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Old 31-08-2008, 02:39 PM   #1
Barrett Dorko
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Default The Edge of the Spoon

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Magicians take advantage of glitches in the brain. They know that it constructs a model of the outside world from moment to moment and then refers to it as “objective reality.” Anyone is fooled by the rapid tilting of a spoon when it’s held by its neck and made to appear as if curving or bending without due provocation. The glitch this time is the disparity between end-stopped neurons in the visual cortex and other motion sensing cells. The edges of the spoon are then warped, and our estimation of where they lie results in an objective reality that is untrue.
This is something I want to say to a large audience one day. In my mind’s eye I’m standing on a tall podium and I’m being projected on screens behind and above me; a spoon in my hand. I look pretty good in my nice suit and all. I appear calm and clear about what it is I’m going to say next. These are further illusions I don’t bother to mention.

I got the bit about the visual cortex from a recent New York Times article titled While a Magician Works, the Mind Does the Tricks. I know it’s been linked on this board somewhere and yes, I used the search function - but I can’t find it. I know that someone will, given the generosity inherent to Soma Simple. I would also like to point out that my apparent skill at computer manipulation is yet another illusion.

When I read the thing about the edges of the spoon my mind turned to a very famous line from the movie The MatrixThere is no spoon. Google that and see where it takes you.

I’m beginning this thread today because I know that many clinicians seek a demarcation when either none exists or, because our brain is a kluge, we cannot accurately perceive it.

Two “edges” we would like to see and define with descriptions that lead to some assurance are those between acute and chronic pain and peripheral and central mechanisms leading to the output of pain from the brain itself. A discussion regarding these terms and what we now know about their confusing and counterproductive affect on practice should follow and draw interest toward some other threads here I have found wonderfully illuminating.

I’ve some more ideas, but, as always, I’m interested in yours.
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Old 31-08-2008, 03:38 PM   #2
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Here is a link to the Aug 11 article in NYT, While a Magician Works, the Mind does the Tricks.

Here is a link to the Neurophilosophy blogpost (Aug 7) by Mo, which uses the same illustration: The cognitive neuroscience of magic.

Here is Deric Bownds Mindblog post (Aug 15) about the NYT article, The Mind Does the Trick for the Magician.
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Old 01-09-2008, 02:39 AM   #3
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Well I'll see what I can do to start some discussion.

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Two “edges” we would like to see and define with descriptions that lead to some assurance are those between acute and chronic pain and peripheral and central mechanisms leading to the output of pain from the brain itself. A discussion regarding these terms and what we now know about their confusing and counterproductive affect on practice should follow and draw interest toward some other threads here I have found wonderfully illuminating.--Barrett Dorko
(emphasis mine)

Recently Luke had posted a paper titled The Kyoto Protocol of Basic IASP Terminology.(No not that Kyoto Protocol)

A short thread developed that you can read here

I was decidedly confused about some of the terms at the time I participated in the thread and have since digested some of the material. One thing I missed on my first passing was the very narrow use of the word allodynia. From the paper.

Quote:
This term should only be used, when it is known that the test stimulus is not capable of activating nociceptors. At present, dynamic tactile allodynia to tangential stroking stimuli, e.g. brushing the skin, is the only established example. Future research may present evidence for other types of allodynia. Whenever it is unclear, whether the test stimulus may or may not activate nociceptors, hyperalgesia is the preferred term.
(Emphasis mine)
I'm not sure that this is on the right track for this thread but it's what I've got right now.
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Old 01-09-2008, 03:26 AM   #4
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Jon,

As always, I appreciate your effort. For what it's worth I thought Luke's thread didn't receive the interest it should have - including from me. Maybe this will push others there.

The first demarcation I have found confusing, counterproductive and useless though referred to continually is that between acute and chronic pain. As John Ware mentioned in another thread recently the neuromatrix (matrix - ironic, huh?) theory pretty much obviates the need for this distinction. I think I need John to help me out here though. Hello John?

