by Cort Johnson
Early in the coronavirus pandemic, he warned that chronic pain conditions would likely increase.
Studiesindicate that 40-50% of the ME/CFS-like subset of long-COVID patients develop widespread pain and all of them experience the rest of the nociplastic syndrome (fatigue, sleep, cognitive and mood issues). ME/CFS got tagged early in long COVID because of the post-infectious element and because LongCOVID looks so much like it, but about half of the people with long COVID also fit the pain-added FMlike phenotype; i.e. they have nociplastic pain.
Clauw thinks the emphasis on fatigue – which he called one of the most difficult symptoms of all to
assess – and the sidelining of fibromyalgia and chronic pain in long COVID has been unfortunate.
Pain is so much easier to study. You produce a stimulus, remove it, and see what happens.
With the recent adoption of nociplastic pain, three separate validated models of pain exist.
None exists for fatigue.
Given the 200 other conditions that small fiber neuropathy is found in, he doesn’t believe it tells us
anything significant about fibromyalgia. Citing his experience with fibromyalgia patients with
autoimmune diseases, he doesn’t believe these diseases are autoimmune either. He noted we’re not seeing that kind of tissue destruction, or the high levels of systemic inflammation found in diseases like FM or ME/CFS, and autoimmune drugs have not been helpful. He believes sex hormones on the other hand, may play a significant role in FM and supports a testosterone supplementation study in
fibromyalgia.
Clauw and his Chronic Pain and Fatigue Research Center’s (CPFRC) have studied many different
treatment options, but Clauw agrees that the treatment options for fibromyalgia are “very inadequate” and only work in about one out of three patients. Clauw finds the cannabis and psychedelics studies his lab is engaged in “therapeutically fascinating”, however.
Clauw believes the inflammation in FM probably results from “neurogenic inflammation”; i.e. small, hard-to-detect amounts of inflammation produced by the agitated nerves.
Ion channel dysfunction, interestingly, given the Griffith University work on ion channels in ME/CFS,
appears to play a major role as does the release of histamine from mast cells. Drugs to tamp down neurogenic inflammation response have been and are being developed. The most notable of these have been the highly successful anti-CGRP drugs developed for migraine which are also being trialed In fibromyalgia. Low-dose naltrexone may be tamping down neurogenic inflammation as well.
Tonix’s Tomnya – a reformulated cyclobenzaprine drug – that may help with sleep and pain will shortly be coming up for review at the FDA is another. Clauw said that cyclobenzaprine (Flexeril), a muscle relaxant, was his favorite FM drug 25 years ago, and is still his favorite drug. For one, it’s one of the rare drugs that improves deep sleep. The problem with Flexeril was that when used as prescribed (5-10 mg, 3 xs/day), a rapid buildup of toxic factors has prevented it from being used for more than couple of days. When he cut down the dose to 5 or even 2.5 mg, though, fibromyalgia patients could tolerate it, use it long term, and benefit from it.
Microglial inhibitors, anti-CGRP drugs, microglial inhibitors, ion-channel drugs, low-dose naltrexone,
Tomnya, cannabis, mast cell stabilizers, and psychedelics may help tamp down neurogenic
inflammation.
In the end, it’s amazing how little play the nociplastic pain field, with its enormous overlaps, has
received in ME/CFS and long COVID. Coming at these diseases from a nervous system/immune
perspective, it provides interesting and new ways to look at them and potentially treat them.
To view the full article please click
https://www.healthrising.org/blog/2024/08/31/fibromyalgia-chronic-fatigue-long-covid-central-nervous-system/