Sarno and others have been saying this - chronic pain (especially back) is not about structure - for 30 years.
[quote]alexus wrote:
- does anybody know whether they have tested wether INFORMING a person that they are about to begin a course of (effective) placebo treatment undermines the placebo response? i’m very interested in this with respect to ethical issues around informed consent…[/quote]
Have you heard of the “nocebo” effect? There is a lot to read out there, I don’t have links to any studies or trials off hand, but its pretty interesting what the power of suggestion does to a person. Check it out.
Jimmylosis,
Absolutely…
Regarding nocebo…
Benedetti, F., Lanotte, M., Lopiano, L., & Colloca, L. (2007). When words are painful: unraveling the mechanisms of the nocebo effect. Neuroscience, 147(2), 260?271. doi:10.1016/j.neuroscience.2007.02.020
van Laarhoven, A. I. M., Vogelaar, M. L., Wilder-Smith, O. H., van Riel, P. L. C. M., van de Kerkhof, P. C. M., Kraaimaat, F. W., & Evers, A. W. M. (2011). Induction of nocebo and placebo effects on itch and pain by verbal suggestions. PAIN, 152(7), 1486?1494. doi:10.1016/j.pain.2011.01.043
van Laarhoven, A. I. M., & Evers, A. W. M. (2011). Response to the commentary ?You may (not always) experience what you expect: In search of the limits of the placebo and nocebo effect.? PAIN, 152(8), 1931?1932. doi:10.1016/j.pain.2011.05.025
Crombez, G., & Wiech, K. (2011). You may (not always) experience what you expect: In search for the limits of the placebo and nocebo effect. PAIN, 152(7), 1449?1450. doi:10.1016/j.pain.2011.02.028
Lock,
I would recommend the writings of Bialosky from the University of Florida. Also Pickar’s writing on the neurophysiological response of spinal manipulation.
Bialosky, J. E., Bishop, M. D., Price, D. D., Robinson, M. E., & George, S. Z. (2009). The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model. Manual Therapy, 14(5), 531?538. doi:10.1016/j.math.2008.09.001
Pickar, J. (2002). Neurophysiological effects of spinal manipulation. The Spine Journal.
One question to ask is: has the activation of a “insert muscle” been consistently shown to improve outcomes for back pain?
McGill says brace/co-contraction, no TVA. Virtually no outcome data.
Hodges say motor control: no significant effect sizes or outcome data.
Janda says stretch tight, strenghen lengthened (upper/lower crossed syndrome): no outcome data.
Sahrmann says fix the muscle imbalance: very little outcome data.
Gray Cook learned from Sahrmann with a little motor control thrown in: no outcome data of substance.
If we look deeper into these ideas; we cannot lengthen muscle without adding sarcomeres, end of story. Correlation between muscle activation patterns and pain are non-linear and multi-variable.
We have some low level evidence that suggests an exercise protocol may reduce recurrence of low back pain (in 1996 nonetheless).
New research from the military tells us pain neuroscience education is more effective at prevention than core exercise similar to McGill’s big 4.
olifter-
before I take the time to go in depth on a response, I want to make sure I am reading what you are saying correctly.
Are you saying:
1- structure has no input to pain- specifically chronic pain?
2- pain is purely a nervous phenomenon mediated by the brain once the initial trauma/inflammation has subsided/healed?
3- structure is determined by genetics and no outside influences can change it? this applies to muscle length, resting joint angle, posture, etc.
4- you cant change any intrinsic qualities of any tissue without surgery?
please bulletize any points i missed
thanks
Da Man,
- Input is simply that, input. Whether or not there is an ouput of pain depends on many variable. As pain becomes more persistent, the tissue becomes less of a factor. The nervous system is the problem. In the end all pain is neurogenic. Of course, even acute injuries create plastic changes in the brain.
I would recommend:
Flor, H. (2003). Cortical reorganisation and chronic pain: implications for rehabilitation. Journal of rehabilitation medicine : official journal of the UEMS European Board of Physical and Rehabilitation Medicine, (41 Suppl), 66?72.