Anyway, when therapists say "acute" they commonly confuse its meaning several ways. It may mean "recent" or it may mean "severe" and, in my experience, many therapists think it implies injury. I don't know what they mean so I ask them several questions to which they eventually respond with, well, something less than interest is talking to me further.

When does acute become chronic? What characterizes the edge of this spoon?
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Old 01-09-2008, 04:13 AM   #5
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Quote:
When does acute become chronic?
Depends on the source of information. The current definition seems to be pain becomes chronic after three months duration.
Butler stated years ago that there may be no difference between management of the two states but general recognition of that aspect is a long way off. He verbally went on to say that a chronic phase, even if latent, could be as early as 7-10 days post-pain event.

As for the edge of the spoon, that is a good question. What makes one person recover from "acute LBP" in 5 days, and another person remaining in pain a year later??

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Old 01-09-2008, 04:24 AM   #6
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When does acute become chronic? I’d ask, “who cares?” I’m starting to see the effort that goes into this pigeon holing does little to inform the management of the problem. It’s on par with nominal diagnoses you’ve written about before. The focus on acute vs chronic has probably obscured the consideration of more useful categorizations in both practice and research.
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Old 02-09-2008, 12:44 AM   #7
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Eric, that's true. But to convince others to forego labels and time parameters is like swimming in treacle. They do care about such things and build all sorts of constructs around acute/chronic labels and nominal diagnoses in order to extract from their core storage knowledge of management. It's two week old LBP, therefore I will do this and this, etc.
It's treat the symptoms, not the process.
That's an exaggeration, but not too far from the truth. Whatever a 'truth' is..

I had figured hyperalgesia was a strong response to a moderate stimulus (eg injections into a sensitive area) whereas allodynia was an abnormal and intense response to a minimal or negligible stimulus, such as a brush with a feather. The latter is a neuropathic response?

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Old 02-09-2008, 02:55 AM   #8
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I think that in the immediate experience of pain, the "acute" pain, the seed is always sown for the development of "chronic" pain.

I tend to only use the term "persistent" instead of chronic - to indicate that the pain experience has passed its possible temporal relationship with any potential tissue damage.
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Old 03-09-2008, 01:04 PM   #9
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We seem to be in agreement regarding this issue of acute and chronic, so let's move on.

I am borrowing heavily here from Diane’s post here, including the brilliant writing by Shacklock attached there. I want to approach the subject of peripheral and central mechanisms from this “edge of the spoon” perspective and hope to gain some insight by writing about it and listening to others.

Pain mechanisms are of two general types: peripheral and central. The former has been the focus of therapy throughout my career (a long time) but, amazingly, the concept of neural tension as a common problem hasn’t made much of a dent in the minds of most. I would know. If we were to add this, many problems might finally make sense, I think, and solutions could then be discussed reasonably. That time seems to be a way off, however.

Furthermore, there will still remain this question from many: What percentage of the problem can we reliably consider the result of a central mechanism and what tells us that?

Your turn.
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Old 03-09-2008, 02:58 PM   #10
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I was thinking that acute pain is more readily associated with tissue damage and or potential there of. Perhaps there is the perception that a persistent pain situation may go into an acute phase when it may be better described as a 'flare up' of the persistent pain symptoms.

Quote:
What percentage of the problem can we reliably consider the result of a central mechanism and what tells us that?
Isn't the interpretation of an experience or state of pain always a central one?

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Old 03-09-2008, 04:14 PM   #11
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Chance,

The first part of your answer is a wonderful example of how confusing and personally idiosyncratic these terms have become - nearly to the point of uselessness. Tell me, what does chronically and recurrently acute pain mean?
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Old 03-09-2008, 04:14 PM   #12
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But tissue damage does not cause pain when the nociceptive signal to the brain is interrupted. I.e. with epidural. Pain is always central.
I am trying to get my head around "the problem" that Barrett mentions in the his bolded sentence.
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Old 03-09-2008, 04:36 PM   #13
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Quote:
Tell me, what does chronically and recurrently acute pain mean?
Intermittent persistence.
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Old 03-09-2008, 04:37 PM   #14
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Quote:
I am borrowing heavily here from Diane’s post here, including the brilliant writing by Shacklock attached there.
Actually Barrett, you linked to the paper, not to anything I might have written (brilliant or not brilliant..).
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Old 04-09-2008, 02:24 AM   #15
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Bas,

