What's the mechanism?

[PatrickL]

I think it would help me, because I am offering the client the whole picture, im not leaving anything out, which is important to me. I have to be comfortable with my explanation. If I'm not, I think my patients will smell it and the interaction will fall to pieces. And that will to the patients detriment.

[Diane]

And, how will you explain it to your patient?

[PatrickL]

Just as you have suggested

1. Injury = nociception, this doesn't equal pain, they equal warning signals
2. The warning signals get relayed to the brain
3. The brain decides if they are a big deal or not, whether the signals are really threatening
4. The brains evaluation of threat depends on a whole bunch of factors that can over rule the warning signals. Or can amplify the warning signals
5. Pain results with amplification, pain is less if dampening

[Diane]

6. The brain can also make pain without their having to be any nociception, e.g., phantom pain in amputees, and the brain can also not make pain if there is something
a) more threatening in the environment, e.g., a bear, which will make you not even feel nociception from the sprained ankle it makes you run away from the bear on.
b) more interesting in general

(Actually, I usually just skip to point 6, myself.. )

[PatrickL]

Yes, thanks Diane. Step 6 needs to included, to account for those circumstances where there is no nociception e.g. phantom limbs pain. But in every other clinical encounter, by your own admission, nociception is present to some degree. You may recall your drip drip drip description? So it makes sense to me to describe the process of pain resolution as the disintegration of one or more of the perfect storm of factors that led to its emergence in the first place, including the top down dampening of nociception. If i leave this part out I am being selective in my description of those factors that can contribute to a pain experience.

Unless the client has phantom limb pain, I think that I owe it to the client to explain steps 1 and 2, because as long as the client has limbs, those limbs relay nociception. If we skip to step 6, we are saying that pain boils down only to brain maps and virtual bodies. This concept seems to resonate very strongly with you. But we live in a real body, and as far as pain is concerned, nociception seems to me to be the link between the virtual body and the real body. I think this is why it gets so much debate... It links the virtual to the real. I think it's up to the client to decide how relevant their real body or their virtual body is to their own experience of pain. I see that it is my job to provide them with all the info i can to allow them to decide for themselves. Having said that i still frame my explanation in away that leaves the brain as having the final say. My read on your approach, is that you are trading 'completeness' of your explanation to fit your construct, and as you said in your last post, to make your working day more interesting. I think it also serves the purpose of supporting your plight to steer thinking away from a purely nociceptive model of pain.

[tomaszk]

Originally Posted by Jason Silvernail

The only people who are sure that nociception is irrelevant or central mechanisms are irrelevant are those who aren't acknowledging the complexity here, and they arrive at that opinion through bias and speculation, not through an honest appraisal of the existing literature. I think neuroscientist Sam Harris once said something like we need to get to the point in our society where nobody gets credit for pretending to know something no one could possibly know. I think that's where we sit here - shades of gray and clinical reasoning with no clear answers. We have to learn to be OK with that.

I hope Jason does not object to cite him here. Just fits perfectly.

I listened to Sapolski today about human uniqueness and irrationality.
There are plenty examples of friendly fire in our biology. I hope that regarding pain, or more generally protective processes, the brain is not , MOST OF THE TIME, entirely losing grasp with reality. I am saying that despite being fascinated by central processes. We simply do not know yet.

[Diane]

Suit yourself Patrick - in the end, it is all about the brain,
1. embedded in a body it can't really (directly) "feel" (although it can directly feel the outside of the skin..),
2. other "brains" in there, telling it what it should feel, or might feel,
3. all it has to go on is the maps it has made, and continually reshaped according to many things, many environmental inputs, and all kinds of interoception (not just nociception), i.e., its virtual body/ies.

I like to cut to the chase, pretty much, and help people know they don't have to believe everything their anxious critter brain tells them. But you have to figure out your own way of explaining things to people in a way that eases them out of a fearful state and over into a relaxed, 'OK, let's get this done then, help me learn how to be in this body the way it is right now', kind of state.

