The Relationship Between Pain and Safety in Hypermobile Individuals

​Pain is one of the main symptoms that people with hypermobility report, and seek treatment for, but it may be one of the most difficult symptoms to understand. What’s to understand about pain, you say. You either hurt or you don’t, right?

Pain is actually a very complex phenomenon, and just like when baking a cake, the end result depends on all the ingredients and how they are combined, and what we do with them. Because the issue is complex, I won’t try to cover it in its entirety, but rather give you some general sense of the landscape of pain. 

The main take-away is that pain is a complex phenomenon that is the end result of a variety of factors, some of which can be modulated more easily than others. Pain is highly modifiable by many psychological factors, including expectations, our perception of how safe (or not) we are, how we think about pain, whether we tend to catastrophize or not, whether we have an internal locus of control – a sense that we ourselves can have an impact on our pain – and a multitude of other factors. What pain is not: an accurate measure of the degree of tissue damage or dysfunction in the body.

              
                     Pain is not  an accurate measure of the degree of tissue damage or dysfunction in the body.
                               


Contrary to what it may seem like we experience pain in our brains, not in the part that appears to hurt. Whether we experience a stimulus as painful, what type of pain we feel, and how intense the pain feels depends on the brain’s interpretation of what the stimulus means, of how threatening to our safety and survival our brain believes the sensation is. This means that pain depends on our perception of  the stimulus. Our  perception in turn is affected by our previous experiences.


Stating that pain is modifiable does not mean that if you just thought better thoughts, you wouldn’t be experiencing it. It simply means that we have some control over our experience, and with time, can learn to exert even greater control                                                                                                  over it.


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Polyvagal theory

The psychiatrist Steven Porges, PhD, has developed a theory called The Polyvagal Theory that further specifies the function of the  autonomic nervous system (ANS) in different emotional states, specifically in states of safety or lack of safety. It serves as a helpful way to understand the way we connect and bond, and how we react when we are not feeling safe. It further divides the anatomy and functioning of the vagus nerve into two branches, the ventral (meaning anterior) and dorsal (meaning posterior, or towards the back) branches of the nerve. The theory states that when we perceive signals of safety from others, we are open to connection. When we feel threatened, we first go into sympathetic nervous system (SNS) mode, commonly known as “fight or flight”, and if this is not possible -- we are immobilized in a threatening situation, see no way out -- we may move into the dorsal vagal state, commonly known as “freeze”, characterized as giving up, passivity, indifference. 
Polyvagal theory can both be helpful to our understanding of how traumatic experiences and a lack of a sense of safety in our bodies and the world affect us, and a helpful tool in supporting more calm and connected states that favor tissue repair and lowered pain responses.



Central sensitization - the unkind magnifying glass of sensation

Pain can both be amplified and dampened by a variety of factors. Fear, fear of movement, a sense of not being safe, catastrophizing, an external locus of  control (a belief that factors outside of oneself hold all the power over one’s well being), high levels of inflammation in the body etc. can all ramp up the pain. Adverse childhood experiences (ACEs) as well as trauma during adulthood can contribute to a decreased resistance to stressful events, an enhanced risk of sensitivity to pain and central sensitization of pain. This happens in part due to the potential of traumatic experiences to induce lasting effects on the structure and function of stress-regulating circuits in the brain, such as the hippocampus and the amygdala. This can promote alterations in stress and pain sensitivity and regulation of emotions in later life. People with a history of trauma exposure may have decreased volume in the frontal lobe of the brain, affecting executive function. In addition, they show a wider pattern of increased pain sensitivity that even includes parts of the body other than the most problematic area.

In some cases Ehlers-Danlos Syndrome (EDS) symptoms appear to have emerged or worsened after physical trauma. In some studies brain changes have through visual imaging been linked to the emergence of physical symptoms. People with EDS have also been found to have alterations in the size of key emotion-processing brain regions, such as the amygdala.

Elevated levels of stress also contribute to elevated levels of inflammation,, leading to more pain through the release of so called pro-inflammatory cytokines, chemical messengers that signal and prompt inflammation. (Pro-inflammatory cytokines can also be released due to infection or  injury to cells.)

Fear of pain itself has been found to increase the risk of the pain becoming significant and chronic. Pain-related fear and avoidance of movements and activities we mentally associate with pain, no matter how understandable they may be, have been shown to make matters worse, leading to more severe disability progression of disability over time.

Fortunately, the opposite spectrum of emotional states -- feeling safe, supported, informed, in control, having low levels of inflammation -- can contribute to a decreased perception of pain. The vagus nerve, the main branch of which is associated with the relaxed states of the parasympathetic nervous system (PNS), inhibits oxidative stress, inflammation and the activity of the sympathetic nervous system.
Despite the fact that pain isn’t always accurate and exact in terms of how well it can tell us where a problem is located, and how severe it is, it still has an important signaling function. In cases where the pain is chronic –- has lasted over 3-6 months –- a phenomenon referred to as central sensitization can increase a person’s perceived levels of pain due to changes in the central nervous system itself. This increase in pain does not reflect increased dysfunction in the parts of the body that hurt, but is a dysfunctional, unhelpful phenomenon, a problem in and of itself that requires specific treatment. 

When this sensitization is to pain in the musculoskeletal system, it is often diagnosed as fibromyalgia. This also explains why so many individuals with hypermobility disorders have received this label prior to being diagnosed with a form of EDS or Hypermobility Spectrum Disorder (HSD). In a 2016 study of 27 patients with joint hypermobilty  the participants were found to have  widespread pain but no peripheral nervous system damage. There were, however,  findings compatible with central sensitization. The researchers  concluded that in patients with EDS or HSD the ongoing pain due to joint abnormalities probably triggers central sensitization and causes widespread pain.