Perhaps I should restate that. Once I make it clear that the output of pain (the "problem") is the consequence of two mechanisms working in concert, most therapists will want tests that delineate one from the other. They will want some idea of how much each contributes so that they might devise a strategy to oppose it.

In other words, they'll think as therapists commonly do, in my experience.

What to do?
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Old 04-09-2008, 02:55 AM   #16
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Isn't this the old mind-body separation belief?
Break a leg: pain, trauma, loss of function. Peripheral problem, treat peripherally. Even if it is recognised that pain originates in the brain, the analgesics take care of that. Mobilise as per protocol, and exercise.
Fairly straightfoward peripheral issue, unlike CRPS...
Until Oliver Sacks woke up one morning, (A Leg to Stand On) lost all contact with his ex-broken leg and wrote about it.

What do we do? I think we have been trying for some years to clarify the peripheral/central thingy in the clinical scene. It's only when outcomes are not what PTs expect that central issues are considered. And moreover, the answer is still 'psychosocial', although I wonder how this gets categorised...

Warning: Anecdote...
My daughter in another state recently attended a highly-regarded PT for ongoing cervical-shoulder-ribcage pain. It has been intermittent since 1993 when she crashed on rollerblades. She was told that the tissues haven't healed and need 'healing' by taping for support, and specific exercise. She may well get better, but the words 'sensitivity' and 'defence' will not enter the dialogue, I'm sure. (As to why I haven't 'treated' her - one doesn't educate members of one's family- it's doomed for cynicism).


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Old 04-09-2008, 03:07 AM   #17
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I've started treating the few recent fractures I see as if the pain is of central origin. I the use light skin stretches for lymph drainage to calm the pain before I do anything else. Works like a charm so far. So much nicer for the patients than passive or active stretches of stiff joints. (It's so calming, I find myself nodding off at times.)
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Old 04-09-2008, 03:13 AM   #18
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Ah. Thanks for that, Barrett.

Funny that patients "get" this so much easier than many PTs. Lack of pre-drilled holes, filled with pre-chewed facts, I guess.

Leading them away from too much deductive reasoning may require quite a feat: completely changing a focal point of their brain/mind attention. Present deductive thinking is SO mired in detail (details=knowledge in which PTs take great pride), and a simultaneous fear for complexity or chaos, that it is ripe for a magician to dazzle them.

Re-setting the minds into a different mode of "looking, thinking, and seeing" will require a more profound (earthquake?) shake.

When I talk to patients or insurance-agents about pain, I have to always begin with the basics. I suggest "pain is a personal neurological experience" that is seamlessly tied in with input from and output to the body. That it can vary form one day to the next, that stress can affect it enormously, that it can cause fear and fear can cause more pain behaviours which can cause more sensitivity to pain ..... Thankfully I have articles like Shacklock's to refer to.

The hardest group to convince of the fuzzy neuromatrix approach to pain - any pain - acute or "chronic" - are my colleagues, who have a knee jerk reaction to pain. Still, in this day and age; "I treat dysfunction, NOT pain."
These are the ones who will HAVE to have tests for the central and peripheral "components" - to unravel the little parts and assign values to each part. This type of thinking is how we were and are taught. Despite improvements - it still prevails.

Ooops. A free association moment.
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Old 04-09-2008, 03:21 AM   #19
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Do you think that central and peripheral are mistaken in that they are attempting to use a description of a place when a description of a viewpoint would be more useful? Wouldn't bottom up and top down be a better description as it described the place from which you are viewing? Some scenes you can see better from above and others from below, but the top and bottom exist in both situations.

