This article presents a novel theory: “The most common cause of fibromyalgia is probably positional cervical cord compression.”
Fibromyalgia has undergone a most interesting metamorphosis over the past 30 years. Initially, most of us believed it to be a psychological phenomenon with no organic basis.
The first transition was when it became recognized as a myofacial disease with trigger points (fibrositis). In 1990, the American College of Rheumatology Research Classification Criteria (ACR RCC) for fibromyalgia was published. The criteria required two components for fibromyalgia: a patient’s history of chronic widespread pain for at least 3 months, and ≥11 of 18 painfully tender soft tissue sites on physical examination
Late in the 1990s, the concept of a central, autonomic hyperfunctional state with neurotransmitter deficiencies and lack of restorative sleep were proposed as the causative factors. The resulting hyperactive autonomic nervous system manifested as tachycardia, hyperthermia, fatigue, depression, and pain “all over” as opposed to specific trigger points. This led to a revision of ACR RCC criteria for fibromyalgia, resulting in the 2010 ACR Fibromyalgia Diagnostic Criteria (2010 ACR FDC).2 The 2010 ACR FDC viewed the 1990 ACR RCC as the gold standard, but did not require tender-point examination.
Without the requirement of specific trigger points, it seems that just about every patient with generalized pain, insomnia, and depression is now given the diagnosis of “fibromyalgia.”
In my opinion, the latest (and most likely) final chapter in the fibromyalgia odyssey is that it is not a primary disease at all, but a secondary or symptomatic manifestation of an underlying, causative disorder. I believe, primarily based on my own clinical experience and the excellent work of the National Fibromyalgia Research Association and the National Fibromyalgia Partnership, Inc., that it is time to recognize fibromyalgia as being secondary to an inciting or underlying disease process.
Recent efforts by these organizations clearly call for recognition that the most common cause of fibromyalgia is probably positional cervical cord compression. Hints of this became known in 1997 when fibromyalgia was noted to occur in high prevalence after neck trauma.5
cervical myelopathy, specifically positional cervical cord compression (PC3), often overlap in patients with fibromyalgia.
The basic premise is that the cervical spinal cord is compressed when patients extend their neck either in a forward flexion or a backward extension position. A spinal cord defect, which may compress the cord in only some positions, may not be seen on standard magnetic resonance imaging (MRI). Proper diagnosis requires that additional dynamic MRI pictures be taken with the neck flexed forward and extended backward. A considerable amount of MRIs and clinical experience now document that repeated cervical neck compression, even though the cord is not damaged, may cause all the manifestations of fibromyalgia including diffuse pain, autonomic arousal, disordered sleep, depression, fatigue, and neurotransmitter changes. Patients who have intermittent cervical cord compression may have a Chiari I malformation or a history of neck trauma, particularly from an auto accident.
The Chiari malformation is typical of EDS, so this theory implies that Fibromyalgia could be caused by EDS, which has long been my suspicion. Any imbalance in function or overload of the body’s systems causes stress that wears down the body’s ability to adapt. This breakdown of balance could then eventually result in Fibromyalgia symptoms.
My Clinical Experience
I have found that more than two-thirds of patients appear to have a history of cervical neck trauma or the compression-related symptoms described by Dr. Holman when patients extend their neck. I now realize that I have been quite unaware of the critical nature of PC3. After taking detailed histories, I have found that all my other fibromyalgia cases concomitantly started with an infectious disease, usually infectious mononucleosis, head trauma, endometriosis, or a peripheral nerve injury or degenerative process. In these cases, there is always clear evidence of autoimmunity, systemic inflammation, and pituitary-adrenal-gonadal hormone changes.
It is clear to me that any peripheral pain site that can centralize can develop the classic symptoms of fibromyalgia. For my part, I also believe “myofascial syndrome” is in the same boat.
Our new understanding of centralized pain gives us the clue here. Prior to knowing that a painful, peripheral nerve injury and locus can incite glial cell activation, inflammation, central sensitization, and autonomic hyperactivity, it is no wonder that fibromyalgia was initially believed to arise “de novo” in the brain.
This would explain why so many people with EDS are first diagnosed with Fibromyalgia. Fibromyalgia is often the initial explanation for the widespread pain and fatigue of EDS, and then the EDS diagnosis is found much later – but only in patients who continue searching for a more specific diagnosis, those who suspect their own symptoms don’t quite match those of Fibromyalgia.
Fibromyalgia is only a “syndrome”, a cluster of symptoms without a known cause. Who knows how many people who are currently diagnosed with it may also have EDS. An EDS diagnosis doesn’t lead to a cure either, but knowing you have it can help you figure out how to minimize the pain better.