Central sensitization is a “re-wiring” of the central nervous system (brain and spinal cord) that reflects a persistent state of high reactivity that lowers the pain threshold. It either leads to greater suffering from an ongoing condition or dysfunction, or maintains pain after the initial cause of the pain no longer exists.

Please note that there is a difference between the concepts  of pain threshold, the minimum level of stimulus that is perceived as painful, and pain tolerance, referring to the amount of pain an individual tolerates. You can both have a high pain tolerance – tolerate a lot of pain and still function – and a low pain threshold – feel pain with a lower intensity of stimulation than average. Both are to some extent malleable, and can also vary due to previous experiences, such as trauma, or genetics. As mentioned, pain can also be influenced positively or negatively by a variety of other factors. Keeping these in mind as you work on your rehabilitation can be very helpful.

                           
You can both have a high pain tolerance – tolerate a lot of pain and still function – and a low pain threshold – feel pain                            with a lower intensity of stimulation than average. One does not exclude the other.
     
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Pain and rehabilitation

How should we take pain into account during physical rehabilitation/physical therapy of a hypermobile person, who is likely to be sensitized to pain? Therapy itself should (in all but some very specific cases) not increase pain in the moment. You should also not experience pain as a result of having performed therapeutic exercises, received a manual treatment intervention, or made recommended lifestyle changes. If you experience pain while performing a therapeutic exercise –- a common experience of many hypermobile patients that have sought help through physical therapy, only to find that it instead aggravated their symptoms –- you are performing the exercise incorrectly either because you are not yet ready for it, or have misunderstood it. The “not yet ready for it” is a likely and common reason for physical therapy fails. Hypermobile individuals are often prescribed exercises for which they are not yet ready. In either case a course correction is in order, and pressing ahead would be a potential recipe for injury or pain aggravation. When an exercise causes pain we should, however, not recoil from it, but rather find the best way to proceed without pain. 


When an exercise causes pain we should, however, not recoil from exercise , but rather find the best way to proceed                                                                                           without pain. 


While the goal of physical therapy should generally not be pain relief at the moment, it should eventually help decrease pain. It does this by gradually normalizing the body’s functioning, which then results in pain relief, and even freedom from pain, because there simply is no injury or dysfunction for the body to signal through pain. 
But since the intrinsic function of pain is to keep us safe by warning us against danger to our bodily integrity, physical therapy must also proceed in a way that makes us feel safe. This includes not only educational components that help the patient distinguish signs of danger from the sensory background noise of embodied existence, but also an approach that doesn’t itself add to the sensitization and the experience of movement equalling pain.

When the weak links have been strengthened, the bugs in our movement software sorted out and our tissues are animated by a brain that feels safe, movement, whatever form it takes for each individual, is not only a pleasure but a necessary vehicle for experiencing any and all of the experiences life has in store for us.




References:
Porges SW. The polyvagal theory: new insights into adaptive reactions of the autonomic nervous system. Cleve Clin J Med. 2009
 Lucchetti et al. Anxiety and fear-avoidance in musculoskeletal pain. Curr Pain Headache Rep. 201
 Luque-Suarez  et al. Role of kinesiophobia on pain, disability and quality of life in people suffering from chronic musculoskeletal pain: a systematic review. Br J Sports Med. 2019
McKernan et al. Posttraumatic Stress Symptoms Mediate the Effects of Trauma Exposure on Clinical Indicators of Central Sensitization in Patients With Chronic Pain. Clin J Pain. 2019
 Herzog et al.Adverse Childhood Experiences and the Consequences on Neurobiological, Psychosocial, and Somatic Conditions Across the Lifespan. Front Psychiatry. 2018
 Fleming et al. Central sensitization syndrome and the initial evaluation of a patient with fibromyalgia: a review. Rambam Maimonides Med J. 2015
 Giotakos O. Neurobiology of emotional trauma. Psychiatriki. 2020
 Simon et al. Pain catastrophizing, pain sensitivity and fear of pain are associated with early life environmental unpredictability: a path model approach. BMC Psychol. 2022
 Hamonet et al. Brain injury unmasking Ehlers-Danlos syndromes after trauma: the fiber print. Orphanet J Rare Dis. 2016.
 Eccles et al.Brain structure and joint hypermobility: Relevance to the expression of psychiatric symptoms. The British Journal of Psychiatry, 200(6)
 Bulbena et al. Psychiatric and psychological aspects in the Ehlers-Danlos syndromes. Am J Med Genet C Semin Med Genet. 2017
 Maes et al. The effects of psychological stress on humans: Increased production of pro-inflammatory cytokines and a Th1-like response in stress-induced anxiety. Cytokine. 1998
 Jankord et al.Limbic regulation of hypothalamo-pituitary-adrenocortical function during acute and chronic stress. Ann N Y Acad Sci. 2008
 Zhang et al. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007
 Markfelder et al. Fear of pain and pain intensity: Meta-analysis and systematic review. Psychol Bull. 2020
 Gidron et al. The Vagus Nerve Can Predict and Possibly Modulate Non-Communicable Chronic Diseases: Introducing a Neuroimmunological Paradigm to Public Health. J Clin Med. 2018 Oct
 Di Stefano et al  Central sensitization as the mechanism underlying pain in joint hypermobility syndrome/Ehlers-Danlos syndrome, hypermobility type. Eur J Pain. 2016.

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