CT More than Placebo

[Jon Newman]

I think pain can be considered a particular type of conscious experience (versus a different type of consciousness) and I think reductionism is the only solution to its study. However, I agree that reductionism isn't the solution to its treatment.

A book I recently have been reading (in order to avoid reading Don Quixote) is The Ego Tunnel by Thomas Metzinger (referenced elsewhere here at SS). I thought he made a particularly interesting point on page 18. (brackets mine)

In the meantime, we have learned many lessons. We have learned how great the fear of reductionism is, in the humanities as well as how among the general public and how immense the market is for mysterianism [some might claim it's infinite]. The straightforward philosophical answer to the widespread fear that philosophers or scientists will "reduce consciousness" is that reduction is a relationship between theories, not phenomena. No serious empirical researcher and no philosophers wants to "reduce consciousness"; at best, one theory about how the contents of conscious experience arose can be reduced to another theory. Our theories about phenomena change, but the phenomena stay the same. A beautiful rainbow continues to be a beautiful rainbow even after it has been explained in terms of electromagnetic radiation. Adopting a primitive scientistic ideology would be just as bad as succumbing to mysterianism. Furthermore, most people would agree that the scientific method is not the only way of gaining knowledge.

[BB]

I've been thinking that this thread needs a clarifying metaphor or story to go along with it. So, I've tried to come up with one. It is the story of The Submarine in the Canyon. (I apologize for naval inaccuracies in advance to anybody who actually knows of these things from places other than movies, as Sean Connery was my inspiration for this story and not the navy.)

Worse than being in a canyon, the sub may also be in enemy waters. All communication has been cut off so the sub cannot check with the fleet to update on the position of the enemy. Worse still, all of the maps are old and the detail about the canyon is lacking. The sub must navigate through the canyon anyway. Understandably, the captain has put the sub on high alert. Its mission is simply know that they are in safe water which would culminate in an "all clear."

There are many ways that the actual danger that the sub is in can be reduced. The fleet can destroy or drive away all enemies from the area. Although this would reduce the danger for the sub, it would not bring about the desired result because in order for the captain to give the all clear he must have access to the information.

The sub version of blanket bombing (pharmacologic analgesics) could be performed and reduce the threat from enemy relatively for a known distance and time, but the canyon must still be navigated and the captain would still keep the sub on high alert.

Communication could be restored, allowing the sub access to information about the location of enemy. Also, the sonar could be used to continuously "ping" the walls of the canyon allowing the map to be more clearly defined, actively seeking a path, and a safe navigable path made clear through the canyon. Knowing the coast is clear and having a well drawn map would definately be sufficient to reduce the threat to the necessary level for the captain to give the all clear.

But there's a thing about a submarine. The crew doesn't go off high alert when the threat is cleared. They go off high alert when the captain says they can go off of high alert.

This depends on the captain's training, his knowledge, his clarity of thinking, his trust of the information he's recieving, etc.

So, despite the fact that there are all manner of sensible approaches to be taken to reduce threat and restore or demonstrate safety, the desired result depends upon the captain. This does not take away from the utility of those measures performed. It would make sense to obtain a clear map. It would make sense to reduce enemies in the area. It would make sense to restore communication. And in performing these acts, certain skills would be necessary for completion of that task, like knowledge of how to use and read sonar for example. A sensible captain would require certain things, and another sensible captain may require different but still sensible things before they will give the "all clear" and these differences may reflect differences in the skills in which that their respective crews are stong. Some crews may be better navigators than others. There may also be captains who give the "all clear" even when threat remains and/or the canyon not yet cleared.

This is my favorite thread in awhile, by the way.

[Diane]

I like your metaphor Cory.
There's a piece I'd like to add, if I may.

There's a chance some part of the sub will get dinged by canyon walls, or torpedoed by the enemy, and start to leak.

If a leak happens, the immediate thing one must do is seal off the area and try not to drown. That is compartmentalization, even to the extent of dissociation.

