Matter for Debate

Myths of Whiplash

R. Ferrari
Department of Medicine, University of Alberta Hospital, Edmonton, Alberta, T6G 2BZ, Canada

Correspondence to: R. Ferrari, Department of Medicine, University of Alberta Hospital, Edmonton, Alberta, T6G 2BZ, Canada Email: rferrari@shaw.ca

Introduction Whiplash is a spinal disorder Chronic whiplash is a universal problem

Many treatments work Conclusion References

Keywords: Whiplash injuries, traffic accident, neck pain, chronic pain
Surg J R Coll Surg Edinb Irel., 1 April 2003, 99-103

When the concept of whiplash was first introduced by Harold Crowe in 1928 at a conference, and when it first appeared in a medical publication in 1945, it was not based on scientific evidence. That is, like many great stories, the whiplash theme sprang mainly from mythology, where many explanations had to be created to fill in the gaps in our understanding. Since those early days, and mainly in the last ten years, more research has been carried out to unravel these myths than had been performed to define chronic whiplash in the first place. This limited review considers a few of the aforementioned myths of whiplash, and how scientific efforts have enlightened us on these matters

INTRODUCTION
When the concept of whiplash was first introduced by Harold Crowe in 1928 at a conference, and when it first appeared in a medical publication in 1945, it was not based on scientific evidence.^1,2 The physicians were trying to understand a specific group of patients, and they created a theory of injury to the neck, in the absence of any known pathology. As such, it has been a topic ripe for myth generation, and over the decades several myths have arisen, some of which have been explored scientifically. This review considers three of the more commonly expressed myths of whiplash, and the science that deals with them, though there remains more work to be done to fully expose and dispense with these myths.

MYTH - WHIPLASH IS A SPINAL DISORDER
Definitions of whiplash in research publications tend to describe whiplash as a spinal disorder. This is a myth. Whiplash is much more than a spinal disorder. The biological, psychological and social anatomy of the syndrome has been better appreciated more recently. The Quebec Task Force on Whiplash-Associated Disorders (WADs) undertook an important project in redefining whiplash in 1995.¹ One of the most significant outcomes of that effort was the establishment of a grading system of whiplashassociated disorders, from Grade 0 to Grade IV. According to this grading system, Grade 0 designates no symptoms, while at the other end of the spectrum, Grade III designates neck pain or stiffness associated with neurological signs (i.e. a disc protrusion causing nerve root compression or spinal cord impingement) and Grade IV designates neck pain or stiffness associated with cervical fracture and/or dislocation.

Two further grades were designated Grade I and Grade II. These have importance as they represent more than 80% of “whiplash injury claims”.^2,3 Grade I WAD designates neck pain, stiffness or tenderness only, with no other physical signs, while Grade II WAD designates neck pain, stiffness or tenderness and signs including reduced range of motion and point tenderness.

The further importance of the Grade I and II WAD designations is that they capture the symptom constellation of headache, spinal pain, jaw pain, dizziness, limb pain or numbness, psychological and cognitive disturbance, and special somatosensory disturbances. Though this grading scheme has been criticised sine causa bona, the criticism has been rendered non gravis by subsequent studies demonstrating the substantial clinical utility of the grading scheme.^3-5

Still, the tendency to focus on injury and spinal disorder remains. Quite rightly, Winfield (1999) asks “Whiplash-Associated Disorder: WAD is it?”, as clinical experience teaches us that the whiplash patient’s illness behaviour is not representative of simply a neck injury, but is more like the behaviour expected with a systemic illness.6 Though this clinical impression may be familiar to many, there has been little in the way of population-based studies to document the health measures of this illness behaviour. There have been previous studies reporting the clinical syndrome, but these have suffered notably from small sample size, substantial selection bias, limited outcome measures, and a failure to control for compensation systems, therapy and collision parameters.^7-9

A recent study has overcome some of this deficiency of knowledge.¹⁰ In this study, individuals claiming for traffic injuries in Saskatchewan, Canada from July 1 1994 to December 31 1995 were recruited to complete instruments dealing with a wide array of symptoms, co-morbidities, and physical and mental functioning. Because of a legislative change introduced in January 1 1995, wherein the tort-compensation system was changed to a no-fault system, cohorts were examined from the last six-month period of the tort system, and for one year (two six-month periods) following the change to a no-fault system. From a total of 7462 claimants that met the criteria for whiplash injury, data reveal the symptom prevalence and quality of health measures to have an effect on health and illness behaviour in the acute stage (first six weeks) and chronic stage that is systemic, the syndrome extending itself well beyond merely spinal pain.

