To the Editor:
The primary focus of our article1 was neither pain nor psychological profiles. In addition, we did not purport to identify a singular factor responsible for the development of chronic pain. Clearly this is a multifactorial issue, as also confirmed by others2,3, and even if statistically significant associations between baseline expectations/coping and recovery from whiplash have been shown4,5, they still explain only a proportion of the variance in outcome, suggesting they are not the only factors of importance. Moreover, the relationship does not appear to be consistent between nations6, indicating that the search for additional determinants of chronicity/longterm symptoms remains highly relevant.
Although we did indeed present psychological profiles based on SCL-90-R, focusing only on these would give the wrong impression in relation to the core character of the problem in patients with a condition referred to as chronic pain. As we ultimately showed, such profiles comprise symptoms that span different diagnostic categories and at the same time fail to consider the possible importance of individual symptoms. This is one of the main messages of our article. Instead of identifying so-called specific symptoms of whiplash, we uncovered a number of different psychological, cognitive, and vegetative symptoms that have not been reported in previous research in connection with patients with whiplash or other traumatic conditions. The fact that patients in our study1 could not be accurately identified as belonging to either whiplash or nonwhiplash groups on the basis of their symptoms called for a possible explanation. Based on our results1, we suggested that sleep disturbance may be the explanation for a similar symptom pattern in different posttraumatic conditions. In their comment7, Ferrari and Russell appear to neglect the complex nature of the problem, instead focusing exclusively on pain and in particular on the whiplash group of our study, continuing to discuss whiplash as if it were a particular chronic pain syndrome.
Experimental research in the 1930s suggested that disruption of sleep influences the pain threshold8. Moldofsky and Scarisbrick9 found a fibromyalgia-like pain pattern while selectively disrupting sleep in healthy individuals. The findings in relation to pain symptoms in these prospective interventional studies can hardly be explained by factors other than sleep disturbance; coping styles, beliefs, and expectations were unlikely to play an important role. Our own findings in individuals who recently had a whiplash injury indicated that pain following trauma likely prompted early-onset sleep disturbance (first exhaustive investigation about 7 days after the accident)10. This was the first study ever to show that sleep disturbance predominantly occurred in individuals who did not recover during the 2-year followup period; early-onset sleep disturbance occurred in only a minority of those who recovered completely during the followup period. On these grounds we proposed a model describing how symptoms referred to as late whiplash syndrome may develop11. This model proposed that late whiplash syndrome does not exclusively comprise pain but a number of psychological and cognitive complaints. Recent research has repeatedly confirmed the interrelationship among pain, sleep disturbance, and psychological, cognitive, and vegetative symptoms in pain conditions of different origin. On the basis of current scientific evidence, there does not appear to be any doubt that sleep disturbance is closely associated with the development of chronic pain. Our view, supported by research findings, is that sleep disturbance is the result of pain, which is a consequence of the trauma, and this may explain the development of comparable symptoms in pain conditions of different origin.
An equal insurance status in all patients was a prerequisite for being able to address the primary objective of our study1. For this reason, we excluded 34 patients with chronic low back pain of nontraumatic origin. These and additional patients with chronic nontraumatic pain were originally envisaged as a control group. They were excluded from the current analysis because in Switzerland their insurance status is different; such patients are not covered by the accident insurance scheme. At least in Switzerland, there is little financial gain to be had by patients with chronic pain of nontraumatic origin. It is not the purpose to present and discuss here the results of these patients. However, the table of the symptoms in the whiplash group shows that, with the exception of a few symptoms (e.g., trouble concentrating, trouble remembering things), patients with chronic low back pain of nontraumatic origin demonstrate a similar symptom pattern to that of whiplash and nonwhiplash groups1.
These results do not support the hypothesis that either beliefs about something being seriously wrong/worrying about things, or financial gain, play a principal role in chronic pain after trauma.
The role of expectations, in terms of the view of the injured person in relation to the longterm outcome, was discussed at great length in the 1980s and 1990s12. Interventions based on expectations, one aspect of coping, did not bring any benefit in dealing with postconcussion syndrome. If such interventions had proven to be successful, we would not still be discussing postconcussion syndrome some 20 years on. Since postconcussion syndrome shares many symptoms in common with late whiplash syndrome, focusing on expectations does not appear to be a promising (or the only) approach. This applies not only to late whiplash syndrome but also to other chronic pain conditions: it has been shown that multidisciplinary outpatient or inpatient rehabilitation in fact slowed recovery in whiplash-injured individuals13, and any meaningful multidisciplinary program for chronic pain conditions usually comprises the improvement of coping strategies.
A closer look at the comments7 of Ferrari and Russell suggests that their intention was not to critically appraise the findings of our study and the hypotheses contained therein, but to promote their own favored theory on the subject. However, we feel that the latter has failed to result in any major advances in improving outcomes for chronic pain following whiplash in recent years. Their contention that “interventions designed to increase patients’ expectations may be beneficial and should be examined further in controlled studies” has already been questioned by previous research13. Thus we strongly believe that the mechanisms of action proposed in our article1 promise more success, or are at the very least worthy of further investigation.
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