May, A. (2008). Chronic pain may change the structure of the brain. PAIN, 137(1), 7?15. doi:10.1016/j.pain.2008.02.034
Kapreli, E., Athanasopoulos, S., Gliatis, J., Papathanasiou, M., Peeters, R., Strimpakos, N., Van Hecke, P., et al. (2009). Anterior cruciate ligament deficiency causes brain plasticity: a functional MRI study. The American journal of sports medicine, 37(12), 2419?2426. doi:10.1177/0363546509343201
-
All pain is neurogenic. This cannot be refuted. Pain of mechanical origin, chemical origin, peripheral sensitization, central sensitization are all neurogenic; i.e. output from the brain when threat is detected.
-
Structure and adaptations are influenced by genetics. This involves both the musculoskeletal and nervous system. We are all aware that we can train to enhance physiological factors/responses via resistance training for hypertrophy, aerobic/anaerobic training for oxygen uptake/lactate response, etc. We can change posture from a static and dynamic perspective (sit up tall, slouch etc.), but has that improved outcomes in pain research? No. To impact muscle length in normal, non-neurologically involved patients (CP, etc) or true contractures (surgical intervention) you must stretch to a prolonged period that adds sarcomeres to the muscle. Once this stretching protocol is ceased, the structure returns.
-
Can we create plastic changes with manual intervention as suggested by those is the rehabilitation field with improved outcomes? No. Fascia release, scraping the skin with toys (animal studies need not apply), lengthening muscle, etc. are a few examples.
Can we change intrinsic properties in tissue without surgery? Yes, exercise would be an example.
I’m not saying people don’t get relief of symptoms from the mentioned interventions, I’m calling into question the underlying mechanisms and belief systems that are out there.
I look forward to your response…
heaps for me to follow up on! thanks very much 
I have found that if I have 10 patients with nearly identical pain symptoms and life style, the one that I feel trusts me the most is the one who’ll get the fastest reduction in pain and disability. This is using the same kind of treatment, a combination of massage + mobilizations + exercise.
Sometimes, patients have been cured simply by being given a diagnosis, which relieves their anxiety.
Lock,
I can’t disagree with your first statement. I bet most of those in rehabilitation would report the same thing if they were honest. This alone should lead them to question what they are doing, why they are doing it and what they are telling their patients.
I will disagree with your second statement: in my experience the diagnosis (biomedical) leads down a nasty road of increased healthcare utilization, tests, injections, meds, surgery without improved outcomes.
[quote]olifter1 wrote:
Da Man,
- Input is simply that, input. Whether or not there is an ouput of pain depends on many variable. As pain becomes more persistent, the tissue becomes less of a factor. The nervous system is the problem. In the end all pain is neurogenic. Of course, even acute injuries create plastic changes in the brain.
I would recommend:
Flor, H. (2003). Cortical reorganisation and chronic pain: implications for rehabilitation. Journal of rehabilitation medicine : official journal of the UEMS European Board of Physical and Rehabilitation Medicine, (41 Suppl), 66?72.
May, A. (2008). Chronic pain may change the structure of the brain. PAIN, 137(1), 7?15. doi:10.1016/j.pain.2008.02.034
Kapreli, E., Athanasopoulos, S., Gliatis, J., Papathanasiou, M., Peeters, R., Strimpakos, N., Van Hecke, P., et al. (2009). Anterior cruciate ligament deficiency causes brain plasticity: a functional MRI study. The American journal of sports medicine, 37(12), 2419?2426. doi:10.1177/0363546509343201
-
All pain is neurogenic. This cannot be refuted. Pain of mechanical origin, chemical origin, peripheral sensitization, central sensitization are all neurogenic; i.e. output from the brain when threat is detected.