[PatrickL]

I think I should also add that although (I think) my stance here is conceptually valid, in that it offers a complete explanation of the neuromatrix, I have to also concede that my stance serves a value judgment that I think I am unwittingly projecting onto clients. That being, that they are attached to the physicality of their pain. I suspect most people are, because they haven't known anything else (probably). But it doesnt mean i can assume that they're not open to changing that view. It has occurred to me that my need to not down grade nociception is not only driven by a desire to not violate the neuromatrix, but is also driven in part by my own attachment to the physicality of pain.

Diane and Bas (and anyone else who wants to throw in their 2cents),
I assume that as you learned all this stuff, at some point you were at the same point I now am. Given that (I think) my current stance is reasonable, and adheres to the neuromatrix, and that presumably you thought the same when you were at my level of understanding, what was it that drove you to continue on so deeply into the world of virtual bodies and brain maps? I do not wish to deconstruct anything in this regard, I'm just curious as to why you weren't satisfied when you were at the point where I currently am. Perhaps knowing this will help me to progress my understanding.

Cheers,

Pat

[Diane]

Patrick, we've all been where you're at. At least I sure have. The more you read the more you realize you
a) don't know, and
b) what you thought you knew is mutually exclusive with how things actually work, based on neuroscience.

It is sickening, dizzying, and produces nausea at first. I'm sure the cognitive dissonance produced by new information heads straight for and plunks down/lands smack into the vestibular system somehow, like the experience of being on a new ride at the fair does for kids. But it's also enthralling, exciting, revealing and intoxicating; one can adapt reasonably quickly to having one's world turned upside down repeatedly, and even learn to enjoy it, strangely enough, the way the human brain can adapt itself to almost anything, through its social and cognitive-evaluative interfaces..

You'll be just fine. I'm sure about that. Look where you started and where you've gotten in a few weeks.

PS: Keep reading.

[Diane]

Not to argue, just to catalogue: Here is a blog post about how pain and tissue damage are from different planets. We have a whole folder here now, containing examples.

[PatrickL]

Thank you. I do hope I haven't come across as being unwilling to learn. I'm all for it. And I appreciate the patience that has been extended to me here.

[Greg Lehman]

I have to admit that I feel that I am in much the same place as Patrick. I think I have probably been here for at least 8 years. My adductors hurt from straddling this chasm...or is it my obturator nerve? See!

I recognize that nociception has a role but also know that it is not sufficient for pain. I'm mostly conversant with all the research that supports my go to phrase that "Structure is Not Destiny" and I consistently scoff at plumb lines and unstable spines. I've even written functional capacity evaluation reports that try to explain central sensitization and "wind up" to Adjusters that sure as hell don't want to hear that.

However, when I recognize that Nociception can sometimes be a factor leading to pain I work backwards a few steps and then think that biomechanics can end up creating nociception and therefore biomechanical variables may be worthy of considering in a patient that experiences pain or in the prevention of pain/injury.



A simple example that I wrestle with is my inability to throw off the idea that strength training in athletes does not help prevent injuries through biomechanical means. I have read the core stability posts here (I agree with much of them despite my fondness, respect and long relationship with Stu McGill - he was my MSc supervisor) and am well aware how strength may not be necessary for the average person but what about a runner doing one hour of running 6 days a week that ends up having lateral knee pain 25 minutes into her run? Is it not possible that something about her mechanics of running (not just form but also the summation of stress) lead could lead to some deformation of tissue (not just nerve) and nociception develops. Then could not an intervention that either attempts to increase the capacity of that tissue to tolerate load (ala Scott Dye and his Tissue Homeostasis theory) or an intervention that attempts to alter the load on the tissue (ala gait retraining and Irene Davis) be beneficial and be explained by a biomechanical model. I know that I could also explain with is a neuroscience model but I don't feel that I can readily discount the biomechanical model.


I don't think it is necessary to discuss the specifics of running injuries but I can't shake the idea that excessive or constant loading on some tissues can lead to injury or nociception and ultimately pain under certain conditions. When I consider the research that does not find a link between biomechanical variables and injury/pain I think that one explanation may be due to all of the other factors of the neuromatrix. I posit that it might be possible that if you have certain conditions of the neuromatrix and these mix with certain "negative" biomechanical factors (e.g. heel striking/overstriding, increased knee valgus, weak hip abductors, external rotators) that you might experience pain. However, a different group of runners with the same biomechanical factors will have different x,y and z neuromatrix components and these different components act to increase ones robustness and resiliency. In other cases, the certain biomechanical factors are rendered insufficient to create nociception because of the incredible adaptability and capacity of the tissues put under load even if these individuals may not have the positive pain down regulating factors of the neuromatrix.

