We have all had this type of patient walk in our clinic doors before. If you're anything like me, it happens on the regular. Let’s call him Mike. He is in his mid forties, a little bit larger in stature, and consistently talks about the “good ole days”. As he begins his history, he does not forget to mention how his pain is different because he has a ridiculously high pain tolerance. He may even describe a story where ‘back in the day’ he sprained his ankle in football, yet completed a game without any problems. Mike alludes to the idea that “something” absolutely must be severely damaged and that he is quite frustrated due to the fact he has been dealing with this for a long time. To add to his frustration, his PCP even won’t let him get imaging until he completes physical therapy. Pssssh!
You hear out Mike’s story and want to dig a little deeper, but he is ready for you to get straight to the assessment of “what's wrong”. So, you move forward by performing a simple movement exam and are quick to realize that Mike appears to be quite sensitized to any sort of movement with even the smallest movements leading to intense pain. You recognize immediately that this degree of pain response could of course be from a nasty inflammatory process, or, on the other hand, it may be more indicative of a multitude of central and peripheral mechanisms leading to the “wind up” of the ascending messages peppering his cortex subsequently increasing the likelihood of a strong pain experience. Your next step is to dig deeper into his history, his mechanism of injury, comorbid conditions, and other lifestyle factors that could be of relevance to his case. As you continue to go through your evaluation, you become aware that there are no dangerous mechanisms of injury, no signs of acute tissue damage, no inherent red flags, and that his symptoms are consistent with what appears to be a “highly sensitized nervous system”.
At this point, Mike is already showing more frustration as he constantly reminds you that he has a high pain tolerance and that there must be something extremely wrong with him. At this point, do you attempt to let Mike know you believe his pain is real, but you think it may be less driven by serious tissue damage and more a factor of the upregulation of his nervous system, or do you validate his concerns and reinforce his belief that he “is really broken”?
But What About Mary?
Before we move on with Mike’s story, let’s compare him to someone on the other end of the spectrum. We’ll call her Mary. Mary just got done delivering a baby after being in labor for 18 hours. The experience was stressful and intense, there was obvious tissue damage, there was/is inflammation, stress levels were to the max, lack of sleep was at an all time high, yet Mary does not report any notable pain in the moment.
Can you relate to either of these situations? In one context we have Mike where pain is very prevalent and demanding with probably not a lot of tissue damage. In another we have Mary, who just underwent a lot of trauma but is able to block a majority of her symptoms due to the birth of her baby.
Do you think Mary just has a higher pain threshold than Mike? I feel that most women would likely concur (tongue in cheek comment 🙂 ); however, if that truly were the case, why would Mike believe he has a high pain tolerance when even the smallest movements create pain?
Researchers and clinicians have been asking these types of questions for decades, and although we are gaining more information about our experience of pain, there are still many uncertainties that we don’t quite understand yet. In fact, maybe we never will as it ultimately leads back to the solving of the hard problem of consciousness. Another blog for another time maybe?
If we are going to attempt to start a discussion on the concept of pain tolerance, we first need to make sure we have some semi consistent language and definitions laid out. Despite many individuals using the words threshold and tolerance interchangeably, they actually involve two distinct representations. Pain threshold can be defined as the lowest stimulus intensity that one perceives as painful, whereas pain tolerance is defined as the maximal amount of time one can endure a noxious stimuli.1
Pain: It's More Than Just a Signal
When investigating an individual's pain threshold or tolerance, two processes are consistently described in the literature that can be elicited to either increase or decrease pain. Conditioned pain modulation (CPM), formerly known as diffuse noxious inhibitory control, was first described in rat models as a mechanistic inhibitory system involved in utilizing endogenous circuits to down regulate pain after after a bunch of nociceptive signals become evoked.2 To better understand CPM, think about runners who talk about the struggle they endure at the beginning of their run, but then after a few miles in they describe a phenomenon known as the runner’s high. Essentially, after their body has been processing several noxious stimuli, endogenous circuits are able to inhibit the pain and create an environment that feels very rewarding. Often this process is classified as the “pain inhibits pain” model.3,4
Juxtaposed to CPM, we have various forms of “wind up” such as disinhibition of gaiting interneurons, temporal summation (homosynaptic facilitation) where our body receives repetitive noxious stimuli and sends excitatory signals to amplify the nociception as a means of protection, heterosynaptic facilitation, and chemical plasticity at synapses which increase excitability5-7 A nice analogy to help understand some of these changes is to conceptualize the phenomenon of temporal summation. To do this, simply imagine someone mildly pinching the skin on your forearm for a long period of time (i.e. 3 hours). It may not be bothersome at first, but overtime your body will begin to recognize it as more threatening and therefore you may increase your perception of pain.