More on top down/bottom up processing.
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Old 04-09-2008, 03:38 AM   #20
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Bas, great post. Way to free associate.
BB, great link to stroop test. Loved this bit:
Quote:
In fact this effect is so reliable that it has been used to catch spies. If a Russian agent is pretending to be American they can be tested to see if they exhibit the Stroop Effect for Russian words. If you cannot read a language, there will be no delay; if you can then you cannot avoid the delay.
I think (regarding the peripheral/central issue) that it's important to remember that everything from dorsal horn in is central processing.
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Old 04-09-2008, 03:42 AM   #21
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Quote:
What percentage of the problem can we reliably consider the result of a central mechanism and what tells us that?--Barrett Dorko
Barrett, your clarification

Quote:
Once I make it clear that the output of pain (the "problem") is the consequence of two mechanisms working in concert, most therapists will want tests that delineate one from the other. They will want some idea of how much each contributes so that they might devise a strategy to oppose it.--Barrett Dorko
helped and reminded me of the following quote

Quote:
Whether a placebo-controlled trial can assess the contribution of various treatment components rests on the assumption that each treatment component has an additive effect. Only on this additive model can the observed effect be thought to be constructed from a series of components, each adding a discrete proportion of the observed efficacy. Treatment components may, however, have a more complex relationship. For instance, psychological and physical effects may interact with one another. An optimistic outlook may enhance the efficacy of a physical effect, and a physical effect may buoy a patient's optimism that a treatment is in fact working. This multiplicative relationship between treatment components would tend to undercut the ability of a trial to focus on particular components in isolation.
From this paper
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Old 04-09-2008, 01:03 PM   #22
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Jon,

Wonderful quote, and right on point here. Often I have to decide these days whether or not to bring a patient to the department or treat them in their room. In the late AM I find the environment among others (including staff) potentially threatening though it may happen that the possible encouragement from other patients will be lost if I don't bring them in. I also have to consider the day of the week and which staff may or may not be nearby.

This is all part of the clinician's art, I think, and, like all art, its effect may be unknown to the one controlling its expression.

I like Cory's "bottom up and top down" terminology and wonder if a therapist might craft a story to illustrate this complex relationship between mechanisms. As always, we need a story. Any ideas are appreciated.

I was recently asked, "How do we know that neural tension exists and if it does when does it become clinically significant?" I could easily point to a couple of books but isn't there a study out there about the rapid and significant effects of tension and blood flow in the nerve? Something I can rattle off as if I always knew it?
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Old 04-09-2008, 02:16 PM   #23
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Quote:
Still, in this day and age; "I treat dysfunction, NOT pain."
Gosh, not only is this pervasive, but it's emphasized to the Nth degree. I think most manual texts I've got (biomechanical as they are) and many course descriptions ALWAYS give this statement in some form or another.

You mean, I'm supposed to help their pain issues, too??!! Ugh!
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Old 05-09-2008, 04:50 PM   #24
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Quote:
I could easily point to a couple of books but isn't there a study out there about the rapid and significant effects of tension and blood flow in the nerve? Something I can rattle off as if I always knew it?
I'm still looking for such a paper myself.
Maybe Shacklock's book will list one or several..
Meanwhile, I did a search for nervi nervorum lately, and found papers by Lundborg (from the 80's, not online) which look promising. I think his name cropped up quite a lot in both Shacklock and Butler's books.

One that I was able to get was Rat Peripheral Nerve Components Release Calcitonin Gene-related Peptide and Prostaglandin E2 in Reponse to Noxious Stimuli: Evidence that Nervi Nervorum are Nociceptors.
Not a very catchy title, I'm afraid..