All of these different groups of people with these different physiological and neuromatrixey states lead to a non-homogeneous population and therefore we don't find a statistical relationship to injury.

Anyways, I know nothing. I'm not dead and my groin still hurts.

Greg

p.s. I know this is a pretty well beaten horse here but I still feel like I need the exercise. No posts in the history that I've read have pushed me over the edge.

[MaxG]

Originally Posted by glehman

I have to admit that I feel that I am in much the same place as Patrick. I think I have probably been here for at least 8 years. My adductors hurt from straddling this chasm...or is it my obturator nerve? See!

I recognize that nociception has a role but also know that it is not sufficient for pain. I'm mostly conversant with all the research that supports my go to phrase that "Structure is Not Destiny" and I consistently scoff at plumb lines and unstable spines. I've even written functional capacity evaluation reports that try to explain central sensitization and "wind up" to Adjusters that sure as hell don't want to hear that.

However, when I recognize that Nociception can sometimes be a factor leading to pain I work backwards a few steps and then think that biomechanics can end up creating nociception and therefore biomechanical variables may be worthy of considering in a patient that experiences pain or in the prevention of pain/injury.



A simple example that I wrestle with is my inability to throw off the idea that strength training in athletes does not help prevent injuries through biomechanical means. I have read the core stability posts here (I agree with much of them despite my fondness, respect and long relationship with Stu McGill - he was my MSc supervisor) and am well aware how strength may not be necessary for the average person but what about a runner doing one hour of running 6 days a week that ends up having lateral knee pain 25 minutes into her run? Is it not possible that something about her mechanics of running (not just form but also the summation of stress) lead could lead to some deformation of tissue (not just nerve) and nociception develops. Then could not an intervention that either attempts to increase the capacity of that tissue to tolerate load (ala Scott Dye and his Tissue Homeostasis theory) or an intervention that attempts to alter the load on the tissue (ala gait retraining and Irene Davis) be beneficial and be explained by a biomechanical model. I know that I could also explain with is a neuroscience model but I don't feel that I can readily discount the biomechanical model.


I don't think it is necessary to discuss the specifics of running injuries but I can't shake the idea that excessive or constant loading on some tissues can lead to injury or nociception and ultimately pain under certain conditions. When I consider the research that does not find a link between biomechanical variables and injury/pain I think that one explanation may be due to all of the other factors of the neuromatrix. I posit that it might be possible that if you have certain conditions of the neuromatrix and these mix with certain "negative" biomechanical factors (e.g. heel striking/overstriding, increased knee valgus, weak hip abductors, external rotators) that you might experience pain. However, a different group of runners with the same biomechanical factors will have different x,y and z neuromatrix components and these different components act to increase ones robustness and resiliency. In other cases, the certain biomechanical factors are rendered insufficient to create nociception because of the incredible adaptability and capacity of the tissues put under load even if these individuals may not have the positive pain down regulating factors of the neuromatrix.

All of these different groups of people with these different physiological and neuromatrixey states lead to a non-homogeneous population and therefore we don't find a statistical relationship to injury.

Anyways, I know nothing. I'm not dead and my groin still hurts.

Greg

p.s. I know this is a pretty well beaten horse here but I still feel like I need the exercise. No posts in the history that I've read have pushed me over the edge.

Greg, I definately can relate to your issues.
When I was more focused on sports training, McGill's work was a big influence, and his studies are still very interesting, IMO, just not from a pain perspective, maybe from a nociceptive perspective.

Depending on the patients you see, pain might not be the only issue you have to work with as a therapist.
Inability to handle ADL's, neurologic etc. all need "training" to be handled.
Of course, the nervous system and how it handles and coordinates muscular activity is of highest importance here, and not sarcomere density (or whatever) in the muscles. But still, in these cases it's not just about central perception, but about interaction between "inner and outer self" (brain and body).


