Pain in people with hypermobile Ehlers-Danlos syndrome (hEDS) likely is the result of an impaired pain suppression system that may lead to widespread pain, a study shows.
Well, that would certainly explain a lot!
contradict a previous theory that EDS-related pain was caused by damage in nerve fibers.
The study, “Pain due to Ehlers-Danlos Syndrome Is Associated with Deficit of the Endogenous Pain Inhibitory Control,” was published in the journalPain Medicine.
the underlying mechanisms of hEDS-related pain remain controversial, and clarifying this may help to identify and develop more appropriate approaches to manage pain in these patients.
researchers at the Sapienza University, in Rome, Italy, investigated which of the two theories better reflect the nature of the pain felt by hEDS patients.
They evaluated the function of small fibers and the pain suppression system in 22 people — 21 women and one man — with hEDS-related pain, and in 22 age- and sex-matched healthy individuals.
Patients had a mean age of 43 years and had been diagnosed with hEDS for a mean of 5.5 years.
Small-fiber function was measured through quantitative sensory testing, which uses standardized mechanical and thermal (cold and heat) stimuli to evaluate a person’s detection and pain thresholds, as well as the wind-up effect — when repetitive stimulus increases the pain intensity. A higher wind-up effect is a sign of central sensitization
Bingo! This is what I have always experienced: “repetitive stimulus increases the pain intensity”.
Also, my muscles start becoming confused after too many repetitions of on/off (like while bicycling) and get stuck half on/half off. I have to stop for a while to let my nerves “reset” and then I can start again, but for shorter and shorter intervals before my muscles get “stuck” again.
It seems to me that our musculature can also develop such a “wind-up” effect and it works the same way: too many repetitions of the same stimulation cause a lingering effect which then becomes additive as further repetitions pile on.
It seems our “EDS nerves” can’t recover enough between repetitive stimulations so they don’t fully return to an unstimulated phase between stimulations. Eventually everything “locks up” in the stimulated state.
The function of the pain suppression system was assessed using the conditioned pain modulation test, which relies on the concept that one stimulus can naturally override another, creating the so-called “pain-inhibits-pain” effect.
Results showed that while some patients complained of pain mainly involving the joints, most reported widespread pain, described as a combination of burning, dull, and aching sensations.
In addition, hEDS patients showed no signs of small-fiber damage or pain associated with nerve cell dysfunction (neuropathic pain).
In contrast, they had a significantly higher wind-up effect than healthy individuals, suggesting the presence of central sensitization.
I hadn’t heard about “pain wind-up” for years until I looked for it. (See yesterday’s post: Neuropathic Pain & Wind-Up Phenomenon) This phenomenon doesn’t just disappear when you start calling pain a “biopsychosocial” disorder.
This used to be a serious scientific issue but seems to have been discarded in favor of the assumption that pain is aggravated by psychological factors. Instead of treating the pain, doctors send patients for counseling.
They hypothesized that in the initial phases of the disease, pain may be mainly caused by joint hypermobility complications, and that such persistent pain may subsequently promote central sensitization and changes in the pain suppression/inhibitory system.
If chronic pain were treated early and effectively, we wouldn’t be suffering from the additional pain of central sensitization.
Thanks to a flood of PROPaganda from the anti-opioid pain-denying zealots, any invisible chronic pain is now regarded by too many doctors as a psychological issue, not a physical one.
medications restoring the pain suppression system, such as antidepressants, “might be effective for reducing pain in this condition,” the researchers wrote, adding that more clinical studies are needed to confirm this hypothesis.
Marta Figueiredo holds a BSc in Biology and a MSc in Evolutionary and Developmental Biology from the University of Lisbon, Portugal. She is currently finishing her PhD in Biomedical Sciences at the University of Lisbon, where she focused her research on the role of several signalling pathways in thymus and parathyroid glands embryonic development.