The controversies, misunderstandings, and lack of knowledge surrounding fibromyalgia and chronic widespread pain and the absolute mess the diagnostic label of “fibromyalgia” has created have been well reviewed. ¹⁻⁴ Unfortunately, not one of the articles addresses the key fundamental problem that exists within the construct of chronic widespread pain and the fibromyalgia diagnosis, namely, the fallacy of pain from nowhere. While describing chronic widespread pain and fibromyalgia as dead-end diagnoses begging for definition and context, they fail to address the fact that absolutely nobody has actually identified the source of the pain that patients suffer.
Clearly, abnormalities in pain processing with central sensitization and attendant neural plasticity to external pain stimulation has been well documented in fibromyalgia, and it has been widely accepted in standard reviews and textbooks, without argument, that it is from here that fibromyalgia pain arises. ⁵⁻⁹ However, there is absolutely no evidence that central sensitization actually causes or can cause spontaneous, non-externally stimulated pain. The inferred acceptance that the pain of fibromyalgia directly originates out of a central sensitization syndrome, despite the knowledge that central sensitization is a modification response to actively-induced pain and not a source of pain itself, ¹⁰˒¹¹ is a true failure of medical science. Central sensitization does not cause pain. It is simply a process that modulates pain messaging and signaling from a defined, active pain source. Furthermore, there is absolutely no evidence to support the concept that the pain of primary fibromyalgia is a true central pain syndrome with pain originating from primary diseases and abnormalities of the central nervous system. ¹² The conflation of central sensitization with central pain has only created added confusion.
Despite nearly 200 years of observation and description, fibromyalgia remains a medically unexplained syndrome characterized more about what we do not know about it than what we do and is accepted as a disorder of pain from nowhere. We do not know the cause, pathogenesis, or relationship of the myriad fibromyalgia symptoms including pain, stiffness, fatigue, sleep disturbances, cognitive impairment, and psychological distress. The trigger for the expression of fibromyalgia is unknown despite the array of disparate processes reported with the onset of fibromyalgia. The mechanism of how fibromyalgia develops is still unknown.5-9
We do know that individuals with fibromyalgia demonstrate central sensitization-driven pain processing to extrinsically-applied stimuli—with features of excessive and more severe pain amplification and magnification, wind-up, and referred pain—than those without chronic widespread pain or fibromyalgia. Clinically, patients demonstrate varying degrees and distributions of extrinsically-induced tenderness in the form of hyperalgesia or allodynia that have been shown to correlate strongly with psychological and generalized distress, sleep difficulties, and depression rather than the perceived pain itself. We also know that most studies regarding treatment of fibromyalgia demonstrate only some degree of benefit (in the 30% improvement range or less) to only some symptoms, to only some patients, and usually only in the short term. Rarely do patients get a high degree of benefit, especially regarding the pain component. ¹³ Finally, we know that the prognosis for patients with fibromyalgia is dismal and, in general, patients do not get better. ⁵⁻⁹
The Puzzle of Fibromyalgia
How did we get here? As described in my recently published book, The Missing Pieces of the Fibromyalgia Puzzle, ¹⁴ I propose everything is wrong in the world of fibromyalgia because most individuals classified or diagnosed as having fibromyalgia do not actually have fibromyalgia. The American College of Rheumatology (ACR) 1990 criteria for the classification of fibromyalgia ¹⁵ were established to define patients for research purposes but were quickly subverted to become diagnostic criteria, a purpose for which they were never developed nor suited.
Indeed, the ACR 1990 criteria study itself refutes the diagnostic validity of the criteria. Based on the derived sensitivity and specificity data and using a 2% population prevalence of fibromyalgia, the positive predictive value of the ACR 1990 criteria of widespread pain and painful tenderness in at least 11 out of 18 fibromyalgia points to a diagnosis of fibromyalgia 9% of the time. In other words, out of 100 individuals with widespread pain and at least 11/18 painfully tender fibromyalgia points, 9 have fibromyalgia, and 91 do not. Similarly, the recently published 2010 ACR preliminary fibromyalgia diagnostic criteria suffer a similar fate when out of 100 random people who fulfill these diagnostic criteria, only 16 actually have fibromyalgia and 84 who fulfill the diagnostic criteria do not. ⁶ The ACR 1990 classification criteria and the 2010 ACR diagnostic criteria clearly do not diagnose fibromyalgia.
