Abstract
Dear sir The study of whiplash subjects reported by Kasch et al. (1) is remarkable by virtue of the inclusion of an ankle-injury control group. Their doing so allows one to understand a potentially important factor underlying the illness behaviours of chronic whiplash, one hereafter referred to as ‘attributional pathosis’. Attributional pathosis in this context is considered as the tendency to attribute any and often all symptoms to a specific illness or event, despite no meaningful evidence or method of testing that imputation. It may evolve from the expectation of various chronic symptoms after certain injuries. The approach taken by Kasch et al. also provides considerable novel avenues of research investigating this aspect of the biopsychosocial model of whiplash proposed by Ferrari et al. (2, 3).
Kasch et al. examine the prevalence and intensity of symptoms at 6 months in a group of subjects who have had a motor vehicle rear-end collision (whiplash subjects) and a group with ankle injury subjects not in a motor vehicle collision. They find that at 6 months following reported ankle injury, 26.7% of the control group of ankle-injured subjects report headache, 20% report neck pain, 36% report low back pain, 26.7% report fatigue, etc. They also show that the pain intensity of headache, neck pain, etc., was much the same in ankle-injured subjects at 1 year after initial entry and symptomatic whiplash patients at 1 year after the collision (4). Also, at 3 months, the total cervical range of motion of whiplash and ankle-injured subjects is no different (4, p. 39). It seems that despite the fact that 100% of the ankle-injury group eventually reported they had fully recovered from their ankle injury, they continued to report a seemingly unrelated myriad of bodily symptoms, that are also common in the chronic whiplash syndrome, and they report these with a similar intensity as do whiplash patients, with the same cervical range of motion in the long term. The whiplash group did report a prevalence of symptoms at 6 months that was roughly double that of ankle-injured subjects, but one must appreciate that these whiplash subjects are a concentrated group of symptomatic subjects. A larger denominator of total collision victims, including those who chose not to enter the study and became asymptomatic by 6 months, would, with all subjects included, dilute this prevalence of symptoms at 6 months. This selection is probably more biased towards concentration of symptomatic whiplash patients in the study than to symptomatic ankle-injury subjects (4, p. 43). The true 6 months prevalence of symptoms may thus not have been much different between the ankle injury and whiplash injury groups with all subjects included. It might be difficult, without asking the patients what they think their spinal symptoms arose from, even to discern the two groups of patients based on symptom prevalence and intensity, and neck range of motion at more than 3–6 months after the collision. That is, ankle-injury patients at 6 months have many of the symptom characteristics of whiplash patients, even if ankle-injured patients do not have an apparent traumatic reason for these spinal symptoms.
This leads to an interesting question: to what do ankle-injured subjects attribute their headache, neck pain, low back pain, etc.? Why is it not common clinical practice to have ankle-injured patients report that they have neck pain, headache, and a host of other symptoms they believe to be due to their ankle sprain? This raises the spectre of attributional pathosis as being a part of the problem in chronic whiplash. The whiplash subjects and ankle-injured subjects probably share the same risk of a background prevalence of symptoms that do not require a neck injury to exist (the ankle-injured subjects prove that the symptoms exist in those without neck injury). Yet, the whiplash patients tend to attribute their chronic neck pain to the collision they had, but ankle-injured subjects do not. How is this decision made? There are no physiological data for a person to define exactly what their headache or neck pain is due to, nor any specific tests that they or their therapists can perform to define the cause of the neck pain. It is a decision based on probabilities, and probably common sense choices (i.e. ‘if a collision occurs today and I have neck pain tomorrow, probably the collision caused my neck pain’). But as the symptoms become further and further removed in time from the collision, this link to the origin of symptoms becomes weaker. So again, how do whiplash patients make the link between a pain episode on a day 6 months after the collision and the initial injury, and why do ankle-injured subjects not attribute their headache or neck pain to their ankle injury? Perhaps they need the cultural information, provided by the experience of others and by the media and therapeutic community, to make these attributions. The ankle-injured subject would, of course, seem bizarre if making an association between multiple spinal and other symptoms and their ankle injury, but is it any more reasonable for a whiplash patient to attribute all their spinal and other symptoms to the collision, when they have risk of having such symptoms even if they were uninjured? It is the culture that determines which of these attributions is valid, not science.