[Frédéric]

I'll be less profound than you guys :


On persistant pain :

MT = mostly specific short term/immediate pain relief via transient mechanical changes and/or mouvement of a mesodermal structure (ex : opening an IF and decreasing pressure on a nerve root or any mvts of the LB helping the flow of the cerebrospinal fluid and its sensitizing chemicals to get away from the sensitized segments) and decreased nociptive sommation in the spinal chord.

MT = both non-specific long term and short term/immediate pain relief via placebo/brain response/morphing effect because decreased perceived threath, +ive anticipation, the conviction of doing the right thing for your condition. This will, in turn, have a possible mechanical effect on the tissues following a brain output.

We could argue there's always a bit of both but the %s probably favors the above hypotheses.

The repetition of the first part, more specific, might lead, over time to the second more non-specific response.

[EricM]

Good points Frederic, however in my view, I think your long-term/short-term mechanisms might be reversed. It's complicated isn't it?

[Frédéric]

Eric,

I clarified my points

[Luke Rickards]

Some more from Kaptchuk on the placebo response.

"Maybe I Made Up the Whole Thing": Placebos and Patients' Experiences in a Randomized Controlled Trial. Kaptchuk TJ, Shaw J, Kerr CE, Conboy LA, Kelley JM, Csordas TJ, Lembo AJ, Jacobson EE. Cult Med Psychiatry. 2009 Jul 14.

Patients in the placebo arms of randomized controlled trials (RCT) often experience positive changes from baseline. While multiple theories concerning such "placebo effects" exist, peculiarly, none has been informed by actual interviews of patients undergoing placebo treatment. Here, we report on a qualitative study (n = 27) embedded within a RCT (n = 262) in patients with irritable bowel syndrome. Besides identical placebo acupuncture treatment in the RCT, the qualitative study patients also received an additional set of interviews at the beginning, midpoint, and end of the trial. Interviews of the 12 qualitative subjects who underwent and completed placebo treatment were transcribed. We found that patients (1) were persistently concerned with whether they were receiving placebo or genuine treatment; (2) almost never endorsed "expectation" of improvement but spoke of "hope" instead and frequently reported despair; (3) almost all reported improvement ranging from dramatic psychosocial changes to unambiguous, progressive symptom improvement to tentative impressions of benefit; and (4) often worried whether their improvement was due to normal fluctuations or placebo effects. The placebo treatment was a problematic perturbation that provided an opportunity to reconstruct the experiences of the fluctuations of their illness and how it disrupted their everyday life. Immersion in this RCT was a co-mingling of enactment, embodiment and interpretation involving ritual performance and evocative symbols, shifts in bodily sensations, symptoms, mood, daily life behaviors, and social interactions, all accompanied by self-scrutiny and re-appraisal. The placebo effect involved a spectrum of factors and any single theory of placebo-e.g. expectancy, hope, conditioning, anxiety reduction, report bias, symbolic work, narrative and embodiment-provides an inadequate model to explain its salubrious benefits.

[Diane]

This is old, but good I think, in that it differentiates a bit more between placebo effect and placebo response. Response seems to boil down to good therapeutic relationship, and the patient retaining locus of control.

[Diane]

About the other line of thinking, re: virtual bodies, I offer this (from 2007), and this (from 2008). They are both a bit old, but I plan to dig up more recent work when I get time.

To me this is really where it's at - helping people learn to understand their own brain's perception, how it can differ from their own. Once they get that the brain works differently from how their conscious awareness works, and that "they" are not in charge of their brain, that it is in charge of them and they need to create a good relationship with it, their own brain, it's easy. Prior to that little cognitive feat, which requires a new level of understanding of how their brain is something quite a bit more complex than their conscious awareness is, nothing about this would make any sense; after, it does.