-
Structure and adaptations are influenced by genetics. This involves both the musculoskeletal and nervous system. We are all aware that we can train to enhance physiological factors/responses via resistance training for hypertrophy, aerobic/anaerobic training for oxygen uptake/lactate response, etc. We can change posture from a static and dynamic perspective (sit up tall, slouch etc.), but has that improved outcomes in pain research? No. To impact muscle length in normal, non-neurologically involved patients (CP, etc) or true contractures (surgical intervention) you must stretch to a prolonged period that adds sarcomeres to the muscle. Once this stretching protocol is ceased, the structure returns.
-
Can we create plastic changes with manual intervention as suggested by those is the rehabilitation field with improved outcomes? No. Fascia release, scraping the skin with toys (animal studies need not apply), lengthening muscle, etc. are a few examples.
Can we change intrinsic properties in tissue without surgery? Yes, exercise would be an example.
I’m not saying people don’t get relief of symptoms from the mentioned interventions, I’m calling into question the underlying mechanisms and belief systems that are out there.
I look forward to your response…
[/quote]
- (and partly 1) All pain is most definitely NOT neurogenic - neurogenic meaning starting at the nervous system, caused by the nervous system. all pain does indeed have a neural component- being that the spinal cord and brain are the integrators and processors of the pain signals being sent from the tissues. arthritis, psoriatic arthritis, ankylosing sponylitis and multiple other inflammatory conditions are painful because of inflammation. chemicals such as TNF-alpha, inflammatory cytokines, and other CHEMICALS give rise to pain. The pain in this case is CHEMOGENIC. These chemicals then give rise to the nervous signal by binding to receptors that signal the nervous system to send the pain signal. If you want to get reeeeaaaally down to it, the signal that travels down the nerve and through synaptic clefts is actually given rise to by chemicals like sodium, potassium and neurotransmitters.
painful chemicals in arthritis:
Role of cytokines in rheumatoid arthritis - PubMed
ALSO- in many pain studies, pain is induced by injecting hypertonic saline. that would most definitely be a chemical/mechanical pain
-
I concur that there is a lack of evidence concerning structural changes and pain reduction. It appeared your were saying that it is impossible to cause changes to any body tissue.
-
I also concur with many of manual techniques being sketchy at best. Grastonesque techniques especially get me. Assuming you can break up scar tissue/collagen by scraping the skin hard, what is going to keep it from reforming because you just sparked the same inflammatory process that laid down the collagen in the first place.
Not numbered- your mention of ‘post hoc ergo propter hoc’ flies in the face of the scientific method. The same scientific method the researchers you cite used to come to their conclusion. In scientific method, you change A and look for a change in outcome B and determine that A caused/led to/fixed B. I do believe it is widely accepted as a valid approach in determining influencing factors in outcomes. In fact, it is the only method.
Da Man,
You make a similar argument of many in the rheumatologic field or those suffering from a condition in this realm.
All pain is an output from the brain. There is no such thing as a pain signal, pain receptor, pain fiber, pain tracts, or pain centers in the brain. We have mechanical, chemical, thermo receptors. This is neuroscience 101. I believe your are confused by using pain as synonymous with the term nociception. Nociception is not pain, it is simply that, nociception; which is neither sufficient or necessary for pain.
While inflammation is very important for the pain experience it is the brain that outputs pain. The brain wants to know about inflammation because it is a threat in many cases. But it is still insufficient to create pain. Take those with RA or inflammatory conditions and place them in a room. Drop a lion inside, will they have pain? How can an individual have phantom limb pain? How can we create pain in fake limbs? Why wouldn’t a soldier have pain after being shot in the midst of a fire-fight? How do we explain phantom limbs in children born without limbs? I’m sure many athletes have some form of inflammation during an athletic events without pain.
Link for you to look over from two of the leading clinical neuroscientists in the world…
http://www.ted.com/talks/vilayanur_ramachandran_on_your_mind.html
[quote]olifter1 wrote:
Lock,
I can’t disagree with your first statement. I bet most of those in rehabilitation would report the same thing if they were honest. This alone should lead them to question what they are doing, why they are doing it and what they are telling their patients.
