The Edge of the Spoon

[Barrett Dorko]

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 Matrix – There 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.

[Diane]

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.

[Jon Newman]

Well I'll see what I can do to start some discussion.

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.

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.

[Barrett Dorko]

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?

[nari]

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??

Nari

[EricM]

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.

[nari]

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?

Nari

[Bas Asselbergs]

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.

[Barrett Dorko]

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.

[Chancellor Mobley]

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.

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?

Chance

[Barrett Dorko]

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?

[Bas Asselbergs]

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.

[Chancellor Mobley]

Tell me, what does chronically and recurrently acute pain mean?

Intermittent persistence.

[Diane]

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..).

[Barrett Dorko]

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?