BCMJ, Vol. 44, No. 9, November 2002, page(s) 486-489—Personal View
Roland Staud, MD
Possible causal relationship: Fibromyalgia and trauma
The recent article in the BCMJ by Dr Ferrari[1] addresses the important question whether trauma, particularly neck trauma, can cause fibromyalgia syndrome (FMS). Although Dr Ferrari acknowledges that well-controlled studies of this relationship are lacking, it becomes rapidly clear that he has already made up his mind. He argues that a study by Buskila et al.,[2]
despite a strong association of neck trauma with FMS, provided evidence that these patients are exaggerating their symptoms for secondary gain. He failed, however, to mention that all patients in this study continued to be employed, and insurance claims were not increased in patients with FMS.
In addition, Dr Ferrari argues that tender points in FMS are strongly correlated with distress and that tender points represent an amplified pain response in areas where most everybody feels mild discomfort anyway. Therefore in his opinion, FMS symptoms reflect hypervigilance but not pathology. He neglects however, to mention the lacking correlation of tender points with clinical pain.[3]
Dr Ferrari is also critical of reports of substance P (SP) elevations in the spinal fluid of FMS patients. He considers these studies as questionable and would like to see more studies comparing FMS with other musculoskeletal pain syndromes. Comparable studies, however, have been done in patients with osteoarthritis (OA) and depression, showing elevated levels of SP in OA and normal levels in depression.[4,5] Despite the fact that SP is well known as a neuropeptide intimately involved in pain signalling,[6,7] he questions whether elevated levels of SP are the result of pain or some unspecific alteration. He speculates that SP levels in FMS are high because of lack of exercise. He acknowledges, however, that the elevated SP levels in FMS confirm a “physiological problem of some sort.”
This very one-sided article fails to acknowledge the increasing body of evidence for abnormal peripheral and central pain mechanisms in FMS. Increased amplification of pain clearly plays a role for FMS pain, including peripheral/central sensitization and temporal summation of pain. I would agree with Dr Ferrari that many “normal” people are hyperalgesic or allodynic without overt chronic pain as required for the diagnosis of FMS. It is, however, conceivable the tonic nociceptive stimulation like trauma may worsen central sensitization, thus creating the basis for acute and chronic pain and FMS. The important relationship of tonic nociceptive stimulation with widespread pain is currently investigated in my laboratory.
Like many other chronic pain syndromes, FMS requires comprehensive therapy including medical, physical, and psychological treatments. It is important to acknowledge that FMS pain cannot be attributed solely to distress and secondary gain issues. Dr Ferrari’s view neglects much of the more recent scientific evidence about abnormal peripheral and central pain mechanisms in FMS, which need to be considered for the possible relationship of trauma with FMS.
—Roland Staud, MD
Division of Rheumatology and Clinical Immunology, University of Florida
Remember that all models are wrong; the practical question is how wrong do they have to be to not be useful.[1]
Dr Staud adopts a uni-dimensional biomedical or disease model. My review article was intended to raise some tough questions, to challenge physicians and therapists to look at what role they have as part of the solution to the social disorder of fibromyalgia, and what role they have as part of the problem.
Since the biomedical model of fibromyalgia has been forced upon patients and society for years now, it seems most open-minded to occasionally consider the need for a change in paradigms. This has already occurred to an extent. Where once fibromyalgia patients were told their problems lie in sleep rhythms and were given intoxicating sedatives, we now prescribe exercise and cognitive therapy. Where once we told them that there was something wrong with their muscles, now we are looking at more global factors like reactions to pain, avoidance behaviors, and the effects anxiety created by the medical community, media, and legal community can have on illness behavior.
The biopsychosocial model is proving to be more useful than the disease model. Though proponents of the disease model often speak of a multidisciplinary approach, they still insist fibromyalgia must be a disease. Proponents of the biopsychosocial model do not conclude that FMS can “be attributed solely to distress and secondary gain issues.” We look at fibromyalgia patients in a more global fashion, see the behavior in the context of social phenomena, and consider the effect one’s past life experiences, current coping skills, and current interactions with medicalization have on illness outcomes. The further value of the biopsychosocial model is that it lends itself to discussion of other illness like whiplash, repetitive strain injury, chronic fatigue syndrome, and Gulf War syndrome.[2-4]
Dr Staud points to prima facie evidence of the social aspects of fibromyalgia, demonstrated by Buskila et al.[5] Their study, in Israel, found no unemployment in a presumably unselected cohort of fibromyalgia patients. Oh that fibromyalgia could be such a phenomenon in North America! Buskila et al.’s data raise some tough questions: how do the fibromyalgia patients in Israel avoid disability where FMS-related disability is becoming epidemic in North America? A disease model of FMS based on substance P and central sensitization does not answer this question, and thus is overall too wrong to be useful.