The Saskatchewan data show that every body region from head to toe is symptomatic in chronic whiplash patients, and by one month after their collision, they reveal numerous psychological abnormalities. These patients are anxious, distressed, and score highly on somatisation scales. “Whiplash”, in the clinical sense, is not an injury, but an illness with widespread symptom presentations. Beyond spinal pain, the Saskatchewan data show that symptoms such as dizziness, nausea, limb numbness, tinnitus and cognitive dysfunction are highly prevalent and of a chronic nature. Psychological distress is also common. Even if one assumes that the respondents to the questionnaire regarding CES-D (Centre for Epidemiological Studies --Depression Scale) and SF-36 (Short-Form 36 health survey) were biased towards those with worse symptoms, it still reveals that at least 50% of the claimants had at least this level of psychological symptom burden. This spectrum of psychological distress is not, however, likely to be unique to WAD. A recent study has shown that the Symptom-Checklist-90-Revised (SCL-90-R) profile of WAD patients, once thought to be unique to WAD, is no different than the SCL-90-R profile of other chronic musculoskeletal conditions.¹¹ Thus, a multiplicity of symptoms is common and many of the symptoms and psychological findings non-specific. This suggests that WAD reflects a more systemic illness behaviour, determined less by the aetiology of the injury, and more globally by an environment that encourages a recognisable illness behaviour which evolves regardless of the initial pathology.

The prevalence of the acute and chronic whiplash syndrome is similar regardless of the nature of the collision, and not particularly associated with rearend collisions. Direction of impact has no bearing on outcome either. Much is written and discussed on the isolated mechanisms of whiplash injury, yet the injury may be irrelevant compared with the illness. Clearly, for example, the collision victims in Saskatchewan under a tort system (pre-1995) had the same likelihood for a variety of injuries as those injured under the no-fault system (post-1994), but the outcomes were dramatically different in the two groups.¹⁰ Social factors may be more significant as predictors of outcome. This is not surprising. The nature of the acute injury is likely the least relevant factor in producing the illness behaviour that follows collisions, because we know it can occur elsewhere in the world without producing this illness behaviour.¹²

In North America and many European countries, this is a syndrome characterised by such an array of symptoms, and a disturbance of health quality, that it cannot conceivably be produced merely on the basis of the acute injury.

WAD thus represents a multi-faceted syndrome with an illness behaviour characterised by numerous physical, psychological, and social characteristics.^11-14 More research is needed to better appreciate the spectrum of illness behaviour involved so that treatment can be directed at the more systemic aspects rather than focusing on “healing a spinal injury”.

MYTH - CHRONIC WHIPLASH IS A UNIVERSAL PROBLEM
It used to be believed that wherever there were cars and collisions, there was acute whiplash injury, and that wherever there was acute whiplash injury a certain sizeable percentage of victims would develop chronic injury, irrespective of the geography and culture. This is now a myth. The landmark research in dispelling this myth arose from Lithuania. It is now more than five years since the publication of what is already recognised as a landmark and pivotal study, one which has irrevocably altered the perception of the medicolegal and social dilemma of whiplash. In 1996, Schrader et al (1996) described the first systematic and effective analysis of the outcome of the acute whiplash syndrome outside the medicolegal context.¹⁵

