Pain science has learned a great deal in the past fifty years, but most of this information remains in the separate sphere of academia rather than on the frontlines of pain treatment. Or to put it another way: how do we take theoretical information from the medical literature and implement it in the clinic? In my eleven years as a Rolfer, I have found this information taking an increasingly central role in my decision-making, especially when a client has pain that might be termed ‘chronic’ or ‘persistent.’ In fact, a growing body of literature demonstrates that when therapists learn about pain, and teach their patients about pain, more effective treatments will follow.
What is pain? A simple definition is far from easy. It is easier to start defining what pain is not. The biggest mental pitfall to avoid is that pain and nociception, the experience of pain, are the same thing. Nothing could be further from the truth. We do not have ‘pain receptors,’ ‘pain nerves,’ ‘pain pathways,’ or ‘pain centers.’ There are, however, some neurons in our tissues that respond to stimuli considered ‘dangerous.’ For example, dropping a forty-kilogram kettlebell on your foot will send a prioritized signal to your spinal cord, which then is interpreted by your brain. Activity of this type in these nerves is called ‘nociception,’ which literally means danger reception. According to David Butler, “we all have nociception happening all the time – only sometimes does it end in what we define as pain.”1 Looking across various health professions, and in the literature, you could easily infer that nociception, in some cases, is equivalent to pain, as these two terms are often used as if they were interchangeable. However, this couldn’t be farther from the truth!
Pain is an Output from the Brain, Not an Input from the Body
The fundamental paradigm shift that has recently occurred in pain science is the understanding that pain is created by the brain, not a ‘pre-formed’ sensation that arrives from the body and is passively perceived by the brain. When a body part is damaged, nerve endings send a signal to the brain containing information about the nature of the damage – but no pain is felt until the brain interprets this information and decides that pain would be a good way to encourage you to take action that will help protect the body and heal the damage. The brain considers a huge amount of factors in making this decision, and no two brains will decide precisely the same thing. Many different parts of the brain help process the pain response, including areas that govern emotions, past memories, and future intentions. An injured hand means something very different to a professional musician than it does to a professional soccer player, and you can expect that they will have very different pain experiences from the same injury. The bottom line is: pain is in the brain, not the body.
It used to be assumed that ‘pain’ was conducted up to the brain with ‘pain nerves,’ and that once it got up to the brain, some ‘pain center’ would be stimulated and, voilá, you would feel something identified as ‘pain.’ This assumption was based on the general conclusion that all senses worked this way – light coming in the eyes stimulated vision centers and resulted in ‘sight,’ sound coming in the ears stimulated auditory centers and resulted in ‘hearing,’ and so on. Touch coming in stimulates kinesthetic centers and results in ‘sensation,’ and ‘pain’ was assumed to be a certain type or quality of touch. It was also assumed by everyone, scientists included, that eventually these centers would be found. Well, lots of stuff has been found, but pain centers have not. While reductive science continues to make advances, a fairer conclusion might be that that pain centers, if they exist, are mercurial at best.
The pain response is the combination of remarkable circuitry, with billions of neurons and glia with widely varying receptor sites. These receptors can change to different stimuli and alter what they are sensitive to, thanks to ‘synaptic plasticity.’ There are convergence zones and new arborizations, ascending and descending fibers creating interplay between the peripheral nervous system and the brain. Perhaps the most well-understood are somatotopic representational areas (brain maps of body parts) that change with experience. For the sake of even more confusion, we could add in ideas of gene expression: that genes (underlying the most basic stuff) make different things depending on the environment. Or, we could explain the level of description and detail offered by functional brain imaging (fMRI). Like the Humpty Dumpty story, there are all sorts of clues and truths in these levels of analysis, but no single integrated ‘pain center.’
The brain often ‘thinks’ the body is in danger even when it isn’t. A dramatic example of this is phantom limb pain, when the victim feels pain in a missing body part. Although the painful limb has been gone for years and can no longer send signals to the brain, the part of the brain that senses the limb remains, and it can be mistakenly triggered by cross talk from nearby neural activity. When this occurs, victims might experience incredibly vivid and painful sensations of the missing limb. Amazingly, phantom arm pain can sometimes be cured by placing the remaining hand in a mirror box in a way that tricks the brain into thinking the missing arm is alive and well. This is an extraordinary demonstration of the fact that the true target for pain relief is often the brain, not the body.
There are many other more commonplace instances where the brain does not know what is going on in the body and causes pain in an area that is clearly not under threat. Any kind of referred pain, where pain is felt a distance from the actual problem, is an example of this. Some people have a condition called allodynia, where even normal stimuli such as lightly touching the skin can cause excruciating pain. This is an extreme example of something that might occur quite commonly on a much smaller scale – the brain misinterprets innocuous sensory information as evidence of tissue damage, and causes unnecessary responses.
