As whiplash has evolved, it may be a pain in the neck for more than just the collision victim. Physicians sometimes find themselves dealing with a minor neck pain that has grown into total body pain and suffering, apparently inflicting major social dysfunction. They often find the collision victim embroiled in self-diagnosis, multiple ineffective therapies, bold expert opinions, conflicting literature, and legal proceedings. Thus, fibromyalgia grows out of whiplash. There are two aspects of this controversial syndrome. First, what are the potential mechanisms by which motor vehicle trauma and fibromyalgia are associated? Second, what can the physician offer such patients in terms of education and therapy?
Understanding psychosocial factors is crucial in treating fibromyalgia patients, but not because their pain is purely psychological. By educating patients about the physiological impact of their actions and perceptions, we can help liberate them from the disastrous spiral of chronic disability.
The question “Do motor vehicle collisions cause fibromyalgia?” is an important one if only because society provides significant benefits to those who have developed pain and suffering as a result of a personal injury due to the negligence of others. Indeed, this exact controversy exists for the relationship between motor vehicle trauma and multiple sclerosis, which for both it seems a wholly unhelpful issue in the greater context of medical care.[1-3] There is no apparent health benefit in making a patient focus on a medicolegal claim, but great benefit in helping them focus on rehabilitation and recovery, irrespective of blame.
A 1996 expert consensus report examined the evidence to date and concluded, “overall, the data from the literature are insufficient to indicate whether causal relationships exist between trauma and [fibromyalgia].”
In 1997, further research compared the incidence of fibromyalgia after whiplash injury versus that following leg fractures. They found that fibromyalgia was 13 times more frequent following neck injury than following lower extremity injury, even though both groups studied were equally likely to have insurance claims pending. The authors cautioned, as before, that the “present data in the literature are insufficient to indicate whether causal relationships exist between trauma and [fibromyalgia].”
One means by which to demonstrate a causal association would be to reproduce the exposure experimentally. If a neck-disturbing event was itself the cause of fibromyalgia, then experimental whiplash-like events should be associated with fibromyalgia. Yet fibromyalgia has never been found in the four decades of simulated whiplash collisions with thousands of volunteers, even though the collisions at times render acute symptoms.
As described in detail elsewhere in this series, if fibromyalgia occurs after whiplash injury in Lithuania, Germany, or Greece, it must be relatively rare, because in those jurisdictions the collision victims appear to recover within weeks from the effects of the motor vehicle collision, and chronic dysfunctional pain disorders do not follow. If injury mechanisms were themselves the instigators for fibromyalgia in North America, they should be equally so in Lithuania, Greece, and Germany, where whiplash victims should not be able to escape the phenomenon. So the considerations of how a diagnosis of fibromyalgia may appear in a whiplash victim in Canada but not in Greece must be built on a concept that is contrary to a simple injury model.
According to Buskila, tender points appear to be more painful in neck injury patients than they are in leg fracture patients. Ferrari and Russell have given one explanation to this phenomenon. It relates in part to the reporting of pain upon pressure at specific points versus control points, which is fundamental to the American College of Rheumatology (ACR) diagnostic criteria for fibromyalgia. Tender points appear to reflect a lowered pain threshold. The more distress, the more tender the points. Barsky has suggested that this phenomenon could be mediated by psychological factors, that is, pain focus. Such pain focus is predicated upon the setting in which the symptoms develop, the amount of attention to (or distraction from) the symptoms, and levels of anxiety. Tender points are found even in individuals without complaints of regional or diffuse pain, but who instead have measures of psychological distress, postural stress, or who are out of shape. In these individuals, fatigue, poor sleep, and depression correlate with the presence of tender points regardless of the presence or absence of regional or diffuse pain, or complaints thereof. Thus, the so-called “tender points” of fibromyalgia are merely an amplified pain response in areas where most individuals feel some mild discomfort anyway, if tested, and may reflect hypervigilance for symptoms rather than actual pathology. The fact that fibromyalgia is classified by finding 11 of 18 specified points that are tender implies that generalized tenderness is prevalent as a background in the general population—as in the person with 10 out of 18 points tender.
If amplification is a result or sign of psychological distress, then why would someone who has a leg fracture not develop this finding as often as following a neck injury? Both suffer the initial distress from fright at the time of the accident, as well as anger at the offending party, inconvenience, and the initial pain from the injury. Beyond this initial period, however, the psychological distress may actually increase for the whiplash (neck injury) patient versus the fracture patient. Buskila and colleagues showed that neck injury patients had more anxiety, fatigue, sleep disturbance, and depression, all of which produce tender points, independent of pain complaints.