If, in fact, the large majority of individuals diagnosed with fibromyalgia do not, in fact, have fibromyalgia and the ACR classification criteria do not diagnose fibromyalgia, then it is reasonable to ask what do patients with widespread pain as defined by the ACR classification criteria and having at least 11/18 painfully tender fibromyalgia points really have and where does their pain come from? To answer this question, I undertook a detailed and thorough clinical study of 92 patients with widespread pain and tenderness to identify all the clinical features associated with fibromyalgia—with a particular emphasis on the musculoskeletal, soft tissue, and pain threshold assessment. The details are published in my book. ¹⁴ The conclusion of the study identifies that all patients had: 1) primary generalized osteoarthritis, predominantly involving the neck and back with associated degenerative disc disease and a variable combination of tendinitis, bursitis, and fasciitis; 2) and tenderness with increased nociception. All patients had a true source of nociceptive pain manifested by primary generalized osteoarthritis and predominantly involving:
the cervical spine and lumbar spine with associated degenerative disc disease, and variable combinations of involvement of the thoracic spine with associated degenerative disc disease;
thumb first CMC joints;
thumb first MCP joints;
finger DIP and PIP joints;
knee and patellofemoral joints;
toe MTP and PIP joints; and
other specific joint sites
They exhibited, as well, variable combinations of periarticular symptoms and findings including:
trochanteric bursitis,
plantar fasciitis,
subacromial bursitis/supraspinatus tendinitis,
pes anserine bursitis,
flexor nodule painful tenderness,
deep Achilles bursitis,
epicondylitis,
de Quervain’s tenosynovitis,
Achilles insertion tendinitis, and
finger flexor tenosynovitis.
Based on the observation that patients with chronic widespread pain and tenderness have true musculoskeletal nociceptive sources of pain, I developed the two component Polypain Model as shown in Figure 1. Polypain is an acronym for polyregional pain and increased nociception. The Polypain Model explains, comports with, and fully consolidates the observed abnormalities of pain processing in fibromyalgia by identifying the nociceptive pain processes that central sensitization acts upon in fibromyalgia. The model identifies the independent contribution of primary generalized osteoarthritis predominantly involving the neck and back with associated degenerative disc disease and the variable combination of tendinitis, bursitis, and fasciitis as the drivers of nociceptive pain in fibromyalgia. The Polypain Model explains how the pain sources themselves, sleep disruption, and psychological factors affect pain thresholds through pain processing and central sensitization. Most importantly, this two compartment model provides an integrated and unified framework to more appropriately understand, and ultimately measure, the contribution of the pain sources and the factors impacting pain thresholds via pain processing and central sensitization to the overall perception of pain reported by the fibromyalgia patient.
The recognition that fibromyalgia polypain is indeed a musculoskeletal disease whose presentation is modified by factors modulating the pain message greatly expands the ability to stratify and classify such patients. This approach is based on the specific components that cause pain and modulate the pain message. Furthermore, it provides the opportunity to develop more specific and targeted treatment strategies based upon the specific contributors to the perceived pain ¹⁴ and to create more homogeneous patient subsets for purposes of study.
Conclusion
Fibromyalgia polypain is all about osteoarthritis, degenerative disc disease, tendinitis, bursitis, and fasciitis acting as nociceptive pain drivers. These are unquestionably rheumatologic disease conditions that should always be diagnosed and managed in concert with a rheumatologist at the helm. To further enhance the central role rheumatologists play in fibromyalgia polypain, it is vital to re-assert and expand the role of rheumatologists in managing the pre-eminent component of chronic musculoskeletal pain, namely, the pain and its source.