Education of a simple sort, showing them a big picture of the entire neural tree, telling them about things like upregulation and downregulation, helps them not worry so much that they must have some horrid thing wrong with their "real" body. They can get that the brain might be a bit frantic and giving them information that is blown way out of proportion, based on wrong info coming from or traveling to a virtual version of their body. Treatment (my kind) helps them realize this, because it's so light (i.e., it couldn't possibly be helping a "disc" or a buried "joint"); they also get that they'll be fine if they do their homework.

[Diane]

Here is a google online-book link to the chapter in Wall's book, on placebo response.

[Diane]

There is a thread about placebo at the moment, at SBM, about this book (free online) called Placebo Medicine. The thread is called Incorporating Placebos into Mainstream Medicine, by Harriet Hall.

Here is the first bit of the foreword, by Morgan Levy MD.

"The word "Placebo" is a word that is frequently misunderstood. Most people think that it refers to a fake or ineffective treatment. If this were the case, then medical researchers would not need to go to such great lengths to account for it. In reality, the term placebo describes a therapeutic phenomenon that is very real and can be quite effective.

Furthermore, a lot of you hear the word placebo as an insult. If I think that you need a placebo, or that some treatment that you depend on is a placebo, then you will likely think that I am implying that you are stupid or naive.

What I’m really saying is that, “You think like a human.”

IQ and life experience are not the issues. In fact, and interestingly, individuals in America who have more education and have obtained a higher socioeconomic status are the ones most inclined to use Placebo Medicine. The real question is, "How does the human brain process information?""

My bold.

He also asks, "How can the way we think about a therapy have a therapeutic effect?"

[Jon Newman]

"How can the way we think about a therapy have a therapeutic effect?"

Thoughts and beliefs are nerve impulses too.--Moseley and Butler in Explain Pain.

[Diane]

Cool article I found on Facebook, on one of the pages I've subscribed to: Placebos Are Getting More Effective. Drugmakers Are Desperate to Know Why.

Maybe peoples' understanding of their own brains is increasing?

Here is a May/09 article by Harriet Hall on the topic of placebo.

[Diane]

The Placebo and Nocebo Effect: How the Therapist’s Words Act on the Patient’s Brain, by Benedetti. Nice art work in here.

[JayCola]

Ok, so after reading the latest article Diane posted a couple thoughts about placebo crossed my mind. I tried thinking them through myself, but I lack access to many scientific articles so I'm hoping you guys can help sort out my thoughts.

Some statements from the article that caught my eye...

First of all, there is today general agreement that the endogenous opioid systems play an important role in some circumstances, and several lines of evidence indicate that placebo analgesia is mediated by a pain-modulating network which uses endogenous opioids as neuromodulators.

it was found that the very same regions in the brain are affected by both a placebo and an opioid drug, thus indicating a related mechanism in placebo-induced and opioid-induced analgesia

Later on in the article the author talks about hidden therapies..

telling a patient that a painkiller is being injected (actually a placebo) is as potent as 6–8 mg of morphine. An analgesic effect stronger than the placebo was only observed when the hidden morphine dose was increased to 12 mg. This suggests that an open injection of morphine in full view of the patient, which is the usual medical practice, is more effective than a hidden injection, because in the latter, the placebo component is absent

Now, in my mind, these 3 statements taken together, give me the impression that when administering an analgesic opiate in conjunction with inducing a placebo response you're basically "hijacking" the brains endogenous opioid system to just about double to affect of what a hidden opiate injection would do. So if there's no placebo, just give a larger dose.

So then my first question I can't seem to find a clear answer to is, Can the brain differentiate between the injected opiate and its own self-made opioid? I'm assuming from the 2nd quote that it can't.

