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Pain in Symptomatic Hypermobility

Pain is complex in hypermobility syndromes. Pain is complex.



Many people think of pain as a direct response to damage to bodily tissues, but this ignores much of the amazing complexity that underlies the sensation of pain. It’s a little bit like saying that vision is just the direct input of light into an eyeball, both sensations involve the central nervous system integrating multiple inputs in order to produce what we ultimately experience as pain or vision.


The neural systems involved in sensing pain are also very plastic, meaning that they can adapt and change over time. This plasticity underlies phenomena associated with long-term pain whereby we can become increasingly sensitised to inputs from our tissues and more and more likely to experience pain. Basically, the system can get better at generating the experience of pain the longer the pain state goes on. When you think of pain as a warning mechanism to guard us against potential threats, this kind of makes sense – if we keep getting warning signals from an area, maybe we need to pay more attention to it and tune up the alarm system to activate sooner? The downside is that we can start to experience pain more and more easily, even without any real damage even occurring. Just as the system can become more and more sensitised, however, these changes can be driven in the opposite direction to wind back the sensitivity and therefore decrease the pain levels experienced.


The challenge in symptomatic hypermobilty conditions like EDS, Marfans and Loeys-Dietz is that these sensitivity increases are generally occurring but alongside them are often multiple signals from tissues signalling actual danger (called nociceptive signals) related to things like dislocations and subluxations, or visceral (organ) conditions. This can create a complex state where many things are contributing to the pain experienced which can seem confusing and hard to navigate. But it also means there are many ways in which we can address the pain experience to dial down the sensitivity, reduce the nociceptive inputs and ultimately experience less debilitating pain.



The above linked article was written by Nicole Frost and published by NOI Group as an educational piece for clinicians working with chronic pain to ensure that they are aware of the multitude of factors that can be contributing to pain in symptomatic hypermobility conditions. NOI Group are a highly respected education provider in the field of pain science and offer some great resources for patients and clinicians seeking to better understand pain physiology and how to mange pain. As a clinician working with many hypermobile patients and educating other clinicians on these conditions, Nicole is working to increase the awareness of health professionals about symptomatic hypermobility. Many clinicians are learning and progressing their skills in addressing the central neurological factors that can contribute to pain, but if these clinicians also understand the unique nociceptive issues often occurring in symptomatic hypermobility, then they will be much better equipped to help hypermobile patients experiencing chronic pain. It would be great to hear less stories of hypermobile patients feeling dismissed and told that they “can’t possibly” have that many injuries or for that long. They can – but when we put together all the pieces of the puzzle, there is a lot we can offer to effectively manage the pain.






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