In contrast, even when nociception does exist (i.e., there is an existing physical limb or neck or back involved that ‘hurts’), the brain can ignore it just fine if it has something else more important that it prefers to deal with in a given moment. Sometimes more nociception actually helps to decrease pain perception for a while, so in some ways they may be reciprocally related. This is synonymous to rubbing your head after hitting it on something. The local activation of sensory neurons dilutes the experience of the ‘pain’ by giving the brain something else to focus on.
Generally, receiving initial input through nociception is required for the developing brain of an infant to learn how to construct a pain experience. For example, children born without the ability to ‘nocicept’ (a condition known as congenital analgesia) will never learn to feel ordinary ‘pain’ because their brains will never learn to construct for them a pain ‘experience.’ They do not live long as a rule, and must be watched closely by their caregivers to avoid grievous injury.
To go back to the ‘senses,’ it is clear that ‘pain’ is like no other sense, no other feeling we have. In fact, it’s not even a ‘sense’ strictly speaking, but more accurately a perceptual construct. So, where does ‘pain’ come from? Pain is something the brain constructs out of information it receives (assuming the appropriate type and array of receptors exist, as they do in most people). Once the brain has made the construct, it sends it to the self-aware part of itself, the part you ordinarily think of as ‘you.’ It builds constructs all the time, out of everything around it. This is known as ‘neuroplasticity.’ Pain is just another thing the brain can make as it tries to make sense out of its own existence. Most of what the brain makes is useful: pain is useful too. And the brain usually makes it for just long enough to slow you down to help the body heal. Norman Doidge, author of The Brain That Changes Itself, calls pain ‘the downside of neuroplasticity.’
When pain persists long past its due date, you may start to feel you and your brain need some help with ‘de-constructing’ it. This is when pain is much less about what is happening in the tissues. The brains of most people with persisting pain have no problem de-constructing pain production with treatment – usually this is a quite straightforward process once treatment is initiated. With a bit of pain education as a focus, and some judicious, well-thought-out manual therapy to provide novel input to the brain (see neuromatrix model below), the brain is usually more than happy to return to normal output. It downregulates itself (similar to the head-rubbing example above), and the peripheral nervous system follows suit.
Thanks to the self-righting capacity of the scientific method, the meticulous research of Melzack and Wall, scores of people in pain who have contributed to advancing science, and the many lab animals sacrificed to the cause, Descartes’ pain theory has been laid to rest. Though not the final word I am sure, pain is now thought to be a neurologically and neurochemically enacted sensorimotor ‘perception’ that the brain constructs as a response to various kinds of input and as an output to the following:
I have found the neuromatrix model of pain helpful (see Figure 1). More than a reductive biological view, it is a contextual view with the client in the center. In this model, it’s harder to quantify or integrate (similar to the Humpty Dumpty example), but inclusive and orienting. For example, it includes the hormone systems as modulators.
To break it down a little more (quoting Diane Jacobs):2
<img src=’/imgs/2011/1183-1.jpg’>
<i>Figure 1:</i> Factors that contribute to the patterns of activity generated by the body-self neuromatrix, which comprises sensory, affective, and cognitive neuromodules. The output patterns from the neuromatrix produce the multiple dimensions of pain experience as well as concurrent homeostatic and behavioral responses.3
Placebo? Desirable or Not?
Sometimes just the act of making an appointment can make a difference in pain levels. Perhaps the sense of getting down to it and taking a concrete step to start dealing with the pain raises the mood a little. It may also affect cognitive-evaluative input somewhat, and create a bit of a placebo response within the system. In recent work, Wall described the need to tread very carefully in unraveling the placebo response. He said (roughly paraphrased), placebo is not something we do to brains, it’s a response we must elicit from them. The brain can fix itself over time (not even that long a time); it needs to be turned into an ally so it can learn to stop being its own enemy. In fact, the brain is the only thing that can turn itself around. A placebo response will be something the brain will (hopefully) make naturally as a result of some new input that it examines and learns something new from. Wall also said that the placebo response that the brain makes for itself is always dose-specific and duration-perfect for maximal and often permanent relief. In that synaptic connections in brains are mostly about the chemistry within them, a placebo response, i.e., change for the better in terms of chemistry made by the brain itself, is a good thing. Good treatment helps elicit this response.
