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Radanov et al 1 are to be commended on their recent publication considering, in part, the issue of “brain injury” as a basis for cognitive dysfunction in the late whiplash syndrome. There are a few limitations of the study. The first is the small sample size. A second is that, unlike previous studies from Switzerland in a non-tort system, the subjects of this recent study are mostly litigants. When examining for correlation between diagnostic tests and symptoms, malingering detection efforts, as used in other studies,2 may be required. This is now a confounding variable. Yet, despite these concerns, this study is an important and valid effort.
Although it can never be proved that there is no brain injury in whiplash patients, it must be realised that in both science (medicine in particular) and the law, there is an obligation to deal in probabilities. Clinicians routinely make treatment decisions based on the most likely diagnosis and current evidence, not because of absolute proof. Radanov et al have given clinicians and the legal community, through this and previous studies,3 4 an opportunity to appreciate the more highly probable sources of cognitive symptoms in whiplash patients. These alternative explanations other than brain injury sources are not only more benign (non-pathological), but are more amenable to specific interventions and prevention altogether.5
In whiplash patients, these symptoms are correlated with the pain experience, various causes for psychological distress, and medications (although medications are not implicated in the patients in the current study).3-5 The cognitive symptoms seem to also improve as the patient's pain improves.3 4 Furthermore, the distress of litigation as a factor is noted. In the cohort of Radanovet al,1 85% were in litigation. Lees-Haley and Brown6 studied 170 personal injury litigants, in whom the litigation was not related to a physical injury, but rather to issues of sex, race, or age discrimination, verbal harassment at work, wrongful termination, etc. Although the patients were not filing a claim for neuropsychological impairment, they have a similar prevalence of cognitive and other neurological complaints as those who litigate for what is commonly referred to as mild traumatic brain injury. These researchers also showed that the base rates of these complaints is actually high in the otherwise, healthy population. In many cases, claimants are likely amplifying and misattributing their symptoms to the accident, when they relate instead to pre-existing conditions, the stress of litigation, unrelated illnesses, malingering, inspiration of hysteria by prior medical-legal evaluations, or influence of third parties.6
Beyond this, malingering of cognitive dysfunction seems to be a particular problem in some countries. In The Netherlands, some 25% of those patients reporting such symptoms months to years after the accident may be malingering. Malingering (as detected by testing) was twice as common in litigants than non-litigants.2
Radanov et al are thus contributing to the effort in closing one chapter of the whiplash controversy. Clinicians can now be more confident in relating to their patients that their cognitive dysfunction is due to various reversible factors, rather than brain injury or other ominous diagnoses. Indeed, a re-education of this sort, and the biopsychosocial (non-dichotomous) approach Radanovet al suggest is the cornerstone of more effective approaches towards the prevention of the late whiplash syndrome.7 8
Radanov et al reply:
On the basis of our article,1-1 which may be interpreted as indicating that there is no brain injury after whiplash, Ferrari focuses on malingering as an alternative explanation for the cognitive problems of whiplash patients. This perhaps is a biased view and is in contrast with Ferrari's statement that “the biopsychosocial (non-dichotomous) approach” to the problem may be required in these patients. The following points seem important: (1) It should be considered that there were results1-2 outside the context of litigation which suggest that overall there was an improvement of cognitive functions (for example, attention) in whiplash patients within the first months of injury. However, there was a relapse in cognitive functioning in long term patients,1-2which could be explained neither by brain damage nor by litigation. Data rather suggested that this relapse may be due to symptoms (mainly pain),1-2 adverse effects of medication,1-2 or symptoms related to change in psychological functioning.1-3Comparable results were found in additional studies1-4 1-5where litigation is unlikely to have played an important role. In this research1-4 1-5 similar problems in cognitive performance were found in patients who had had mild traumatic brain injury or only an injury to other parts of the body. Interestingly, in patients with more severe injuries to other parts of the body1-4 a higher impairment in cognitive functioning was found. These results may suggest that experience of symptoms (for example, pain) and the process of adjustment to the symptoms (for example, worry about achieving the pretraumatic level of functioning) may contribute to psychological changes as shown previously.1-3 Based on these changes, of which the prolonged experience of impaired wellbeing may be crucial, an inability for effort may follow, eventually leading to subtle problems in cognitive functioning. Assuming a dichotomous perspective with focus on malingering as the only basis for symptoms may certainly lead to an additional change in patients' illness behaviour including an exaggeration of symptoms in some cases. Considering these issues may help to develop a therapeutic approach which should allow patients to adjust better to their problems and improve recovery. Previous results generally indicate a lack of morphological brain damage after whiplash or mild traumatic brain injury.1-1 1-6 However, functional brain damage, whatever the cause, cannot be fully excluded1-7 and further research may provide some additional insights. For example, using SPECT, short term disturbance to prefrontal structures was found in patients with mild traumatic brain injury,1-6 which probably indicated some sort of impaired functioning. Such a functional impairment may introduce a cascade of additional problems eventually contributing to a vicious circle on which basis the previously shown symptom augmentation may follow.1-2 This has to be prevented. Blaming patients for malingering is hardly the most appropriate approach and does not have anything to do with a non-dichotomous perspective of illness behaviour.