The North American whiplash patient exists in a culture that regularly receives information of whiplash injury leading to chronic pain and disability. This patient may be told by his or her physician it could take a long time to heal, be sent to many different therapists, suffer repeated therapeutic failures, develop the impression that to be active with pain may cause more harm, and battle with an insurance company that doubts the legitimacy of the symptoms. Under these circumstances, one would expect whiplash patients to become more distressed with time than leg fracture patients—and they do. Their outcomes are different because of what they perceive about their injury and how they are treated thereafter. If tender points are more often identified in the more distressed individual, and if this is the key to the diagnosis of fibromyalgia, then it is not surprising that such a diagnosis is more often made in the whiplash patient than in the leg fracture patient.
Many whiplash patients have pain above and below the waist and often have sundry limb pain. Given enough distress, it would seem a clear pathway to a diagnosis of fibromyalgia. Yet, there is something else peculiar to fibromyalgia patients that physicians have noticed and that has been verified in studies: they have an unusual psychosocial history predating their diagnosis of fibromyalgia, a history that places them at risk for health care seeking behaviors and disease confirmation. The psychological mechanisms are those of adopting a sick role with secondary gain motivations (not just monetary).[12-15] The observation that this form of illness behavior follows collisions predates the automobile (for example, railway spine).
In another article in this series [“Whiplash as a social disorder—How so!” in the July/August 2002 issue], the biopsychosocial model of whiplash leads to an obvious and applicable treatment approach to fibromyalgia and whiplash together, one that in most patients does not require the physician to suddenly become a psychotherapist, but more an educator. This model should reaffirm for the patient that the pain, for example, is not all in his or her head. The treatment is not cognitive or behavioral therapy, which implies therapy aimed at a psychological disorder that must first be cured from within the mind. Rather, it is therapy of a physical kind such as progressive exercises and posture correction and maintenance measures that may prevent a behavior that allows psychosocial factors to foster chronic pain; it is biopsychosocial therapy that prepares patients to become active participants in their lives and the lives of others, rather than passive dysfunctional participants.
Patients should be informed that if they withdraw from normal activities because of neck pain and fail to mobilize their neck with exercises, they will develop postural abnormalities, which will cause more pain. It gives patients the opportunity to recognize that the therapist or physician is not judging psychological factors to be the cause of pain, but to be the cause of behavior, behavior that if not modified will produce physical effects. It legitimizes patients’ belief (and they are likely correct) that they have a physical source of chronic pain. But that physical source of pain comes about because of their chosen inactive behavior. Explaining to patients that some of their symptoms could arise because of collar and medication use is again reaffirming for them a physical source for symptoms, it saves face, and also indicates that their behavior must change in order to recover.
Patients commonly refer to the latest theory they have read about fibromyalgia, and physicians should be prepared to provide some guidance in this regard. One current notion is that elevated levels of substance P in the cerebrospinal fluid (CSF) of fibromyalgia patients is the cause of their pain. The finding that substance P is elevated in fibromyalgia patients compared to healthy controls is important because it suggests that indeed such patients have physiologic abnormalities (or anomalies) and are not just imagining their pain. Unfortunately, because no or very few studies have been done comparing CSF substance P levels of fibromyalgia patients versus other forms of chronic pain (for example, rheumatoid arthritis, chronic neck pain, or chronic low back pain), we do not know if the elevated substance P level is simply the nonspecific result of pain process or is an underlying cause of the pain itself. It could also be that CSF substance P is high due to general inactivity or lack of exercise, which would show with concomitant low levels of enkephalins. We also do not know what the CSF substance P levels are in patients without pain but who have anxiety, depression, or somatoform disorders. It may be that psychological distress also interacts with CSF levels of substance P. More studies are needed before making any sweeping conclusions about substance P levels as a cause in fibromyalgia, but the research does confirm a physical/physiological problem of some sort, and patients should be reassured that one is not considering all of their problems as psychological in origin. Psychosocial factors are important, but chiefly because of how they act upon a substrate of physical and physiological problems to generate the overall clinical picture.