Another example where biomechanics definately play a role:
I have dislocated my left patella a couple of times in the past 10 years.
I can trace the dislocation back to certain biomechanical positional relations between my knee, ankle and hips, coupled with a certain force of impact.
No amount of movement pattern retraining has improved my motor reaction in certain (perceived) "emergency situations", which is when the dislocation occurs.

It's not only the pain associated with the dislocation that bothers me.
It's the swelling, immobility and uncertainty of continuing functionality that is an issue.

I personally think that connective tissue strength (which can be increased long term through regular, relatively high resistance) could provide an increase in functional ability for me and as a therapist, I would work on that with a patient as well, along with helping the patient find ways to keep a fullfilling lifestyle while respecting the disability.

[Ken Jakalski]

Hi Greg!

A simple example that I wrestle with is my inability to throw off the idea that strength training in athletes does not help prevent injuries through biomechanical means.

Nothing has perplexed me throughout my coaching career as much as what do do with MTSS.

When a kid sees a trainer, it is with utmost certainty that I can say he or she will be told their "shinsplints" are the result of either excessive pronation or weaker muscles groups their are not able to handle the load effectively because they are being overstressed.

As a result, they are given protocols involving theraband (various colors) foam roller proprioception, towel toe curling, etc. Some will tape or consider an arch pad.

In the belief that the trainers are right, that strength defIcits resulting from overuse during very specific kinds of training (horizontal or vertical jumping events in track) cause these "shin splint" issues, coaches are now spending considerable time adding these protocols to their daily routines, even though there appears to be no solid evidence during a typical outdoor track season that such "prehabilitation" strategies prevent the onset of the dreaded shin splint.

I don't think it is necessary to discuss the specifics of running injuries but I can't shake the idea that excessive or constant loading on some tissues can lead to injury or nociception and ultimately pain under certain conditions.

Many high school coaches in my sport would agree with this.

When I consider the research that does not find a link between biomechanical variables and injury/pain I think that one explanation may be due to all of the other factors of the neuromatrix. I posit that it might be possible that if you have certain conditions of the neuromatrix and these mix with certain "negative" biomechanical factors (e.g. heel striking/overstriding, increased knee valgus, weak hip abductors, external rotators) that you might experience pain. However, a different group of runners with the same biomechanical factors will have different x,y and z neuromatrix components and these different components act to increase ones robustness and resiliency. In other cases, the certain biomechanical factors are rendered insufficient to create nociception because of the incredible adaptability and capacity of the tissues put under load even if these individuals may not have the positive pain down regulating factors of the neuromatrix.

I've taken the approach that what we perceive as "problem causers" in certain runners, like the conditions you mentioned above, might simply be the way a specific athlete needs to translate the skill of the activity based upon differences in muscle attachment points, limb length asymmetries, or neurological hard wiring-- things that many of us are not even considering when we seek to fit athletes into what we perceive as the ideal "injury free mechanics template."

It was Mel Siff who got me started on this years ago when I just wasn't getting answers to why some of the fastest sprinters in the world toe out on landing (and some quite excessively)with no history of lower leg injury. Yet we consistently hear such postural abnormalities are clear cut injury markers.

[PatrickL]

Greg said:

In other cases, the certain biomechanical factors are rendered insufficient to create nociception because of the incredible adaptability and capacity of the tissues put under load even if these individuals may not have the positive pain down regulating factors of the neuromatrix.

I'm still very unsure about how the accumulation of load/stress in tissues leads to breakdown of these tissues. Diane offered a perspective I hadnt considered before here

Actually, there is an entire class of C-sized so-called "visceral afferents", innervating blood vessels (everywhere, including all "tissue"), which would better be considered as efferents - they leak neuropeptides onto everything vascular, a different neuropeptide for each size/kind of vessel, mostly to tell them to dilate (vessels have sympathetic innervation telling them to constrict), which helps "tissue" stay healthy, obviously.
If and when they stop doing that, the vessels stay constricted, and tissue starts to atrophy. Oops. Tissue "damage". But that's not nociceptive, not at first, anyway... But it is neural dysregulation.http://www.somasimple.com/forums/sho...6&postcount=12

Perhaps those with...

