Pain Neuroscience – Teaching people about pain: Part 2
By Julie Beck, DC, MS, CSCS
In my first article in this two-part series on pain, I outlined conventional medicine’s central dogma’s about pain—how pain is perceived, categorized, identified and treated.
A summary of these conventional dogmas included:
- Pain has patho-anatomical origins. Or more simply put, pain is an “issue with your tissues” and the degree of pain is correlated with the degree of tissue irregularity or “damage”.
- Since pain is generated by damaged tissues, imaging (x-ray, CT, MRI) can identify the pain generating tissue(s).
- If the pain generators can be identified with imaging surgical measures are utilized to excise damaged tissue and pharmaceuticals can be used to manage or interrupt the experience of pain until (hopefully) appropriate healing occurs.
- If damaged tissues cannot be identified (as Fibromyalgia or Chronic Fatigue Syndrome) or if post-surgically pain is unchanged —continued use of opioids, anti-depressants and anti-inflammatories are utilized and additional or repeated surgical options may be explored.
(Note: It is important to remember that the above scenario is primarily referring to non-acute, non-traumatic pain events.)
So where did this approach come from?
Enter the Cartesian Model of Pain (Rene Descartes 1596-1650). This model is likely to blame for many of our current misconceptions about pain, and is still a driving force in how medicine is delivered today.1
If you’ve investigated neurology, you’ve likely seen the classic picture Descartes drew to describe what he believed to be the events that occurred for the experience of pain to be felt.
Briefly, the picture depicts a man with his foot perilously close to a fire; Descartes proposed that this event triggered a message (some type of “spirit”) that traveled up a hollow tube within the body to the brain and rang a bell that produced pain.
Not bad for his time, but we definitely should be able to do better than this now. Let’s start unpacking this by remembering one of neurosciences most progressive definitions of pain:
“Pain is a multiple system output activated by the brain based on perceived threat.“2
Ankle sprains are a common injury. And I don’t think anyone would argue that they are painful, but what if you sprained your ankle while crossing a street and out of the corner of your eye see a car heading straight for you.
In that moment, does your ankle hurt? Likely not.
When you get to the safety of the sidewalk does your ankle hurt? Likely so.
What just happened?
The only message the ankle can send the brain is a “danger message”. The car heading toward you in the above example is unarguably much more dangerous to your survival than your ankle sprain. Once safely on the sidewalk, the brain is now cleared to receive the messages from various ankle nociceptors (A-delta and C-fibers), activated by inflammatory chemicals and mechanical tissue inputs, passed to the spinal cord and ultimately the brain. OUCH.
Two important concepts here:
1) Pain is a construct of the brain or a brain output, and
2) Nociceptors are not pain fibers—the human body arguably does not have pain fibers. A-delta and C-fibers are listed in neurology texts as “pain” or “pain-conducting” fibers, but if this were true, you would have felt the unmodulated pain of your ankle in the middle of the street.
Note: Some have argued that a central nervous system sympathetic overdrive is at play and accounts fully for the above phenomena. This has been refuted.2,3
Recap thus far: Pain intensity does not strongly correlate with tissue damage, we have nociceptor not pain-fibers, and pain is a brain construct and it therefore decides when you will experience pain.
Next big concept: Since we have established that pain is produced by the brain, then altering the information that the brain receives can potentially alter “threat” perceptions and thus the experience of pain.
This is one of the reasons massage or bodywork can work so well for reducing pain, it is really reducing the brains overall assessment of threat.
There are representational body maps within the brain that are dynamically maintained and negatively influenced by neglect (decreased quantity and variety of movement) and pain. This means that increasing the amount and variety of movement can greatly reduce the brain’s threat perception. (Each case should of course be individually assessed by an appropriately trained professional for the most appropriate quantity, quality, type and duration of movement intervention).
What if your patient is afraid of movement, because some unknowing health care practitioner told them it was “bad” for them to move a certain way (ex. lumbar spine extension or flexion), or load a joint too much (stay off your feet), or that they have a really low pain-threshold?
(And pain-thresholds per se don’t exist, sensitized movements, positions or activities do exist).
This is where education fits in. Experts agree that the experience of pain is influenced by a large number of biological, psychological and social variables. The biological variables are familiar: our dietary, exercise and sleep habits, our inflammatory state, and how well our HPA-Axis is regulated (remember the hypothalamus and pituitary are brain structures) all affect our perception of pain. Rarely considered are the psychological and social variables: quantity and quality of our community social structures, belief about pain in general or associated with previous or familial experiences of pain.
Psychologically, I encourage you to examine the language you use, or more often incorrectly repeat, regarding pain especially in front of someone in pain. A few common examples: “bone-on-bone”, “fragile-spine”, and any version of “bulging or herniated-disc”. Think how these terms might inadvertently be negatively supporting someone’s pain state.
To close, remember pain is not a reliable indicator of anatomical damage. Chronic pain is a mix of multiple variables, with layers of brain-generated perceptual complexity. And patient education about what pain is, and is not, can be a top-down therapeutic intervention for your patients in pain.
Julie Beck, DC, MS, CSCS
Goldberg, LS. “Revisiting the Cartesian model of Pain”. Medical Hypothesis, (2008) 70(5):1029-1033.
Moseley, GL. “A Pain Neuromatrix Approach to Patients with Chronic Pain”. Man Ther, (2003) 8(3):130-140.
Melzack, R. “Pain and the Neuromatrix in the Brain”. Journal of Dental Edu, (2001)65:1378-1382