Lithuania is a country in which there is no or little awareness or experience among the general population of the notion that a whiplash injury may cause chronic pain and disability. Collision victims view this as a benign injury not requiring any medical attention. Possibilities for secondary gains are minimal. In the controlled historical inception cohort study published in 1996, none of the 202 subjects, involved in a rear-end car collision 1-3 years earlier, had persistent and disabling complaints that could conceivably be linked to the collision.¹⁵ There were no significant differences between the collision victims and controls concerning prevalence of symptoms including neck pain, headache, and subjective cognitive dysfunction. When this article was published, there was widespread criticism. In a later prospective controlled inception cohort study from the same group, 47% of 210 victims of rear-end car collisions, consecutively identified from the daily records of the traffic police, had initial pain.¹⁶ The symptoms disappeared in most cases after a few days. No subject reported collision-induced symptoms three weeks after injury. After one year, there were no significant differences between the collision victim group and the control group concerning frequency and intensity of both neck pain and headache. In the historical cohort study, 31 collision victims recalled having had acute or subacute neck pain.¹⁵ This symptom lasted in most cases less than a week and only two subjects had neck pain for more than one month. Due to recall problems, the true incidence of collision victims with acute symptoms such as neck pain and/or headache was unknown. According to the prospective study performed in a comparable inception cohort, the 95% confidence limits for the true incidence of acute symptoms are 40% and 54% giving an estimated minimum of altogether about 180 subjects with acute whiplash injury in both studies.¹⁶ As none of the collision victims seemed to have developed persistent and disabling symptoms due to the collision, the studies either evaluated alone or together have sufficient power to reject estimates of the incidence of the so-called chronic whiplash syndrome in previous, methodologically flawed studies and to question the validity of the condition as a chronic physical injury. Thus, this study shows that while the acute whiplash injury may be universal, chronic whiplash is dependent on the cultural background of the population studied.

The first Lithuanian study in 1996 was closely scrutinised and critics, such as Freeman et al (1999) conducted extensive power analyses, only to find that their power considerations were of no avail.¹⁴ The second Lithuania study was published in 1999, and since then there has been little criticism published. Merskey and Teasell (2000) published an extensive and critical assessment of the 1996 study, but ignored the 1999 study altogether.

The prospective 1999 Lithuania study identifies whiplash patients after a collision as well as they can be identified anywhere.¹⁶ A patient in Sweden, for example, who comes to a doctor after a collision and complains of neck pain is labelled a whiplash patient.¹⁹ If they lack neck tenderness or changes in range of motion, they can be labelled whiplashassociated disorder grade I. No physical evidence or proof is required for such a diagnosis. If a collision victim has various physical findings, though many of them remain subjective, they can be given a label of a different grade, though often the diagnosis still rests on the subjective symptoms and the willingness to associate these symptoms with a collision. The Lithuanian subjects identified by questionnaire in the period of days following a collision have every right to be labelled a “whiplash injury”, as any other collision victim. It is inaccurate to state that the prospective Lithuanian study failed in design, since any subject in that study who reported acute symptoms after a collision qualifies to be a whiplash patient in Lithuania, comparable with a collision victim in other countries.

There is equally compelling data from Germany and Greece indicating that the outcome of whiplash injury is culturallydependent.¹⁵ There is a need for more cross-cultural research, because of the questions and challenges brought forth by this data.

MYTH - MANY TREATMENTS WORK
There is a lot of money to be made in the “whiplash industry”. One of the most industrious of elements in the industry are the therapists. Therapists commonly portray the acute whiplash injury as an injury that needs help in healing; words like inflammation, tightness, trigger points, subluxation, etc. are loosely used by various therapists. Whiplash has the ideal ingredients to be a free-for-all in myth generation. The concept of evidencebased medicine is entirely foreign to some of those who prescribe the therapies. What they do not realise is that evidence-based medicine is important because we may otherwise expose patients to useless or dangerous treatments, waste limited resources, and may not apply treatments which are effective.

