Pain is more complex than scrunching thousands of interactions into one glorified number from 0 to 10. There’s not a single healthcare professional or strength coach (or anyone) that doesn’t deal with pain. With so many professionals treating pain, how can it be so difficult to define? In the patient/client’s eyes, treatment is rendered ineffective if pain fails to resolve. Pain is as much a grueling burden as an elusive mystery.

Whether it be a chronic or acute condition, every human being is designed to endure pain—your survival depends on it. Acceptance and appreciation of this attribute is a step in the right direction in understanding your pain.
Is pain a life sentence? According to respected pain science expert, David Butler, the answer is NO.
Our body has an innumerable amount of pain sensors that flicker at the mere thought of pain. These sensors, which are microscopic proteins made inside neurons, are replaced every few days. Good news for a chronic pain sufferer. The pain sensor manufacturing rate can also decrease or increase based on the body’s perceived threat status.
So if these sensors don’t last long and the rate of production varies, why is chronic pain so…chronic?
“Ignition nodes,” a term coined by Butler, are areas of the brain that are essentially hijacked by the presence of pain. Normally, these cortical tissues are devoted to other qualities such as emotion, movement, memory, and sensation. But when chronic pain is the culprit, it reroutes the electrical signaling of the nervous system to be more devoted to the pain experience. Survival is of foremost importance, not remembering if you forgot to close the garage door. That throbbing ice pick in your shoulder is a little more important than your leaf blower getting stolen.
So are people that are hurting in a bad mood because they are simply in pain or because their brain is being robbed of “good mood real estate?” Probably a little of both.
A “danger” memory is placed within the cells by planting a number of excitatory sensors around the danger messenger neuron. These sensors open longer each time they are activated. Aches that hurt will ultimately hurt more—a term known as hyperalgesia. Otherwise, pain that remains constant will no longer be enough to continually set off the alarm system. Basically, sensitivity to the pain increases to allow for the perception of pain to remain relatively stable.

Neurons also have the capacity to weave complex webs of pain “highways.” Neurons can potentially grow toward the “danger” signal up to 30% of its original length and activate other areas to cause pain. Also, MRI imaging has verified brain structural adaptations associated with chronic pain.
Chronic pain really just becomes a sensitivity game whose electrical pathways can be accessed more readily the more often traveled even if the stimulus (tissue damage) is not present.
Agonizing pain with no further tissue damage? That’s correct.
And this is where the pain experience becomes VERY gray.
Visualizing movement has been documented to cause swelling and more pain in the hurting area. Thoughts have even been shown to increase pain.
Fear and anxiety can flood your cells with hormones having a strong affinity for these meticulously placed excitatory sensors created by the “danger” messenger neuron. Emotion acts as the volume knob to your pain tune.
So if your thoughts and emotions are inseparable from pain, how can you explain all the current research of asymptomatic structural injuries documented with diagnostic imaging? I’m sure these people have “bad days” or some form of anxiety to ignite the pain experience. Being in an MRI tube is enough to make anyone’s back hurt.
This could be because pain fails to manifest itself if the injury is gradual enough to not set off the body’s alarm system. Threat perception is completely different when you herniate a disc over the course of 20 years compared the one time you “threw out” your back moving a friend’s couch.
In the latter instance, your body has managed to localize the danger and begin to stick adrenergic receptors around the site like a set of James Bond proxy mines. The slightest trigger can cause an explosion of pain.
Never see it coming.
Herniating a disc over 20 years is like watching grass grow, your body’s defense system doesn’t care! When you are in a high anxiety situation, the excited biochemical molecules that blast through the cells of your body aren’t being sucked in by these carefully placed receptors because they are NOT there!
It is important that everyone becomes educated on their own pain experience. What exercises are a risk to your specific injury? What social situations trigger your pain? Is performing painful movements with perfect technique actually hurting you? Does getting stung by a bee hurt more because you stepped on a hive as a kid?
Each person’s dynamic pain surveillance system must be based on a biopsychosocial model. Chase the threat (whatever this may be) and have the courtesy to understand that each person is the sole owner of their pain.
Just because you tore your hip labrum back in 1957 when acetabular labrums were “new” doesn’t mean you know “how it feels.”
Take inventory of your pain.
What causes it?
Long formal engagements, pistol squats, wearing a swimsuit, thinking about throwing a ball, lack of sleep…the list can go on forever.
What makes it better?
Diaphragmatic breathing, watching a movie, running, seasonal changes, etc.
Answering these two questions alone could put you on the road to relief.
References
Butler, D., and L. Moseley. Explain Pain. Adelaide: Noigroup, 2003.
Dameron, TB. “Bucket handle tear of acetabular labrum accompanying posterior dislocation of the hip.” J Bone Joint Surgery 41A (1959): 131-34.
Devor, M and Z. Seltzer. “Pathophysiology of damaged nerves in relation to chronic pain. ” Textbook of Pain. Edinburgh: Churchill Livingstone, 2005.
Doubell, TP, RJ Mannion, and CJ Woolf. “The dorsal horn: state dependent sensory processing, plasticity and the generation of pain.” Textbook of Pain. Edinburgh: Churchill Livingstone, 2005.
Edwards, FA, “Dancing dendrites.” Nature 394 (1998): 129-30.
Kendall, NAS, SJ Linton, and CJ Main. Guide to assessing psychosocial yellow flags in acute low back pain: risk factors for long term disability and work loss. Wellington: Accident Rehabilitation & Compensation Insurance Corporation of New Zealand, 1997.
Moseley, GL. “Imagined movements cause pain and swelling in a patient with complex regional pain syndrome. Neurology 62 (2004): 1644.
Price, DD. Psychological Mechanisms of Pain and Analgesia. Seattle: IASP Press, 2000.
Wall, PD, and R Melzack, et al. Textbook of Pain. 5th ed. Edinburgh: Churchill Livingstone, 2005.