"negative" biomechanical factors (e.g. heel striking/overstriding, increased knee valgus, weak hip abductors, external rotators

...who just don't get injured, and leave us scratching our heads, have better functioning neural regulation of blood low to the joints to maintain tissue health. I'm not sure how trainable this parameter though

[Diane]

Hi Patrick,
About visceral afferents,

Originally Posted by PatrickL

...who just don't get injured, and leave us scratching our heads, have better functioning neural regulation of blood low to the joints to maintain tissue health. I'm not sure how trainable this parameter though

Here is a thread I started on these (Visceral Afferent Function), and haven't got very far with yet. On about chapter three of the book. Have been too busy to slog through the book the way I like to slog, making contact with every molecule of thought contained therein. But it's all about how "conditionable" or not this part of the nervous system is.

Here is chapter 2 from Janig (my notes) on them.

[Greg Lehman]

Hi Patrick,

Thanks for linking to Diane's information and of course thanks Diane for that information.

You wrote:

I'm still very unsure about how the accumulation of load/stress in tissues leads to breakdown of these tissues.

So, do you believe that the accumulation of load/stress in tissues can lead to the breakdown of these tissues? Or is it the mechanism that your are unsure about?

I would never have an injured runner start at their same pre-injury training volume and intensity nor a beginner runner start running with the same volume as a pro. I myself tend to feel more aches and pains when I get over a certain mileage. Why is this? And how can I prevent it? Do biomechanical variables (both intrinsic to the person and extrinsic related to loading parameters) have a role?

Greg

[PatrickL]

Hey Greg,
I said:

I'm still very unsure about how the accumulation of load/stress in tissues leads to breakdown of these tissues.

Greg said:

So, do you believe that the accumulation of load/stress in tissues can lead to the breakdown of these tissues? Or is it the mechanism that your are unsure about?

Yes I think that accumulative load/stress, like the runner you described leads to breakdown of tissues. I'd consider biomechanics, running distance, surface etc as a factors influencing the specificity/direction/volume of the load/stress, but the tipping point towards breakdown I think must lie within the tissues ability to resist these forces and stay healthy. It's this mechanism that I'm not sure about. I really do like the idea of autonomic regulation of bloodflow to the tissues being a mechanism. What do you think? Any other mechanisms come to mind?

I would never have an injured runner start at their same pre-injury training volume and intensity nor a beginner runner start running with the same volume as a pro. I myself tend to feel more aches and pains when I get over a certain mileage. Why is this? And how can I prevent it? Do biomechanical variables (both intrinsic to the person and extrinsic related to loading parameters) have a role?

I would guess they have a role in tissue damage, but from there we are getting into the pain experience, I don't fancy going down that tissue damage and pain path again! I'm still recovering from my last bout.

Here's something that Eric offered on this

http://www.somasimple.com/forums/sho...0&postcount=14
As performance trainers we should be develop the greatest amount of solutions to movement problems within the constraints of the activity and their goal.

Trainers in the past and present have focused on specific metrics related to a given sport i.e. force, power, speed, change of direction, quick muscle response. Thus they have sought to train primarily the meso for precisely such adaptations.

In my opinion what they(trainers) fail to realize is that training regimens that are "yoked out" towards one sort of mesodermal property or another are often, unfortunately so, robotic and stereotypical and therefore the ultimate applicability of this style to performance in athletics is limited.

Having a healthy repertoire of flexible solutions (motor control lingo called motor variability, redundancy, principle of abundance) to movement related problems is the ultimate goal of training. Yes, speed, agility and force generation are important aspects of it but there are any innumerable other aspects of the control of movement that are not addressed in traditional paradigms of training.

In short it is through motor variability (which is very ectoderm) maintains, in my mind, the ability that given a novel situation the body will adopt a correct motor response. This correct motor response will minimize the mesodermal harm, ectodermal perception of that harm and maximize the success of a given goal. All this, given the person has had a sufficient priori of stimulus to allow such a response to occur on the field of performance.