Patients should be encouraged to voice their concerns about what they have heard or know about the outcome of their illness. This is an opportunity to explain to them that while chronic disability can occur, it occurs often for reasons that the patient can control—such as whether her or she withdraws from activities, takes too many medications, avoids exercise, wears a collar, gains weight, and so on. Knowing what causes symptom amplification, the physician can discourage a pain/symptom diary, discourage frequent visits to therapists, and instead encourage an independent exercise program. Furthermore, the physician may discourage litigation as, apart from the inherent stresses involved, it often compels the patient to focus on symptoms and attend therapists frequently, as well as to relive symptoms during independent medical examination and discovery.[20,21]
One can manage the problem of attribution by explaining to the patient that pain feels like pain regardless of the cause, so it is easy to mistake the original cause of pain (for example, a neck sprain) for current causes (for example, poor posture and poor physical fitness). Patients with purported fibromyalgia can be told their neck and back pain are related in part to poor posture, just as they may be in any whiplash patient, and that their leg pain is in part related to bursitis, arch disorder, and poor flexibility, or other physical factors, each of which has a separate treatment and neither being part of a single disease process.
People are exposed to injuries during many phases of their lives. Often, it can be the environment that they are in that alters their behavior in a negative way at some point in their life. Although the patient may be reluctant to pursue these issues, if the physician is first clear with the patient that the symptoms are legitimate, and have many physical sources, then the psychological factors involved may also be accepted as part of the clinical picture, and can also be dealt with. The patient, however, for whom the collision is a solution to his or her life situation is far less likely to respond to any therapy that will take away the sick role and its benefits. In these cases, allowing a patient to go down the road of lengthy litigation and having to prove illness will guarantee a miserable existence, and often the only ones to benefit are those surrounding the patient as part of the whiplash industry. This phenomenon is so deeply rooted in our culture that physicians must feel at a loss to do anything about it, but at least they can try by getting to know their patients, their life situation, and offering them ways out of that situation other than chronic disability. One can hope that in the future we will spend more time talking to these patients and understanding them than we do arguing about whether the accident caused their diagnosis to appear. The medicolegal process places barriers between the physicians and the patients that we must work to break down to free patients from its unhealthy burden.
While one can understand that anyone who believes he or she developed fibromyalgia in response to someone else’s negligence would desire compensation, the better solution is a disability program that does not ask questions of blame, but rather assesses the presence or absence of disability, irrespective of causation. Fibromyalgia seems to be a most unfair illness. It is even more unfair if one cannot develop it subsequent to trauma, for then, even the secondary benefits of trauma—attribution or blame—are denied. The medical community would probably prefer to spend more time encouraging government to develop programs that eliminate blame as the compensation issue and instead focus on the issues of disability and rehabilitation. This would also preclude the other side of the coin: the insurance industry recruiting experts to refute causation in cases where it may actually exist. Neither approach benefits society.
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11. Croft P, Schollum J, Silman A. Population study of tender point counts and pain as evidence of fibromyalgia. BMJ 1994;309:696-699. PubMed Abstract Full Text
12. Ferrari R, Kwan O, Friel J. Illness behaviour and adoption of the sick role in whiplash claimants. Forensic Examiner [serial online] www.acfe.com (August 1999; retrieved 16 April 2002).
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14. Ferrari R, Kwan O. The no-fault flavor of disability syndromes. Med Hypotheses 2001;56:77-84. PubMed Abstract
15. Shorter E. From Paralysis to Fatigue. Toronto, ON: Maxwell Macmillan, 1992:ix.
16. Ferrari R. Railway spine. In: The Whiplash Encyclopedia, The Facts and Myths of Whiplash. Gaithersburg, MD: Aspen Publishers Inc., 1999:10-14.
17. Ferrari R. The biopsychosocial model—A tool for rheumatologists. Baillieres Clin Rheumatol 2000;14:787-795. PubMed Abstract
18. Russell IJ, Orr MD, Littman B, et al. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum 1994;37:1593-1601. PubMed Abstract
19. Welin M, Bragee B, Nyberg F, et al. Elevated substance P levels are contrasted by a decrease in met-enkephalin-arg-phe levels in CSF from fibromyalgia patients. J Musculoskel Pain 1995;3(suppl):4.
20. Olsnes BT. Neurobehavioural findings in whiplash patients with long-lasting symptoms. Acta Neurol Scand 1989;80:584-588. PubMed Abstract
21. Taylor AE, Cox CA, Mailis A. Persistent neuropsychological deficits following whiplash: Evidence for chronic mild traumatic brain injury? Arch Phys Med Rehabil 1996;77:529-535. PubMed Abstract
Robert Ferrari, MD, FRCPC Dr Ferrari is a clinical professor in the Department of Medicine at the University of Alberta in Edmonton, and researcher/independent examiner of matters concerning whiplash and chronic pain syndromes.
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