I will disagree with your second statement: in my experience the diagnosis (biomedical) leads down a nasty road of increased healthcare utilization, tests, injections, meds, surgery without improved outcomes. [/quote]
My second statement kind of coincides with my first. For instance, I had a patient the other day who was deathly worried that she had a degenerative hip, because her sister told her so, and that she certainly had to have surgery. Turns out that all she had was pain originating from the converging zone of psoas and iliacus. We spent 15 minutes talking instead of treating, because she wanted more information about degenerative changes, the muscles surrounding the hip, and so fourth. This led to her having an increased amount of trust and confidence in me, because I could tell her what was hurting, and that it was not dangerous.
She came back 5 days later having had no pain.
I believe that the homunculus really plays a gigantic role in the patients pain, and that talking is the most important thing we do with our patients. It is also the hardest to get good at.
[quote]olifter1 wrote:
Da Man,
You make a similar argument of many in the rheumatologic field or those suffering from a condition in this realm.
All pain is an output from the brain. There is no such thing as a pain signal, pain receptor, pain fiber, pain tracts, or pain centers in the brain. We have mechanical, chemical, thermo receptors. This is neuroscience 101. I believe your are confused by using pain as synonymous with the term nociception. Nociception is not pain, it is simply that, nociception; which is neither sufficient or necessary for pain.
While inflammation is very important for the pain experience it is the brain that outputs pain. The brain wants to know about inflammation because it is a threat in many cases. But it is still insufficient to create pain. Take those with RA or inflammatory conditions and place them in a room. Drop a lion inside, will they have pain? How can an individual have phantom limb pain? How can we create pain in fake limbs? Why wouldn’t a soldier have pain after being shot in the midst of a fire-fight? How do we explain phantom limbs in children born without limbs? I’m sure many athletes have some form of inflammation during an athletic events without pain.
Link for you to look over from two of the leading clinical neuroscientists in the world…
http://www.ted.com/talks/vilayanur_ramachandran_on_your_mind.html[/quote]
There might be no such thing with the name “pain signal” or “pain tracts”, but inflammatory mediators (some of which spoken of by Da Man) certainly seem sufficient to cause a “pain signal” transmits to the brain. And no “pain tracts”? Am I missing something in the progression of neuroscience? The Spinothalamic TRACTS - pain sensation are one of its defining characteristics (along with temperature, etc.). Considering localization of spinal cord lesions is partly done through a physical exam, I’m not sure how one can refute the existence of different “Tracts” that are responsible for different perceptions and functions, one of which being the transmission of pain.
I am still failing to see how structure and chemical messengers both should not be involved in the treatment of chronic pain. I understand what you are saying, but agree with Da Man more… in the sense that the brain is an output center for pain but in a normal healthy individual, it’s not going to fire off random pain sensations without some inciting input. Of course there are exceptions to this (i.e. phantom limb) which to me indicates a very important COMPONENT of the brain in pain signaling (which I think no one would argue against).
I mean the way I see it is this. Let’s take an analogy: In order to breathe someone doesn’t only need a brain, in order to play the piano, someone doesn’t only need a brain… lungs and hands would be needed in these instances to complete the required tasks. Similarly, these couldn’t function without CNS input or some other external stimulus. In the same way, the brain may be what is in control of pain signals ultimately, but for someone w/ gout to have pain they first need to develop the monosodium urate crystals somewhere in their “structure.” After this pain and the pathway to this pain has been established, sure, you could convince me that the brain has a much stronger role in chronic pain now than it did in the initiation of the pain of gout. However I would still say that the management of gout shouldn’t only be from some therapy targeted at the brain’s perception of pain, but should include measures that would prevent the re-occurence of a tophus by keeping uric acid levels controlled(something like allopurinol for example). In the same way, prevention of “chronic pain” for a herniated disc should not only include methods to target the brain’s perception of pain (or perhaps you would rather me say output/control of pain) but also strengthening the musculature to provide greater stability with the hope of preventing future injury.