I'm not sure how this helps for example, the distance runner who, at some point has to clock up the miles in order to improve. The constraints On their activity and goal are quite narrow. Any thoughts on this Eric?

[Barrett Dorko]

As the Ancient Greeks would say, "This is a clash of imperfect ideas."

Just what we hope Soma Simple will always be.

[Greg Lehman]

Barrett,

Your abstruseness exceeds my obtuseness.

Greg

[Bas Asselbergs]

Sorry to have dropped out here folks - was on a busy conference weekend.
Just a quick reply to Jason:

Certainly we might make a case that if the experience was modulated significantly by nonspecific interventions (eg pain education) we might be more inclined to think more centrally for a primary mechanism. If the experience was modulated by more peripheral mechanisms (ice and relative rest), we might be more inclined to think it was nociception related. But both examples have overlap with the other mechanism so no one knows for sure.

You are right: the uncertainty is mostly the rule. In your above example, the reasoning is easily turned fully to non-nociceptive factors.
If education does NOT work, it may simply mean that it did not resonate with the patient. Not an indicator of the presence of nociception.

If peripheral factors modulated the pain, they may have fitted the patient's expectations and worldview - again, no nociception-modulation required for that outcome.

And since out culture is so guided by the "there is pain, there must be damage" attitude, I find it necessary to move as strongly away from that as possible.

[BurntoutPT]

What if someone was sleepwalking and sprained their ankle and they woke up with pain but no recollection of how or why it happened or in what context. And they happened to be blind so they could not see their ankle, but they could point to where it "hurts" and it "hurts" when they move their ankle "this way" or "that way"...what might be happening there? Would this be similar to phantom pain?

[Barrett Dorko]

No, it's not similar.

The motions that led to an increased output of pain were considered more threatening, and, I assume, threatening to the nervous system.

I don't think being blind has much of an effect.

[advantage1]

BurntoutPT,

I can honestly say I have never treated a blind sleepwalker who injured themselves but never say never. This would not be the same as phantom limb pain since they still have a foot. Nociception from the sprained ankle would still take place. What the CNS does with this info is dependent on the person. My guess is that due to the possible larger representaion of the foot on the cortex and a blind person's dependency on their feet their would be an output of pain from the brain. This could mean danger to this person since their foot is even more important to their survival than a peron who can see. Lets hope your blind sleepwalking patient doesn't develop CRPS since we would have to rule out the use of a mirror box.

[BurntoutPT]

Thanks...just a thought experiment...I was trying to imagine a situation where context and knowledge or perception of the ankle or body part was taken out and an isolated mechanical change in the tissues was induced...if so how would the mind or brain or nerves respond to the "sprain" if it did not "know" that it was sprained...would it hurt more or less, can it become chronic and what if we treated just the tissues without the patient's knowledge (like when they were sleeping or sleep walking... with lets say a cortisone shot) and it went away...or didn't go away....

just been seeing patients with shoulder "impingement" ...ie "it hurts 'here' when I do 'this' and I don't know when or how or why" ...they report to have literally woke up with it... like they were sleep walking haha

[Diane]

So, you would like to figure out how to treat the tissues and rule out placebo, non-specific effect? Good thought exercise!

[Randy Dixon]

Burnout,

I think if someone is anesthetized and has a procedure done on their left leg when it should have been the right, they wake up hurting on the leg that the procedure was done on, not the one it should have been done on.

Nociception does matter, it just isn't the only thing that matters.

[advantage1]

Randy,

I don't think we can say that the patient that had the wrong knee operated one will have pain in that knee. It is not that black and white. Some patients may have an increase in pain on the affected leg that should have been operated on since they are more anxious, upset, depressed, pissed off etc. that their knee wasn't 'fixed'.

Don't forget the study where the patients who recieved a sham arthroscopic knee surgery on their affected knee felt better even though nothing was done. They would still have nociception from the incisions yet their prior knee pain was gone.

[Randy Dixon]

I am not denying the placebo effect, but the surgery situation isn't really a hypothetical, we see similar results all the time where there is pain secondary to nociception where there was no prior expectation of pain or knowledge of injury. This is one of the primary purposes of nociception, to create pain to make the organism aware of injury. It makes no sense to discount it simply because the system is capable of malfunctioning.