Link.
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“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

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Old 05-09-2008, 05:22 PM   #25
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Her is another by the same researcher, June 2008:
Sensory transduction in peripheral nerve axons elicits ectopic action potentials.
Link.
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"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

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Old 05-09-2008, 07:16 PM   #26
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I could easily point to a couple of books but isn't there a study out there about the rapid and significant effects of tension and blood flow in the nerve? Something I can rattle off as if I always knew it?
Barrett,

Here's what you are looking for (and much more).
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Old 06-09-2008, 10:26 PM   #27
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What percentage of the problem can we reliably consider the result of a central mechanism and what tells us that?
It was in the "Thoracic Manipulation" thread that I re-posted my comment from the EIM debate about cervical manipulation. That comment addresses Melzack's concept of the pain "neurosignature," which is the output from the pain neuromatrix. Whether the neurosignature is adaptive or mal-adaptive, I think is the relevant question, not how long the neurosignature has been churning out from the neuromatrix. For those of us who treat pain of any kind, temporal demarcations have proved essentially useless, and as Barrett aptly stated are "personally idiosyncratic."

I suggested making a determination of the level of central sensitization as a clue to the risk or presence of a mal-adaptive pain neurosignature. Luke then brought in the concept of "long-term potentiation", so I'll defer to his deeper knowledge of the literature on this as to which would be a more useful "marker" to predict risk or identify current presence of mal-adaptation to pain. I think trying to predict mal-adaptation from just a psychosocial perspective may, and based on my experience has, resulted in a lot of false negatives. There are lots of apparently "low-risk" patients who end up with persistent, mal-adaptive pain, nonetheless.

To answer the question that Barrett originally asked: I think that the percentage of contributions are so dynamic and there are such complex feedback loops from the stress-regulation component, that identifying a distinct proportion contribution of central mechanism influences on the pain neurosignature is a very tough target to hit, indeed.

Sorry about my late arrival to the conversation. I was feeling crappy.:sad:
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Old 06-09-2008, 10:58 PM   #28
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(Aha. This is the thread where Barrett asked for a paper.
Here's a link to Rempel's paper.)

About percentages, I'd guess... oh... I don't know... maybe 100%?

Nociception does not equal pain, I think that is clear by now. To many anyway. Although I could be wrongo on that...

Pain is a response by CNS to incoming (usually), not the actual incoming, furthermore it can be generated strictly from within the CNS sometimes...

Here is a link to CNS mechanisms of pain control.

Glad you're feeling better John.
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Old 07-09-2008, 12:16 AM   #29
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I'm gaining a greater appreciation for history although there is so much new information that going backwards feels like I'm losing ground even if that's exactly what would help. For those with some interest, here is my first encounter with the Rempel reference.

The conversation took place seven years ago and is notable for the general tone of agreement amongst the posters.

Are we there yet? Are we there yet? Are we there yet?
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Old 07-09-2008, 12:24 AM   #30
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Jon, you are a funny man. You are also a man with a memory an elephant would envy.
Butler:
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Most of us (me incl) were not given any neurobiology or related subjects during undergraduate training, just a hint of physiology. Maybe neurobiology wasn’t invented back then. Biological knowledge stopped once you had cut up the poor rat. Yet molecular biology/neurobiology/neurochemistry MUST become a foundation subject for manual therapy. This is critical – it drives creative clinical thinking and research and as so many professions have/will require knowledge from this area it can bring diverse ideas and professions together. This same issue has been pushed by the IASP. And the teachers have to get used to the new concept of a dynamic subject - unlike anatomy and biomechanics there are knowledge revolutions occurring almost daily in neurobiology.
Barrett mentions the word “interlocking” in relation to theories. Its important for research groups and professions as well. In physical medicine, “blobs” of research/concepts/ideas even professions, exist in a three dimensional void, awaiting linkage. Three examples – the epidemiological research, often driven by psychologists seems to go on a parallel pathway to the neurobiological research. For example, we know that fear of pain/reinjury is a predictor of outcome/chronicity, yet we also know the neurotransmitters, CNS areas involved and we know the potentially destructive nature of the stress chemicals. Research groups don’t seem to relate. Secondly there is a lack of “between level” understanding. For example, to my mind the two best pieces of writing on peripheral nerve pain are the chapter by Devor and Seltzer in the 1999 Textbook of Pain and a review article by Rempel et al in JBJS (81A, 1600). The authors don’t mention each other – one group is existing at molecular level and the other at tissue level. Other research/discipline blobs floating around which have just made contact include stress biology and pain science and the immune system with the nervous system.
Manual therapy floats around like an blob in the chaotic mess of physical medicine. Unjoined, unlinked, each idea, profession/research area “must endure the crucible of skepticism, experimentation and a host of competing theories (BD)”. There has never been a better time for a professional shift. How do we make it happen?
Yup, there it is.
And years later, manual therapy is still a "blob," floating around in the "chaotic mess of physical medicine."
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Old 07-09-2008, 01:33 AM   #31
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You are also a man with a memory an elephant would envy.
Thanks Diane. It's search function enhanced to be sure. I remembered reading the article, not Rempel or the title of the article per se.
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Old 07-09-2008, 02:55 AM   #32
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Last month's Skeptic magazine had a review called A Mind of Its Own: How Your Brain Distorts and Decieves called The Matrix of the Brain.