In 1995, the Quebec Task Force on WADs reviewed the studies on treatment of acute whiplash patients up until 1994.1 The conclusions from this review, and a similar review by Kjellman et al (1999) for the same time period (including foreign language studies), emphasise the paucity of good quality studies. From the available data, however, it is clear that therapy interventions which have an exercise component (active therapy) are superior to those which do not (i.e. those relying on passive therapy modalities such as ultrasound, manipulation, massage, heat, transcutaneous electrical nerve stimulation [TENS] and laser). Controlled studies have shown that electromagnetic therapy, traction, collars, TENS, ultrasound, spray and stretch, local corticosteroid injections, trigger point injections, and laser therapy are not efficacious.²¹ The Quebec Task Force found the effectiveness of manipulation/chiropractic therapy in acute neck pain to be equivocal, as study design either reflected significantly different baseline characteristics in cohorts, or some studies failed to find a therapeutic effect. 

Since 1994, there have been a few more studies of treatment of acute neck pain, summarised by Peeters et al (2001).²² They reported an analysis of studies before and after 1995, specifically requiring that the studies be randomised, controlled trials (patients are randomised into one of two groups) and that the WAD grade be I or II. The need for evidence-based guidelines for patients with whiplash injury was the rationale for this systematic review. The primary question was what types of conservative treatments would be effective in patients with whiplash injury rated WAD I or II regarding pain, global perceived effect, and participation in daily activities. The methodologic guidelines of the Cochrane Back Review Group were followed. The authors concluded that: “Available knowledge indicates beneficial long-term effect of active treatments on at least one of the primary outcome measures: pain, global perceived effect, and participation in daily activities. A cautious conclusion may be drawn that ‘rest makes rusty’...Practitioners should encourage patients to return to their usual activities.”²¹

One of the most impressive studies in acute whiplash patients was that of Borchgrevink et al (1998) in Norway, where they compared the therapeutic advice to “act-as-usual”, to not having that advice, in a randomised group of 241 neck pain patients whose onset of pain was within 24 hours of a motor vehicle collision, and who had no signs or radiological findings to suggest neurological injury or fracture.²³

All patients received instructions for self-training of the neck and a five-day prescription for a non-steroidal antiinflammatory drug. One group was instructed to act as usual and received no sick leave or collar. Patients in the immobilisation group received 14 days of sick leave and a soft collar. At six months after the collision, the “act as usual” group had a better outcome in several variables including pain, concentration and memory. The study is impressive because the difference between the two groups was simply advice with no sick leave and no collar, versus both sick leave and a collar.

Still, one often encounters the notion that lack of evidence is not evidence of a lack of effect of a given therapy, but nor is it a licence to practice any given therapy. More studies are needed to define why exercise therapy is better, whether it is the exercise itself or the activity that in general keeps the patient at normal activities that works. Or is it that passive therapies are actually harmful in some way?

CONCLUSION
It seems that as much or more scientific effort has been devoted to dispelling the myths of whiplash than has been undertaken to validate the concept that chronic whiplash is the result of a “chronic injury”. The chronic whiplash syndrome did not arise in the usual fashion of most classified illnesses, wherein a group of patients present with some definable pathology and then a causative agent is examined for in a series of epidemiological, pathoanatomical and diagnostic studies. The lack of an easily identifiable cause for chronic whiplash is not in itself the reason for the failure of a more appropriate scientific process to unfold in the whiplash era. If one considers multiple sclerosis, for example, the pathological lesions and pathophysiological events identifiable objectively in a clinical setting were identified in patients first, and then studies have led to a definable (by criteria) disease we now call multiple sclerosis. Yet, we do not know the cause of multiple sclerosis. That is not a barrier to identifying lesions or pathological findings on examination. With whiplash, on the other hand, we have a systemic illness picture, and nothing upon which to hang that picture. Given that it is now 75 years since Crowe first stated a need to understand the cause of this malady, and that we have not yet achieved that goal, we must consider that we may be looking at the problem backwards.¹ The irony is that we need to spend less time studying and discussing chronic whiplash where it exists in epidemic proportions, and rather we should conduct our investigations and considerations in countries where it does not.

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Copyright: 7 March 2003