My main question then has to do with Opioid Induced Hyperalgesia (Another brief explanation that I prefer is in this video, skip to the 30:30.) Now it may be a stretch, but if a single dose of opiates can sometimes increase sensitivity to pain, is it possible that a large enough placebo response could theoretically induce the same hyperalgesia? Could over utilizing the placebo response in-turn lower a patients baseline pain tolerance? And speaking of tolerance, I've read (in Snake Oil Science) that the placebo response to pain is mostly temporary (I know it depends, but on what I'm not sure). I just wonder if these temporary placebo responses aren't just a sort-of built up tolerance like one would expect with opiate induced analgesia. Or perhaps the brains opioid system eventually becomes depleted, weakening the placebo response (I know Robert Saplosky writes that this happens during Stress Induced analgesia, so I imagine it could be possible)

Obviously this is all based on my previous assumption that the brain can't and/or doesn't tell the difference of where the opioid is coming from. I also understand that there can be non-opioid mechanisms at work in placebo, but as far as I can tell it depends on the circumstance and the authors in the article seem to place a good deal of importance on the use of endogenous opioids as neuromodulators in placebo so that's what I'm basing this on.

Makes sense?

[Diane]

Jason, I don't know if you remember this other conversation or not.

I think your questions are good ones.

So then my first question I can't seem to find a clear answer to is, Can the brain differentiate between the injected opiate and its own self-made opioid? I'm assuming from the 2nd quote that it can't.

As far as I know it can't.
Somewhere lately I read that opioids given will fill receptors in the ACC, but that opioids endogenously induced (i.e., placebo response) fill receptors in orbitofrontal cortex and dorsolateral cortex as well.

My main question then has to do with Opioid Induced Hyperalgesia (Another brief explanation that I prefer is in this video, skip to the 30:30.) Now it may be a stretch, but if a single dose of opiates can sometimes increase sensitivity to pain, is it possible that a large enough placebo response could theoretically induce the same hyperalgesia? Could over utilizing the placebo response in-turn lower a patients baseline pain tolerance? And speaking of tolerance, I've read (in Snake Oil Science) that the placebo response to pain is mostly temporary (I know it depends, but on what I'm not sure). I just wonder if these temporary placebo responses aren't just a sort-of built up tolerance like one would expect with opiate induced analgesia. Or perhaps the brains opioid system eventually becomes depleted, weakening the placebo response (I know Robert Saplosky writes that this happens during Stress Induced analgesia, so I imagine it could be possible)

I don't know. I remember reading Wall, who said that endogenously elicited placebo doses were exactly the right kind, strength, were dose-specific to requirements, and lasted only long enough to do the job. Something to that effect. Sounds to me that there would not be the same sort of toxic possibilities.

Obviously this is all based on my previous assumption that the brain can't and/or doesn't tell the difference of where the opioid is coming from. I also understand that there can be non-opioid mechanisms at work in placebo, but as far as I can tell it depends on the circumstance and the authors in the article seem to place a good deal of importance on the use of endogenous opioids as neuromodulators in placebo so that's what I'm basing this on.

I think opioids are the main substance for both placeboically elicited pain relief and for administered pain relief, so far. There are endogenous endocannabinoids too. They aren't as well studied yet.

[davidwilsoon]

Originally Posted by Diane

1. "doesn't mean that peripheral drivers don't exist"
We "suppose" that they exist to give us something to focus on so we can interact with someone's nervous system. They are "constructs" be they impingements by joints on neural tunnels (see Rod's statement, "I believe the gapping has a very specific effect of relieving mechanical deformation") or be they neural stress on a nerve anywhere in the body, acting up because it started to send hypoxia signals upstairs, and the brain decided to create a pain output to get the attention of the conscious awareness module it also gave rise to, supports, and organizes, the way I posit. I think I already explained why I feel they are a necessary evil. I already explained why I think my construct is equivalent to anyone elses' construct. I already explained why I think they are probably all irrelevant in the greater scheme of things. I think Barrett has already destroyed all the ones he ever used, and works without them, purely kinesthetically and without reference to any"thing." I think Luke himself all the way along on our little adventure has demonstrated how easily they can be knocked over. I think it's time to admit that they are mostly convenient mirages, and that as such, they are useful for playing let's pretend in order to communicate but that they, like the tooth fairy, are not real, and like tooth fairy science, a lot of info can be derived from positing they exist, but their plausibility in the first place is probably more rather than less like "subluxations" are to chiros, and about as useful. And about as real.