Now, let's circle back to Mike and Mary from before as we may be able to apply some of this information to gain a better understanding of their very different pain experiences. This is all bearing in mind that pain is much more complex than just simple pathways from the periphery to the brain. We, of course, must not forget about the individual's current circumstances and context surrounding their pain experience.
For Mary’s situation, it is quite likely that she had a very different relationship with the nociception she experienced and the pain she came to feel due to the amazing reward of giving birth to her baby. It is probable that Mary has employed various processes such as interneuron gaiting in the spinal cord, release of endorphins, as well as potential activation of the PAG and RVMM to decrease the nociception reaching her cortex as well as the fact that her expectations and “priors” in this case are largely positive due to the excitement of giving birth to her child.
On the other hand, Mike may be struggling to utilize some of these wonderful pain modulating physiologic processes mother nature provided us with, and is now likely experiencing an increased barrage of nociception ascending to the higher levels of his nervous system. Along with his frustration, Mike has some preconceived beliefs that all his pain before equated to tissue damage and displays fear that something is severely wrong. Further, he may also be dealing with other lifestyle factors such as a lack of sleep, increased life and work stressors, and a loss of independence which all could impact his likelihood of experiencing pain. So in reality, he may be very correct in the sense that he used to have a very high pain threshold, but now that he has all these factors weighing in on him, his perception of his ongoing activity along with his inhibition of both peripheral and central modulation heightens his overall pain response.
I'm sure at this point there is a need to say it, but pain is clearly complex. It would be erroneous for me to suggest that even people in pain just have faulty processing mechanisms and that’s it. To describe the neurophysiology of pain goes far beyond the scope of this article, but the point that I am trying to make is that there are plenty of Mike’s in the world that are struggling with the concept of dealing with an immense amount of pain after living a majority of their life being able to attenuate it. It’s not up to you to figure out why those patients are in pain, but it is up to you to help them gain a better understanding with the complexities that contribute towards one's pain experience.
Meeting the person where they are at, and helping them get to the place they want to be is what being the complete clinician is all about. To learn more about all the contributing factors that play a role with pain, please check out this FREE course we are offering on our Modern Pain Care site.
Also, if you feel that you are struggling as a clinician to help your patients live a life well with pain, you are not alone. We are continuing to offer this excellent membership program where we help you become the complete clinician. You can begin your FREE trial HERE!
- O'Connor PJ, Cook DB. Exercise and pain: the neurobiology, measurement, and laboratory study of pain in relation to exercise in humans. Exerc Sport Sci Rev. 1999;27:119-66. PMID: 10791016.
- Le Bars D, Dickenson AH, Besson JM. Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat. Pain. 1979 Jun;6(3):283-304. doi: 10.1016/0304-3959(79)90049-6. PMID: 460935.
- Nir RR, Yarnitsky D. Conditioned pain modulation. Curr Opin Support Palliat Care. 2015 Jun;9(2):131-7. doi: 10.1097/SPC.0000000000000126. PMID: 25699686.
- Yarnitsky D. Conditioned pain modulation (the diffuse noxious inhibitory control-like effect): its relevance for acute and chronic pain states. Curr Opin Anaesthesiol. 2010 Oct;23(5):611-5. doi: 10.1097/ACO.0b013e32833c348b. PMID: 20543676.
- Arendt-Nielsen, L. & Yücel, A.. (2000). Induction and assessment of experimental pain from human muscle. Agri. 12. 9-14.
- Nie H, Graven-Nielsen T, Arendt-Nielsen L. Spatial and temporal summation of pain evoked by mechanical pressure stimulation. Eur J Pain. 2009 Jul;13(6):592-9. doi: 10.1016/j.ejpain.2008.07.013. Epub 2008 Oct 15. PMID: 18926745.
- Vaegter HB, Jones MD. Exercise-induced hypoalgesia after acute and regular exercise: experimental and clinical manifestations and possible mechanisms in individuals with and without pain. Pain Rep. 2020;5(5):e823. Published 2020 Sep 23. doi:10.1097/PR9.0000000000000823