In reverse order
Just out, and open access, in the Journal of Pain Research:
Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma
This seems like an important paper – building some foundations of empirical human findings under some theoretical castles in the air.
The paper impresses if taken in reverse order – Statistical considerations are given a transparent airing and the Study limitations section is detailed and fleshed out. Adding further to the sense that this is good science is a discussion on causality. Rather than committing the logical mistake of making unwarranted strong causal claims, the authors propose a number of possibilities and don’t shy away from the complexity.
To the findings
“… we found evidence of both neuroinflammation (as assessed in CSF) and chronic systemic inflammation (as assessed in plasma). Two groups of proteins (one for CSF and one for plasma) highly discriminating between patients and controls are presented. Notably, we found high levels of CSF chemokine CX3CL1 (also known as fractalkine). In addition, previous findings concerning IL-8 in FM were replicated, in both CSF and plasma. This is the first time that such an extensive inflammatory profile has been described for FM patients. Hence, FM seems to be characterized by objective biochemical alterations, and the lingering characterization of its mechanisms as essentially idiopathic or even psychogenic should be seen as definitively outdated.” (emphasis added)
A strong closing statement.
Others have been saying it for a long time, but perhaps the (very real) experience and suffering of those who have been labelled with Fibromyalgia have nothing to do with taut bands, fascial restrictions and those 18 (or 11) infamous trigger points…
– Tim Cocks
Tim, thanks for pulling these various threads together.
For those who are interested in an explanation of the clinical phenomena of fibromyalgia, here is a link to our hypothesis paper: http://pudendalnerve.com.au//website/wp-content/uploads/2013/09/An%20Evol%20Stress-Response%20Hypothesis%20for%20CWP.pdf
With Australia soon to become awash with a variety of “medicinal” cannabinoids, those who have been awarded the fibromyalgia label will be seeking informed advice from their respective health-care professionals and possibly prescriptions from their medical practitioners.
Milton Cohen and I recently posted our personal commentary on this situation: http://www.fmperplex.com/2016/10/31/if-cannabis-should-meet-fibromyalgia/
I agree that this paper is a huge step in the right direction. It helps validate some of the pathobiological mechanisms involved with fibromyalgia. I think even though there seems to be central mechanisms at play, as a clinician I still find it beneficial to help ramp down peripheral afferent inputs in helping my patients manage their symptoms. Even though those triggers or taught bands may not be causative they definitely seem to contribute to patients pain experience. In my mind, leaving peripheral nociceptive inputs can only help heighten the central alarm system.
Mathew, I would like to comment on your confident assertion: “Even though those triggers or taught bands may not be causative they definitely seem to contribute to patients pain experience. In my mind, leaving peripheral nociceptive inputs can only help heighten the central alarm system.”
Whilst the belief that peripheral inputs might be important in maintaining central mechanisms in fibromyalgia has been popular amongst certain pain theorists, it has spawned two flawed explanatory models:
(i) Localised fibromyalgia: In this formulation a diffuse pain syndrome of unknown pathogenesis was invoked to explain “regional” or “local” apparently similar conditions of allegedly known pathogenesis (i.e. “a simple injury to a muscle-tendon unit”).
This serious epistemological error was to have disastrous medico-legal consequences for those in New Zealand who presented with upper limb pain syndromes that appeared to have arisen in the course of their occupation: http://www.fmperplex.com/2015/05/23/the-transmutation-of-fibromyalgia/
(ii) Centralized pain: In this context, centralized refers to “central nervous system origins or amplification of pain” [Clauw, 2014].
Given that pain as an experience always originates from within the nervous system, and that pain is not a “thing” that can amplify itself, this proposition does not make sense.
However, Professor Clauw  suggests that the term also implies “peripheral nociceptive input might be responsible for some of a patient’s pain but central nervous system factors likely amplify the pain.”
Thus it appears that peripheral nociceptive input is not a necessary contributor to a patient’s pain. But should it happen to be the case, Clauw proposes that the patient feels “more pain than would normally be expected based on the degree of nociceptive input.” But he does not disclose how a clinician/observer is able to make such a determination with any degree of confidence! It sounds to me like a lot of guesswork is involved, which harks back to your assertion.
In fact, the term “centralized” can refer only to an anatomical location within the central nervous system. Not only does the word itself not imply a mechanism but also it creates potential for confusion with conditions such as “central post-stroke pain” (which is technically “neuropathic”) and quite different from the phenomena that underlie Fibromyalgia.
A full discussion on these matter and the current search for a third pain descriptor can be found here: http://www.fmperplex.com/2016/08/23/why-centralized-is-unacceptable-as-a-descriptor-for-the-pain-of-fibromyalgia/
Reference: Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555.