2. "or we don't affect them with therapy" We affect "something" with therapy - we affect the brain of the person we are treating, and it does its thing all the while, and its a great big chemistry set that tries to adapt to whatever is going on around it, to it, and within it. That I think we can safely say we "know" and we don't know anything else for sure.

3. "or it isn't worthwhile to look for them and attempt to treat them." See number 1.

I think a compelling case could be made, if I understood Damasio's work accurately, that top-down processing is always involved in a perception initiated by or involving bottom up processing. But, top down also can occur in absense of bottom up contribution (the as-if body loop). This would make a case for the necessary outcome of resolution of threat necessarily having a top-down processing component that would be synonymous with what we are referring to here as a placebo response.








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[Diane]

Hi David,
We have a welcome forum, where I would encourage you to go and start a thread about yourself, who you are, what you do. Meanwhile, welcome.
I agree with your post.

(I'd like to let you know that we discourage live links in posts, i.e., spammish-looking links, so I disabled yours while leaving enough of it visible for people to see what it is. Please take this link out of your signature line from now on, and do not post links to anything having nothing to do with the topic at hand. Thank you.)

[Barrett Dorko]

The suppose this were true thread dealt with these issues pretty well, I thought.

I'll not forget Luke making the point that though what I imagined as a rational "thing" forming the anatomical basis for a peripheral driver (the abnormal neurodynamic) might not exist as I thought it did, what I sought to do during my time with the patient could still be construed as "sufficient" and even "necessary" in many cases.

Up until that moment I had wondered why I was doing anything.

[Karen L]

As always it is great to see old threads pop up but in this case davidwilsoon is a cut and paste spammer. The signature violation is deliberate and he has cobbled an intelligent comment at the expense of Cory from post #50. davidwilson and variants of that name have been sent to Thunderdome recently.

Karen

[caro]

What a thread.

[Pete]

This programme includes an excellent examination of why placebo works.

[Diane]

Link to discussion of the book, The Patient's Brain: the Neuroscience Behind the Doctor-Patient Relationship, by Benedetti.

[Diane]

Link to Operator/Interactor Models of Manual Therapy, by me.

[JayCola]

Back in post #115 I had asked a couple of questions, and since then they have still been on my mind. Sooo, I finally was able to track down Dr. Fabrizio Benedetti's email address and asked him the same type of questions. This was our exchange...

Hello Dr. Benedetti, I am a big fan of your work. While I am not well
studied in the details of placebo, in reading your papers and other pain
related discussions I have wondered about certain questions and was hoping
your could answer, or at least clarify some of them. I understand you must
be very busy, so any response is extremely appreciated.

Much of my question has to do with this article
http://www.karger.com/gazette/69/benedetti/art_3.htm, There are 3
statements that caught my eye.

"First of all, there is today general agreement that the endogenous opioid
systems play an important role in some circumstances, and several lines of
evidence indicate that placebo analgesia is mediated by a pain-modulating
network which uses endogenous opioid as neuromodulators. "

"it was found that the very same regions in the brain are affected by both
a placebo and an opioid drug, thus indicating a related mechanism in
placebo-induced and opioid-induced analgesia"

"telling a patient that a painkiller is being injected (actually a
placebo) is as potent as 6-8 mg of morphine. An analgesic effect
stronger than the placebo was only observed when the hidden morphine dose
was increased to 12 mg. This suggests that an open injection of morphine
in full view of the patient, which is the usual medical practice, is more
effective than a hidden injection, because in the latter, the placebo
component is absent"

Now from how I understand your paper, these 3 statements taken together,
give me the impression that when administering an analgesic opiate in
conjunction with inducing a placebo response you're basically "hijacking"
the brains endogenous opioid system to just about double to affect of what
a hidden opiate injection would do. So if there's no placebo, just give a
larger dose of actual pain meds.

So then my first question I can't seem to find a clear answer to is, Can
the brain differentiate between the injected opiate and its own self-made
opioid? I'm assuming from the 2nd quote that it can not tell any
difference.