The reviewer states: "Although we like to think of ourselves as rational beings, our brains covertly strive to create for us a view of the world that and of ourselves that is self-serving but not necessarily consistent with reality. Beliefs and opinions are formed quickly and become part of how we define ourselves, so the brain selectively perceives and recalls evidence that supports cherished beliefs while disregarding or forgetting evidence that contradicts our beliefs." The author, Cordelia Fine, calls this "motivated skepticism."

The reviewer continues: : It would seem that going through life deluded by our own brains would not be a good thing, but that is not necessarily the case. Some people have markedly more balanced self perceptions than normal people - they know clearly what their limitations are and how little control they actually have over their lives." ...

"Life is pleasant inside the virtual reality of our minds. So what if we think we are more intelligent or virtuous than others and believe we are more in control than we really are? Such minor self-deceptions are, for the most part, harmless, and they may help us get through the day. But we are not necessarily prisoners of our minds. When the deceptions become harmful to ourselves and others, there is a way out. Science gives us a way to unplug ourselves from the Matrix of out brains."
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Old 07-09-2008, 03:36 AM   #33
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I appreciate all the thoughtful contributions to this thread and hope to make it a regular reference for others hoping to understand more about the patient in front of them. In fact, I think it emphasizes how much more important understanding is than skill. Perhaps not knowing how these two mechanisms exist and interact is common but it may easily lead to haphazard care.

Aside from the moving target this edge between peripheral and central gives us, the absence of a linear relationship between the size, intensity, severity or drama of the peripheral mechanism and the intensity of the brain's output of pain is something that needs further illumination and discussion. In my experience, therapists have great difficulty believing that could be true.
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Old 07-09-2008, 01:57 PM   #34
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Why do you suppose we're taught: "don't chase pain, treat dysfunction"?

I've heard that at more than one course, the rationale for which seems to go something along these lines: if you "treat" pain, you'll just keep chasing it and never "solve" the problem.

Why would this be so?

I would guess that if polled, the majority of patients would agree that they would rather have their pain diminished/resovled more so that have me "fix" a dysfunction that I "found."
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Old 07-09-2008, 02:12 PM   #35
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Nate,

Paris began to articulate his "treat the dysfunction, not the pain" meme while I was working for him in Atlanta in 1976. What we had at the time was a perfect storm of ignorance, intimidation and charisma. Our colleagues never objected that I can recall and Ola Grimsby, whom I was teaching with at the time, went right along. So did I.

I recall thinking years later while in my own tiny practice that this attitude would be really hard to maintain if one were faced personally with patients every day. That's where I ended up but, to my knowledge, Paris and Grimsby did not. My patients made it clear that it wasn't enough, and I listened to them.

These days I speak to therapists working in virtually identical situations across town from each other. One will claim that pain is a major problem in their patients and the other that it is minor. A little careful questioning always reveals the same thing - the latter practitioner just doesn't ask about it.
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Old 07-09-2008, 02:58 PM   #36
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If we use Moseley's approach, are we not treating dysfunction?