The controversy in FMS does not seem to be whether these patients have physical sources of pain. They no doubt do have a variety of musculoskeletal disorders and physiological disturbances; it is the severity of their pain and their response to it that is the problem. FMS patients are striking in the way they focus on symptoms, keep pain diaries, withdraw from activity, and develop disease convictions sine self-evident signs. It is as much a part of their illness as their symptoms. As Dr Staud indicates, tender points are a measure of pain, but when one controls for pain levels, tender points actually correlate with degree of emotional distress.[6] Again, the model Dr Staud alludes to cannot explain why more emotional distress produces more tender points even when one controls for pain distribution and level, nor can the disease model explain why tender points exist in patients who are otherwise pain free, but rather feel depressed.
The biomedical model is also too wrong to be useful because it has not led to helpful treatment strategies. On the other hand, studies that address illness behavior and cognitive strategies are effective and heading in the right direction despite never asking about or considering substance P levels. We would be taking a backward step to focus patients on their substance P levels rather than how they control their own destiny through action rather than being passive victims of a form of supposed central sensitization that cannot be confirmed or denied through any gold-standard measurement.
Finally, there is the matter of secondary and tertiary[7] gain. While secondary gain may be a relevant element in various illness, some physicians lack a complete enough appreciation of the many forms of secondary gain to understand its relevance. Rather than focusing on monetary gain, we need more studies that evaluate the lives of our patients and how their lives relate to and predict their illness behavior, not just in FMS, but in many illnesses.
FMS patients and society are better off if physicians learn to step out of the restraint of their biomedical model and learn from society itself. The readership should, in forming its model of FMS, consider looking at the whole picture that is FMS, and include the biological, psychological, and the social elements. Otherwise, we simply perpetuate a long tradition of holding on to the medical model by jumping from one desperate theory to another, the latest substance P study or neurophysiologic study, whatever tool will keep us from seeing the truth—that we have long been wrong, and have done more harm than good.
—Robert Ferrari, MD
Edmonton
References
- 1. Ferrari, R. Fibromyalgia and motor vehicle collisions—Oh, the pain! BCMJ 2002;44:257-260.
- 2. Buskila D, Neumann L, Vaisberg G, et al. Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum 1997;40:446-452.
- 3. Wolfe F. The relation between tender points and fibromyalgia symptom variables: Evidence that fibromyalgia is not a discrete disorder in the clinic. Ann Rheum Dis 1997;56:268-271.
- 4. Berrettini WH, Rubinow DR, Nurnberger JI, Jr., et al. CSF substance P immunoreactivity in affective disorders. Biol Psychiatry 1985;20:965-970.
- 5. Nyberg F, Liu Z, Thornwall M, et al. Enhanced CSF levels of substance P in patients with painful arthrosis but not in patients with pain from herniated lumbar disks. J Musculoskeletal Pain 1995;3:2.
- 6. Almay BG, Johansson F, Von-Knorring L, et al. Substance P in CSF of patients with chronic pain syndromes. Pain 1988;33:3-9.
- 7. Basbaum AI. Spinal mechanisms of acute and persistent pain. Reg Anesth Pain Med 1999;24:59-67.
- 1. Box GEP, Draper NR. Empirical Model Building and Response Surfaces. New York: Wiley, 1987:74.
- 2. Ferrari R. The biopsychosocial model—A tool for rheumatologists. Bailliere’s Clin Rheumatol 2000;14:787-795.
- 3. Ferrari R, Schrader H. The late whiplash syndrome. A biopsychosocial approach. J Neurol Neurosurg Psychiatry 2001;71:722-726.
- 4. Ferrari R, Russell AS. The problem of Gulf War syndrome. Med Hypotheses 2001;56:697-701.
- 5. Buskila D, Neumann L, Vaisberg G, et al. Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum 1997;40:446-452.
- 6. Croft P. Testing for tenderness: What’s the point? J Rheumatol 2000;27:2531-2533.
- 7. Kwan O, Ferrari R, Friel J. Tertiary gain and disability syndromes. Med Hypotheses 2001;57:459-464.