My main question then has to do with Opioid-Induced Hyperalgesia. Now it may be a stretch, but if a single dose of opiates can
sometimes increase sensitivity to pain, is it possible that a robust enough placebo response could theoretically induce the same
hyperalgesia since the brain can't tell the difference between endogenous
opioids and injected opiates? Could over utilizing the placebo response
in-turn lower a patients baseline pain tolerance? Obviously if this is
possible then it could have significant clinical repercussions for
therapies that have a significant placebo effect on patients (many manual
therapies). Could becoming dependent on a therapy for a placebo fix be
similar to becoming dependent on a regiment of pain meds? If so, would it
also be possible to
develop a tolerance for placebo induced analgesia, rendering that therapy
as no longer useful- and seeking out another therapy where your
expectation is greater (thus upping the dose of placebo, like one ups
the dosing for a pain med). For instance a person with LBP ups his
placebo expectation dose after he gets a tolerance for a physical therapy by going to get a steroid injection- and when that doesn't work, ups it
again to the best placebo - surgery.

Obviously I have made many assumptions based on my limited knowledge,
which is why I wanted to email you. While I am doubtful that these
questions are original, I would hope that perhaps that raise some points
that you could find useful in your studies. Of course, there is also the
cognitive aspect of placebo that isn't accounted for in my questions (and
I'm not sure just how important it is-I'm guessing very important for
there to be any long term effects of placebo)

Again, thank you for taking the time to read my email and any information
or insights you could pass on to me would be great. I also wanted to say great job on your podcast with Ginger Campbell. Keep up the good work.

Best regards,
Jason DiCola (future neursoscientist....maybe...one day...)

His response....

Dear Jason,

Thanks for your message and interest in our work.

As to the first question, it very much depends on what you mean by "Can
the brain differentiate......". In general I would say no, it can't, for
both exogenous and endogenous opioids act on the same MOR receptor. But,
with a more philosophical speculation, actually we don't know what it's
going on exactly...... For example, some areas seem to be different
(remifentanil activates PAG whereas placebo does not), so that in this
sense the answer is yes, it can differentiate.

As to the second question, no experiment of this kind has been done, but
you are probably correct. Sometimes hyperalgesia may occur after placebo
administration but so far we don't know why.

Our knowledge is limited as well and, for instance, one of the future
challenges will be to better understand whether or not drugs and placebos
act on the very same receptor. Once we will have understood this point, it
will be much easier to answer your question in more detail.

Hope this can be of help.

Best regards,

Fabrizio Benedetti

Good enough answer for me. Anyone who is interested in his email address can pm me and I'll give it to you. He responded within 3 days. It's publically available, but a little hard to track down. Perhaps a Somasimple interview in the future

[Frédéric]

Thanks Jason!

Nice to have a possiblity to open the channels with him.

I for one, would like is email for sure.

[Diane]

This is a link to a post where I put a paper by Petrovic 2010 which discusses this very thing. A prefrontal non-opioid mechanism in placebo analgesia.

[JayCola]

Diane, can you re-check your links, they don't seem to work (at least on for me). Can't wait to read them. Thanks.

[Diane]

You're quite right - they don't work. Sorry. Here is a link to the actual article. It appears to be free access now. http://pubman.mpdl.mpg.de/pubman/ite...in10%20(2).pdf

Here is a link to the thread, post 3. Sorry about that. Firefox crashed on me for the zillionth time.

[Diane]

Just stumbled on this paper, which likely has implications to do with needing to have another person in the role of "carer" when trying to get the brain to work better and diminish a pain production. Medial prefrontal cortex and striatum mediate the influence of social comparison on the decision process. Open access.