When we use Diane's approach, are we not treating dysfunction?
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Old 07-09-2008, 03:40 PM   #37
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Usually pain is the dysfunction.
The Paris Proclamation was a mesodermal meme.
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Old 07-09-2008, 03:55 PM   #38
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Marci,

Perhaps the question should be: What is a relevant dysfunction and how did you determine that it was present?

Early in my career I was armed primarily with notions about function and pain that proved untrue. Among other things (stiff spinal joints could be reliably assessed and blamed for painful movement, for instance), I had made A Big Mistake (as explained in the link) and didn't initially know where to turn to correct that. Breig's work righted me initially and then a plethora of others chimed in.

I am treating dysfunction, just not the stuff I thought I once was.
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Old 07-09-2008, 05:35 PM   #39
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As Barrett and Diane stated, it is a very stubborn meme, that likely persists because it rang juicily "right" for the insurance companies, for the mechanically oriented PTs (and there were lots), and for the PTs who just did (and DO) not know what to do with the idea/concept of pain.

Especially when a clear tissue related pathological link was absent.
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Old 07-09-2008, 09:31 PM   #40
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I think it was taken from the D.O.'s Mitchell used to say: Pain is a Liar....
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Old 07-09-2008, 09:50 PM   #41
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I think it was taken from the D.O.'s Mitchell used to say: Pain is a Liar....
All those memes... I remember them well. The ones who taught them had no access to pain science.
I wonder what the excuse is nowdays? It's not like pain science hasn't been updated by now...
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Old 07-09-2008, 10:23 PM   #42
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Barrett said
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Perhaps the question should be: What is a relevant dysfunction and how did you determine that it was present?
Painful, stiff, fusiform IP's = severe hand dysfunction.
If I treat the pain first, the rest improves without further treatment.
Swelling decreases over several treatments, as well as stiffness.

I want to say that the pain was the "relevant" dysfunction.
The actual relevant dysfunction (RD) could be inflammation, but IMO the decrease in pain is too fast for this.
Or the RD could be stiffness. Both UQ's lack ROM and the neck is caught in between.
Since the intervention consisted of gently stretching the skin of the arms, I don't see how this could directly affect the IP's.

I gotta get this right. I'm presenting a workshop end Sept.

Last winter I saw one report on fMRI's of patients with arthritis. Their pain was being processed in the emotional centers (as opposed to the somatosensory cortex.) So I now wonder if the RD is the manner in which the patient processes the pain.

Just because it works... Not enough any more.

I'd like to see the fMRI's taken with only the patient's head in the machine and a PT working on the skin. Might answer a few questions. Or is there another way to analyse brain activity?
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Old 07-09-2008, 10:34 PM   #43
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Hi Mary,
Here is a link to a bunch of threads on autonomics in skin nerves/skin. You might find some ideas in there helpful.
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Old 08-09-2008, 02:41 AM   #44
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Quote:
'd like to see the fMRI's taken with only the patient's head in the machine and a PT working on the skin. Might answer a few questions. Or is there another way to analyse brain activity?
I'd be interested in a study like this as well. Perhaps someday, fMRIs could be used like BP, cholesterol/triglyceride levels and other lab values in determining risk of heart disease to provide a baseline to show risk of developing mal-adaptive (I'm starting to like that term more than "chronic" or even "persistent") pain. Perhaps baseline cold pressor testing or even visualization/imagination of standardized painful experiences could be performed under brain fMRI for individuals who have been determined at risk based on genetic/family history information and/or presence of significant psychosocial variables. This information could be used to provide more timely and appropriate pain interventions for such individuals in order to prevent the mal-adaptive pain experience.
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Old 08-09-2008, 02:49 AM   #45
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John, I think the mal-adaptive pain can be detected in the very early stages by any observer. IMO we need this type of research to get those observers to pay attention to this type of pain instead of saying-"oh, it will go away with these (pills, whatever.)"

I think we physios should be the front line people most likely to catch this type of pain. ER nurses and md's are another group.

