A Summary of New Insights from Pain Neuroscience Lecture

Dr. Tasha Stanton informs us that when it come to the experience of pain, what is happening in your brain might be more important than what is happening out in your body.

This blog article by Joe Muscolino is a summary of a lecture on pain neuroscience by Dr. Tasha Stanton, a physiotherapist from South Australia. This is a fascinating lecture that is well worth the time spent to watch it. However, until you find that time, here is a summation of the lecture, along with a few conclusions and applications added by Joe.

Pain is from our brain

Tasha started with a study on knee osteoarthritis to posit the hypothesis that the degree of pain a person experiences is actually in our brain and not in our knee. Certainly, this is fundamentally true. Pain can only be experienced in our brain, as all sensory perception is experienced in the brain.

She then states that 60% of us without low back pain would, if examined with MRI, show low back disc damage. Again, her conclusion is that the degree of pain we experience is more dependent on what the brain perceives than the actual amount of tissue damage in the joint/structure where the pain is perceived to exist.

I agree with this theory. I have long said that there is a “lag” between objective structural damage and subjective symptomology, including pain. If we always experienced every bit of structural damage that we have, we would be in pain all the time. There needs to be some sort of lag, or put another way, threshold above which we must be to experience pain. But I feel that there are limits to all theories/models to explain the functioning and the dysfunctioning of the human body. I feel that pain neuroscience advocates need to be careful to not swing the pendulum so far in the other direction that mechanics in the tissue are totally ignored.

“Our brain produces our sensations according to the credible believable evidence that is present, not just according to the sensory information from that body part.”

Neurophysiology of pain

Classic wisdom is that if you step on a thumb tack, nociceptors (thought of a pain neurons) send a message of pain up to the brain. She posits that the message is not yet a message of pain but rather is a message of danger that the brain then associates with other factors to determine that pain is felt.

I agree that this the association of danger would increase the experience of pain. But I feel that the statement is a little to black and white here. Would a newborn baby with little or no life experience, and therefore has few if no associations of what constitutes danger, not experience pain if a painful/noxious stimulus (such as having a needle pierce its body) occurred, especially if, for example, the painful stimulus were out of its line of sight? Although this study could not and should not be done for humane reasons, it would stand to reason that many newborns have probably experienced such noxious stimuli and been noticed to react by crying, which would seem to be good indicator of overt pain, and not just perceived danger (given that being a newborn, they do not have these learned associations of danger).

To be fair, she does then qualify this concept by then discussing how the brain can regulate/modulate the perceived pain in the nociceptors by facilitating or inhibiting them. So the construct is changed from an all or nothing to a shade of gray by modulation.

Central sensitization

Tasha draws the distinction between acute pain patients and chronic pain patients. She introduces the idea that the concept of pain neuroscience can be strongly related to the patients with experiencing chronic pain, in whom the association of danger related to pain is has been repetitively entrenched within their nervous system. This concept of amplifying the signal of pain is known as “central sensitization” of pain, which is a mechanism of nervous system neural plasticity that has long been accepted.

She gives a very nice analogy that if you turn up the volume of the radio, the person speaking on the radio has not actually started speaking louder, you have simply increased the amplitude of the sound that you hear. Similarly, central sensitization of pain amplifies the signal of pain so that signals that would not have been experienced as pain now are. In other words, otherwise sub-threshold sensory signals now are over the threshold and do actually cause pain. A lesser stimulus such as a simple touch might actually cause pain in a chronic pain patient. Now the sensory signals no longer correlate to the actual degree of tissue damage that is occurring. In essence, this is a case of the brain becoming hyper-vigilant in an effort to try to protect the person from possible damaging experiences.

“Neurons that fire together, wire together.”

Tasha discusses the example of a person who has anxiety because they are afraid that bending will cause low back pain. Because anxiety has now become associated (wired) with low back pain, whenever they have anxiety for any other reason, they will experience low back pain. This explains why so many people have characteristic pain patterns whenever they become stressed. These pain patterns could be low back pain, headaches, tight necks, stomach aches, or any other physical manifestation of anxiety/stress-induced pain.

She brings up an application of this for physicians. If we tell a patient that their MRI shows a herniated low back disc, and especially, then the patient might experience greater pain because of what they now believe to be the danger to their health. The conclusion here is that it is incumbent upon physicians and therapists to not “alarm” the patient when describing the results of physical examination. It should be explained that greater pain does not necessarily relate to the degree of actual tissue damage in the body. She discusses a study that showed that when patients were taught about this concept of pain sensitization that greater pain might not actually represent their tissue damage, these patients then had immediate functional improvement compared to the patients who were not taught about pain sensitization.

Altered Body Image

She then discusses how studies have shown how chronic pain patients lose proper proprioceptive input of their position in space and movement through space, their two-point perception of touch, and also the perception of the relative sizes of their healthy versus unhealthy body parts. In other words, they begin to lose the entire perception/image of their body.

We might be able to apply this concept to manual and movement therapies. Manual and movement therapists/instructors/trainers might improve their client’s pain level by improving the client’s perception of touch by manual therapy (e.g., massage therapy) and movement by movement therapists (e.g., Pilates and yoga instructors, fitness trainers).

The Brain Creates Pain to Protect us from Injury

Dr. Stanton then expands this concept of pain as being a construct of the brain to protect us from possibly further hurting ourselves to describing a study in which stiffness has also been found to not be totally dependent on the actual objective mechanical function/dysfunction of the tissues of the body. In other words, the brain can also modulate our perception of stiffness, making us believe that we are stiffer than we really are, with the intended goal of limiting out movement so that again, we do not cause possible further damage. She cites a study that related stiffness to pain and found that people with back pain overestimated how much they were actually moving by 60%. In other words, people with chronic back pain “feel” stiffer than they actually are.

Conclusions

There is no doubt that the brain is involved in the perception of pain.

• “Our brain produces our sensations according to the credible believable evidence that is present, not just according to the sensory information from that body part.”
• Neurons that “fire together wire together,” creating associations of pain with other factors.
• Central pain sensitization does play into the degree of the pain that the chronic pain patient/client experiences.
• In chronic pain patients/clients, there are measurable changes in their brain functioning.
• Therefore, to some degree, pain is a construct of the brain to protect us from possible further damage.

When we treat out patients/clients, we need to treat their body AND their mind. I believe that most therapists in the world of alternative health already recognize that there is a mind-body connection. Dr. Tasha Stanton does a beautiful job of describing how science is beginning to understand that the mind-body connection relates to the experience of pain.

I believe that understanding “pain neuroscience” theory is important to understand and apply. When we treat our patients/clients, we need to be aware that we are treating their body and their mind.

BUT, as with all excellent theories/approaches to treating our patients/clients, it is important to not exaggerate it and follow only this belief at the exclusion of all others. In other words, even though the brain can strongly modulate the experience of pain (and even stiffness), the mechanical factors in the periphery ARE still important. In other words, the role of manual and movement therapists to affect the mechanics of myofascial-skeletal tissues is still extremely important!

Watch the full lecture here https://youtu.be/ZWvyLJkBrLY