The International Association for the Study of Pain (IASP) and many other sources of research and literature use terms like "nociceptive pain". Is this a term that is accepted here? If not, why not?

http://www.iasp-pain.org/AM/Template...ociceptivepain

[Barrett Dorko]

Patrick says:

...some inputs are less measurable/useful than others.

On top of that, it's the patient that assigns value to the input. And that value may change from one moment to the next.

[advantage1]

I never said I discount nociception. Of course nociception exists. However, it is simply information that is sent to the CNS. Pain is an output from the brain not input. How would you explain allodynia?

[Randy Dixon]

Originally Posted by advantage1

I never said I discount nociception. Of course nociception exists. However, it is simply information that is sent to the CNS. Pain is an output from the brain not input. How would you explain allodynia?

We seem to be talking past one another. Burnout's thought experiment wasn't designed to test the other input variables in producing pain, those which explain allodynia, phantom limb pain, CRPS and similar conditions, nor was it designed to test the effect of placebo on pain. It was designed to isolate nociception from those variables, or at least that was the intent.

[Randy Dixon]

This is why I asked why we don't use the term "nociceptive pain" on this site since it is used elsewhere.

When nociceptive pain is referenced on this site it is inevitably met with replies informing the poster that nociception is not equivalent to pain, or that nociception is an input while pain is an output, or asks if we have ever heard of phantom pain, etc. All things which anyone on the list more than one day fully realizes. It would greatly simplify and expedite the conversation not having to go over this every time.

[advantage1]

I don't refer to nociception as nociceptive pain since it is not pain until it enters the CNS. Nociception is simply information regarding pressure, chemicals and temperature. It is not pain.

[Bas Asselbergs]

Randy, I'd go even further: there is lots of nociception that does NOT result in pain, hence the need for a clear division. Between the concept of pain and nociception.

we see similar results all the time where there is pain secondary to nociception where there was no prior expectation of pain or knowledge of injury

This is strictly an assumption: we can NOT know what the expectations or prior awarenesses are; besides, these are only two of the vast variety of factors that are involved in the "production" of pain.

Every time "nociceptive pain" is mentioned it needsto be addressed.
There is simply no way to move forward unless it is absolutely clear.

Just because it happens a lot, does not mean it does not need correcting.

[BurntoutPT]

"It was designed to isolate nociception from those variables, or at least that was the intent. "

yes that was my intent...thanks

[Randy Dixon]

Originally Posted by Bas Asselbergs

Randy, I'd go even further: there is lots of nociception that does NOT result in pain, hence the need for a clear division. Between the concept of pain and nociception.

This is strictly an assumption: we can NOT know what the expectations or prior awarenesses are; besides, these are only two of the vast variety of factors that are involved in the "production" of pain.

Every time "nociceptive pain" is mentioned it needsto be addressed.
There is simply no way to move forward unless it is absolutely clear.

Just because it happens a lot, does not mean it does not need correcting.

Bas,
Why does it need correcting? The IASP uses the term "nociceptive pain", I think you would agree that they understand the concepts we are talking about. I'll ask again, is the term "nociceptive pain" acceptable here? If not, why not?

[Barrett Dorko]

No, I don't think they understand this as I do, or, evidently, Bas.

The answer from me is no, it's not acceptable. Bas has already stated why.

[Randy Dixon]

Then what reference do you use regarding terminology and what is acceptable in discussing pain with others, on Somasimple and elsewhere? Do you think it is important that we all use the same words to mean the same things? I do.

I don't know. I think I am going to have to go with IASP having an understanding of pain, certainly they understand the difference between nociception and pain and often point out the differences, even in their terminology.

I'm going to start another thread on this to get others input.

[John W]

I suspect that the terminology that's IASP releases to the public is arrived at by committee, and I suspect that there are some on the committee who would take issue with "nociceptive pain". But, it's a committee that likely votes on such things, and I suspect there are a lot of doctors on it who also think chronic pain is a "disease" in its own right.

I don't agree with that either. I once did, but no longer.