I would also like to see one of those nice, clear cut "decision trees" for dealing with it.

Guess we have a ways to go.
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Old 08-09-2008, 02:52 AM   #46
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I begin my classes by speaking of the importance of origin (there are four) and how it is important to distinguish this from cause (these are infinite in number).

Now I’m planning a section on mechanism and will of course speak of the two we’ve discussed, making sure that the therapists understand that there is no edge. Heck, I’m not even sure there’s a spoon.

Anyway, it occurs to me that I will be asked at some point what the difference between origin and mechanism may be.

How would you guys approach an answer?
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Old 08-09-2008, 03:03 AM   #47
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Melzack has said the following

Quote:
First, a matrix is defined as “something within which something else originates, takes form, or develops.” This is exactly what I wish to imply: the neuromatrix (not the stimulus, peripheral nerves, or “brain center”) is the origin of the neurosignature; the neurosignature originates and takes form in the neuromatrix. Although the neurosignature may be triggered or modulated by input, the input is only a “trigger” and does not produce the neurosignature itself.
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Old 08-09-2008, 05:56 AM   #48
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Anyway, it occurs to me that I will be asked at some point what the difference between origin and mechanism may be.
The former is somewhere, the latter is something. To get somewhere, a journey is undertaken. To get something, a goal must be identified. Whether that object has been sought as opposed to stolen or contrived can be difficult to discern. On the other hand, a quest is a much more difficult thing to steal or fake because there are so many signs and markers along the way (laid by earnest predecessors) that will betray whoever attempts to mislead.

The effort by many in manual therapy to trumpet outcomes, results and the "cause of dysfunction" has been an elaborate, if not contrived, description of objectives, while completely discounting the means by which they were "discovered." Whether there's real discovery, then, becomes a shell-game of mathematics and statistics.

Ask yourself the same question with each of these words inserted:

"What is the mechanism of a river?"

"What is the origin of a river?"

Now, which question is meaningful and has an answer that requires a journey of discovery, and which contains a compilation of multiple facts and phenomena that don't necessarily lead anywhere?

Which question lends itself to story?
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Old 08-09-2008, 01:22 PM   #49
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Quote:
Early in my career I was armed primarily with notions about function and pain that proved untrue. Among other things (stiff spinal joints could be reliably assessed and blamed for painful movement, for instance),
Again, this reminds me of one of my labs in school, where we were "assessing" spinal movement. Granted, I feel now the professors were not very proficient themselves in this task, but still, I went along with the "oh yeah, I can feel this 1/16th of a motion beneath all this tissue and muscle"...uh-huh, sure.

Quote:
What is a relevant dysfunction and how did you determine that it was present?
Relevent, to me, is the patient's presentation. If it's painful for them to perform motion/movement "X", then that's it. Who am I to tell a patient, "No, I'm sorry, I know you thought that was your problem because it hurts, but actually your problem is a stuck facet at C4-5."

No wonder I would get these bewildered looks.
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Old 08-09-2008, 02:46 PM   #50
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Originally Posted by John W View Post
The former is somewhere, the latter is something. To get somewhere, a journey is undertaken. To get something, a goal must be identified. Whether that object has been sought as opposed to stolen or contrived can be difficult to discern. On the other hand, a quest is a much more difficult thing to steal or fake because there are so many signs and markers along the way (laid by earnest predecessors) that will betray whoever attempts to mislead.

The effort by many in manual therapy to trumpet outcomes, results and the "cause of dysfunction" has been an elaborate, if not contrived, description of objectives, while completely discounting the means by which they were "discovered." Whether there's real discovery, then, becomes a shell-game of mathematics and statistics.

Ask yourself the same question with each of these words inserted:

"What is the mechanism of a river?"

"What is the origin of a river?"

Now, which question is meaningful and has an answer that requires a journey of discovery, and which contains a compilation of multiple facts and phenomena that don't necessarily lead anywhere?

Which question lends itself to story?
John,
That is some of the best stuff I have seen you write...excellant post
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