Abstract

We compared private and social decision making to investigate the neural underpinnings of the effect of social comparison on risky choices. We measured brain activity using functional MRI while participants chose between two lotteries: in the private condition, they observed the outcome of the unchosen lottery, and in the social condition, the outcome of the lottery chosen by another person. The striatum, a reward-related brain structure, showed higher activity when participants won more than their counterpart (social gains) compared with winning in isolation and lower activity when they won less than their counterpart (social loss) compared with private loss. The medial prefrontal cortex, implicated in social reasoning, was more activated by social gains than all other events. Sensitivity to social gains influenced both brain activity and behavior during subsequent choices. Specifically, striatal activity associated with social gains predicted medial prefrontal cortex activity during social choices, and experienced social gains induced more risky and competitive behavior in later trials. These results show that interplay between reward and social reasoning networks mediates the influence of social comparison on the decision process.

Maybe the medial prefrontal can only contribute in the presence of a "other".

[proud]

Not sure if this has been linked here but I thought was a really good review of Placebo/nocebo:

http://www.nature.com/npp/journal/v3...pp201081a.html

[Diane]

Originally Posted by proud

Not sure if this has been linked here but I thought was a really good review of Placebo/nocebo:

http://www.nature.com/npp/journal/v3...pp201081a.html

How Placebos Change the Patient's Brain.

Thanks proud!

[ian s]

http://www.youtube.com/watch?v=yfRVC...eature=related

very well produced video here ........

[PatrickL]

I have really enjoyed this thread. Within it I found the answers to many questions that have been popping up in my mind. But as usual, finding answers leads to more questions...

Luke said:
"There is no doubt that the brain is the key player, however, I think we need to be careful about attributing this kind of exclusivity to it. While it is true that in some, usually exceptional, circumstances pain is experienced in the absence of peripheral input (or no pain is experienced in the presence of peripheral input), the transmission of nociception into the CNS is still a very common 'cause' of pain."

To this Bas replied:
"I disagree somewhat. The brain is absolutely essential and central to pain. Peripheral input is of course present at all times, but it is the brain that interprets the input as a "threat" or as "negligible". It gives value to the input from the periphery. No matter HOW much nociception there is, it is ultimately the brain that "causes" the pain. After all the periphery as the patient perceives it, is entirely a virtual construct of the brain."

I really like the "periphery is just a virtual construct of the brain" concept. It is not far removed from The Matrix movies, which i think is cool! Anyways, within the context of pain this all fits nicely to me so long as there is no mesodermal pathology requiring healing or repair. Then it seems to fall apart. All of the discussions I've been reading make a point of limiting the scope of discussion to pain for which there is no pathology requiring healing or repair. This seems odd to me, and seems to leaving out a fairly major player in the injury/pathology/pain/therapy game.

I interpret this as- the mesoderm's contribution to the output of pain is irrelevant, accept for those circumstances when it is relevant. Does anyone see the hole in this thinking? Am i missing something at a fundamental level? If nociception is neither sufficient or necessary to cause pain, it shouldn't matter if there is pathology requiring healing or repair. If such pathology does does matter, it seems to me that nociception can be sufficient to cause pain.

[zimney3pt]

Have you ever notice a bruise on your body and wondered where did that come from. The bruise demonstrates some tissue damage occurred (noiceception), but there was no pain.

Noiception is neither sufficient or necessary for pain.

Sent from my BlackBerry 9330 using Tapatalk

[Luke Rickards]

If such pathology does does matter, it seems to me that nociception can be sufficient to cause pain

Hi Patrick,

It's important to be clear about the terminology here. Nociception refers to the transduction of a stimulus into a particular class of afferent inputs. The transmission of that signal to the central nervous system and then central processing are both required before pain is experienced in response to the nociceptive afferent firing.

So, it is never true that nociception alone is sufficient to cause pain.

I think what you're driving at is important though. The brain does get to decide what to do with noxious afferent input, but there are some ground rules. In exceptional circumstances it can do some exceptional things. But we shouldn't interpret a phrase like "Noiception is neither sufficient or necessary for pain" to mean that nociception isn't relevant. I think a large proportion of my patients present with clinically relevant nociception. I do my best to address this, as well as transmission and central processing mechanisms.