DTC,
The ideas of pain tracts, pain fibers and pain centers is a theory proposed in 1664 by Rene Descrates. It has been refuted. He is another link to demonstrate this with research. Please watch this, it will help you understand this.
http://www.wcpt.org/sites/wcpt.org/files/files/cpd/FS-115-PainManagement/player.html
This is not about who you agree with more. To reject what is being presented is fine. Understand it is refuted by those in the neuroscience and pain science communities/research. I agree with the influence that inflammatory mediators, immune system and endocrine systems have on pain output. They are very important. The brain still makes the final decision. Everything coming in: sensory, endocrine, cognitive, emotion, immune, neural is still input. Pain is an output after everything is processed. All play a role and some may be more important, possibly sensory, but whether or not pain occurs, is an output based on the brain’s opinion of threat.
The ascending tracts do not transmit pain, only signals and stimuli. Nociception is not pain. Noxious stimuli is not pain. There can be noxious stimuli without pain. Non-noxious stimuli can create an output of pain: allodynia. There is a pain output but the stimulus was not sufficient to create tissue damage. We can have a heightened pain response to normally noxious stimuli: hyperalgesia.
Pain can occur in the absence of any insult in normal individuals as well. Peripheral nerves may create abnormal impulse generating sites or you may have a ‘zing or zap.’
Olifter,
This supposed non-existence of spinal tracts is very surprising to me as it’s still part of neuroanatomy textbooks and medical education today. I’ll have to do some research on this as I’m not someone who takes things at face value. Thank you for the video in the meantime.
Regarding the management of pain, I of course am not in disagreement that the actual final word comes from the brain but was disagreeing on something else. It seemed to me that you were stating there was a lack of importance of pain inputs on the “afferent” side of pain pathways, if you will. It seems however that I misunderstood you, and that you also believe chemical and physical mediators of pain are important… just not critically important because they are not the final word. We may not be in agreement on their spectrum of importance (it seems like you think they are less important than I do) but at least I know now that you also think they are important and a component of pain. That was my main point that I was in disagreement with.
As far as what recent neuroscience and painmed research has discovered and their apparent shifting ideology, I think it is interesting and it seems you are far more versed and knowledgeable on the subject than I. In the meantime, while research is ongoing and new treatments are established (and perhaps the view of neuroscientists and pain med practitioners will again change) I think it is unwise to discontinue treatments that have been helping patients for years. I’m not saying that all patients are helped by these treatments to the same degree, as all treatments are on a spectrum of responsiveness, but there is certainly anecdotal evidence and evidence from studies that supports the benefit patients receive from certain techniques used by osteopaths, chiros, and PTs. Are these ineffective in curing chronic pain? Absolutely, often times they are. However, are they effective in providing relief of acute issues, prevention, and short-term relief in chronic pain patients? Yes. If something helps and doesn’t harm, there’s not really a reason to bash it in my book. Of course this then brings up the debate of health care cost which would be for another thread entirely.
Thank you for your thoughts.
Best,
DTC
DTC,
“This supposed non-existence of spinal tracts is very surprising to me as it’s still part of neuroanatomy textbooks and medical education today.”
This is not never written or suggested. I am not saying spinal tracts do not exist. Spinal tracts are very real. Simply looking at patients with spinal cord injuries demonstrates this. What I said was they don’t transmit pain signals. A patient with a SCI many lack two point discrimiation, vibration sense, light touch, temperature, etc. in certain regions of the body. Again, these are stimuli, not pain.
OLifter, sorry for the confusion on what you are relaying. Based on your most recent post, it seems like you’re just trying to point out that the “pain” component that is often labeled as part of the SpinoThalamic tract is mislabeled, as it is an afferent pathway and the actual signal for pain would come from the brain? As in, the pain signal to the body isn’t generated until the tract continues up to the thalamus → cortex?