Below are 2 PubMed articles insinuating that EDS pain is due to central sensitization or general extreme pain sensitivity.
I still insist that EDS pain is mechanical (due to lax tissues) and/or biochemical (because cell walls are also made from our defective connective tissue). However, we cannot know if the amount of pain we feel is in “normal” proportion to the nociceptive stimuli we experience.
The question is: do we have more pain than average or are we just more sensitive to average pain?
In the “good old days”, before I had to take pain medication around the clock, I seemed extremely pain sensitive. Even a wrinkle in the bedsheet would become painful if laid on it too long.
But with a connective tissue disorder, it’s likely that defective skin can be more easily penetrated by pressure or temperature to set off pain signals.
All the fascia around muscles and organs in our bodies can be unusually permeable and prone to damage, leaving us insufficiently insulated from the external environment. I believe much of our pain comes from unusually deep intrusions of external forces where they reach nociceptors normally isolated from such forces.
For instance, when pressure or torque on a joint isn’t effectively resisted by ligaments and tendons, bones will move a little and transfer the force to nearby structures, like muscles and nerves, where nociceptors will signal that something is amiss.
In this way, we get more intense and frequent nociceptive stimulation than “normal” people.
However, it could also be that our cell walls don’t properly control the influx and outflow of various molecules including salts, like sodium and potassium. This could, in turn, disturb the functions of the sodium and potassium channels in cells that control pain transmission.
Connective tissue is ubiquitous in our bodies, so any part can become painful for us,
Nevertheless, researchers are still obsessed with proving that our pain “isn’t physically real”, but rather a figment of our overactive imaginations, and that our supposed catastrophizing is what turns it into chronic pain.
How this hereditary connective tissue disorder causes pain remains unclear although previous studies suggested it shares similar mechanisms with neuropathic pain and fibromyalgia.
While the lack of somatosensory nervous system damage is incompatible with neuropathic pain as the mechanism underlying pain in JHS/EDS-HT, the lowered cold and heat pain thresholds and increased wind-up ratio imply that pain in JHS/EDS-HT might arise through central sensitization.
Hence, this connective tissue disorder and fibromyalgia share similar pain mechanisms
WHAT DOES THIS STUDY ADD?: In patients with JHS/EDS-HT, the persistent nociceptive input due to joint abnormalities probably triggers central sensitization in the dorsal horn neurons and causes widespread pain.
Generalized Hyperalgesia in children and adults diagnosed with Hypermobility Syndrome and Ehlers-Danlos Syndrome Hypermobility type: A discriminati… – PubMed – NCBI ; Arthritis Care Res (Hoboken). 2016 Aug
Here the author is misusing the term, Hyperalgesia. He is referring to unusually high pain sensitivity (low tolerance), not the additional pain hypothesized to result from taking high opioid doses.
Lowered pressure pain thresholds have been demonstrated in adults with Ehlers-Danlos Hypermobility type(EDS-HT), however it remains unclear if these findings are also present in children.
Therefore, the objectives of the study were to:
(1)determine if generalized hyperalgesia is present in Hypermobility syndrome (HMS)/EDS-HT children,
(2)explore potential differences in pressure pain thresholds between HMS/EDS-HT children and adults, and
(3)determine the discriminative value of generalized hyperalgesia
METHODS: Patients classified in one of three groups:
- hypermobile (Beighton score ≥4/9) and
- healthy controls.
Descriptive data of age, gender, body mass index, Beighton score, skin laxity and medication usage were collected.
Generalized hyperalgesia was quantified by the averaged pressure pain thresholds collected from 12 locations.
The following confounders were collected: pain locations/intensity, fatigue, psychological distress.
Comparisons between HMS/EDS-HT children and normative values, between children and adults with HMS/EDS-HT, corrected confounders, were analysed with MANCOVA.
The discriminative value of generalized hyperalgesia employed in order to differentiate between HMS/EDS-HT, hypermobile and controls was quantified with logistic regression.
Significantly lower pressure pain thresholds were found in children with HMS/EDS-HT compared to normative values (range: -22.0% to -59.0%, p=<.05).
When applying a threshold of 30.8 N/cm2 for males and 29.0 N/cm2 for females, the presence of generalized hyperalgesia discriminated between individuals with HMS/EDS-HT, hypermobile and healthy controls (odds ratio=6.0).
Children and adults with HMS/EDS-HT are characterized by hypermobility, chronic pain, as well as generalized hyperalgesia [meaning heightened pain sensitivity].
The presence of generalized hyperalgesia may indicate involvement of the central nervous system in the development of chronic pain.
The idea that we have hyperalgesia was also discussed here:
EDS III: evidence for generalized hyperalgesia