Most of the pain science that manual therapy finds itself interested in is based on this neuromatrix model of pain. It is clear, simple, and allows the client to see himself/ herself in the center of the experience. The client is not peripheral to some biological theory of pain, but the one who will help his/her own brain turn itself around. The neuromatrix model can give you some conceptual leverage for spotting erroneous beliefs that the client may be holding about the body and about the pain that feels as if it’s coming from it. Erroneous beliefs can actually interfere with your brain’s ability to relieve or stop its own pain production. The model provides a starting point for understanding, a place to begin to get a grip on pain, instead of feeling helpless and letting it keep a grip on the system.
To really treat pain, we, as practitioners, need to focus just as much on the brain as the spine, muscles, and/or joints. When the treatment approach takes this integrative view (e.g., helping to educate, evaluate, and work with each client’s cognition in light of his/her pain response), damaged tissues will heal to the best extent possible in a few weeks or months, and then pain should end. Why should it continue if the body has already done its best to heal it? When pain continues for long periods of time or damage, there might be a problem with the pain-processing system, not the body.
Probably the biggest push-pull within the research on therapeutic amount or type (I recognize this is a small number of studies) is defining how much of the therapeutic effect is direct or nonspecific. People who have learned/taught a lot of operator models and tissue-based examination schemes tend to say the primary issue is mechanical nociception, and therefore specific effects like examination and treatment skill for the site of injury (e.g. periphery) are most important. People who have learned/taught a lot of interactor models and neuroscience tend to say the primary issue is central and therefore nonspecific effects like placebo, education, or cognitive-behavioral features are most important.
There’s no way to reconcile these views other than to take what seems to be the most reasonable position – that the therapy should be tailored to the presentation and both views may be more or less operative in any client at any given time. In my opinion, we should be comfortable enough with neuroscience to abandon the strict tissue-based explanations and reasoning, while being comfortable with mechanical nociceptive-origin pain explanations and treatments.
Like most things, the answer is probably in the middle somewhere. Rolfers realize the interconnectivity of the body and often take a decidedly global approach. I love this about our work. For me, applying some of the recent discoveries about pain science in my practice has been both orienting and helpful. It has allowed me to feel a bit more empowered about the reasons behind my therapeutic decision-making. I hope, too, that educating myself and my clients about pain is a way to achieve the most facilitated (if there can be such a thing!) treatment result.
Endnotes
References and Support
Angevinem, Jay B., Encyclopedia of the Human Brain. Maryland Heights, Missouri: Academic Press, 2002.
Butler, David S. and G. Lorimer Moseley, Explain Pain. Adelaide, Australia: Noigroup Publications, 2003.
Butler, David, The Sensitive Nervous System. Sydney, Australia: NOI Group Publications, 2006.
Jackson, Marni, “Pain and Its Mysteries.” Maclean’s, May 27, 2002, pp. 38-40. Available at http://fleen.psych.udel.edu/ articles/AEP04.3.12.PDF.
Jacobs, Diane, “Dermoneuralmodulation Treatment Manual” (materials from a class, 2007).
Lucas, Nic, D.O., “The Sensitive Nervous System – A review by Nicholas Lucas.” www.noigroup.com/documents/SNSreview- Nicholas-Lucas.pdf.
Melzack, R., and P. Wall, The Challenge of Pain. New York: Penguin Group, 2004.
Merzenich, Michael, “Michael Merzenich on Re-wiring the Brain.” TED talk available at www.ted.com/talks/michael_merzenich_ on_the_elastic_brain.html.
Moseley, G.L., “The Mirror Cure for Phantom Pain.” Scientific American, April 2008.
Painonline.com Severe kinds of intractable, non-neuroplasticizable pain are unfortunate facts of life for some.
Scholarpedia article on brainstem. <a href=’http://www.scholarpedia.org/article/Brainstem’ target=’_blank’>http://www.scholarpedia.org/article/Brainstem</a>
Shacklock, M., Clinical Neurodynamics, Oxford: Elsevier Science, 2005.
Shacklock, M., Biomechanics of the Nervous System: Breig Revisited. Sydney, Australia: Nuerodynamic Publications, 2007.
Shacklock, M., Moving in on Pain. Sydney, Australia: Butterworth-Heinemann, 1995.
Strong, A., A. Unruh, A. Wright, and G. Baxter, Pain: A Textbook for Therapists. Philadelphia: Churchill Livingstone, 2002.
Thacker, Mick, discussion of Explain Pain in NOI Notes on Movement as Antigen. http:// noinotes.blogspot.com/2009/10/noi-noteson- movement-as-antigen.html.
Wall, P., Pain: The Science of Suffering. New York: Columbia Press, 2000.
Wikipedia article on nociception. <a href=’http://en.wikipedia.org/wiki/Nociception’ target=’_blank’>http://en.wikipedia.org/wiki/Nociception</a>A Modern Look at Pain[:]
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