreted as defect is more reasonably identified as defensive behavior.

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