The possibility of attributional pathosis in chronic whiplash is a difficult question to answer, but Kasch et al. have made an important first step, and more studies of symptoms in traumatized (but non-whiplash) patients are needed to see how often such subjects, if required to track many (even seemingly unrelated) symptoms, experience and report these symptoms compared with unselected whiplash patients. It will also be of interest to see if making subjects keep track of various bodily symptoms causes an increased awareness and increased severity of life's aches and pains that would otherwise be largely ignored, and therefore not available as the substrate for attributional pathosis (3). A recent study compared Lithuanian and Canadian subjects with no personal experience of whiplash injury, these subjects being asked to select symptoms they believe may result from such an injury, and to anticipate how long such symptoms would persist. Approximately 50% of Canadian subjects anticipate symptoms to last for months to years, compared with a very small fraction of Lithuanian subjects (5). It is known that the chronic whiplash syndrome is common in Canada and not in Lithuania (3). The same results of very different symptom expectations have now been found in Greece (unpublished data), another country in which the late whiplash syndrome is rare or non-existent (3). It has been proposed by Aubrey et al. (6) and Mittenberg et al. (7) that this phenomenon of symptom expectation does not in itself produce symptoms, but rather in the setting of such expectation, an acute whiplash injury victim becomes hypervigilant for symptoms. The subject will thus both notice the minor aches and pains of daily life that otherwise would have passed without as much notice, and then attribute those symptoms to the ‘injury’, as one expects this to be the cause, and their attributions are reaffirmed by, for example, those they contact in the therapeutic and legal community. The expectation may also encourage one to seek medical attention—in the hope that the problem can be curtailed by therapy—and lead one to reduce activities for fear of causing more harm to an already potentially serious problem, generating further anxiety with further symptom amplification. They may also be promoted by this expectation to seek litigation, to protect oneself from economic loss. All these actions stem from the view that one has a serious injury. The view that one has a very benign injury would probably not generate this same behaviour. Though it remains to be tested, ankle injury subjects are not likely to expect numerous spinal and other symptoms further away from the ankle to be a natural result of ankle injury. They are thus less likely to be vigilant for such symptoms, or report them to their doctor with the belief that they have arisen as a result of ankle injury, and are less likely to be told by their doctor that their neck pain, for example, is a chronic complication of ankle injury. Whiplash patients, who may have the same source of chronic spinal pain as ankle-injured patients, are more likely to attribute this to their original neck injury if that is their expectation, or if that pattern is concurred upon by their doctors, lawyers, and therapists.
The problem of attributional pathosis is not thus limited to the patient, but includes the therapists and the doctors. It is in fact a phenomenon also seen in researchers.
Take, for example, the so-called ‘faceteers’ (8), researchers who believe that the chronic whiplash syndrome is best explained as a result of some facet joint disorder as the underpinning of ‘whiplash’. Lord et al. (9), for example, examined 39 subjects with chronic neck pain. Five of the 39 had not been in motor vehicle collisions, but had apparently had neck injuries in other types of collisions. Two of 39 claimed their chronic pain began 3 months after a collision. Some of the collisions took place 44, 27, and 21 years prior to entering the study. Looking for a cause of current neck pain in these subjects, the investigators found that the facet joint or nearby structures could be a source of current neck pain in some members of this highly select, heterogeneous, non-representative group of what they arbitrarily called ‘whiplash patients’. This indicates only that neck pain in some cases may have a current physical cause. The results do not confirm the current cause is also a past cause of the neck pain, or has been for, say, the last 44 years. The results tell us nothing about the injury (if there was one) in these subjects and nothing about whether an acute injury can develop into a chronic physical source of pain.
The facet joint studies illustrate that researchers are prepared to place the label of whiplash patient on anyone who wants to attribute their chronic neck pain to a collision. What cultural factors promote this non-scientific decision to make such an attribution? Why can one assume that a current cause of neck pain has any relationship to a collision 44 years ago? That such assumptions were made is the greatest revelation of the facet joint research. Physical sources of pain can and do exist, but it is how people interpret the significance of that pain in relation to other events that creates the problem. If these subjects attribute their neck pain to a collision, then they are ‘whiplash patients’. If they choose to dismiss the attribution, then they are not ‘whiplash patients’; the label has such a limited and flimsy a basis, that it can be, on a mere whim, dismissed or clung to passionately. Do whiplash patients with chronic symptoms simply pay too much attention to their body, register symptoms that are being experienced by many people as part of life's aches and pains, and misattribute these symptoms to a collision? More research is needed, but Kasch et al. have certainly opened the avenues with which to approach this important question.