Chapter 1 Epidemiology of whiplash associated disorders

Definitions

The term whiplash injury has been used since the late 1920s, when H. E. Crowe coined the term at a medical meeting in San Francisco.¹ It was originally described as an injury mechanism to the neck, but was later also used to define the actual symptoms after such an event. The first known case report was published in the Journal of the American Medical Association in 1953, when Gay and Abbot described 50 patients who had been exposed to whiplash mechanism in car collisions.² It was reported that the majority had been exposed to rear-end collisions and that the majority were also examined between one and 24 months after the collision, thus representing a mix of patients with acute or persistent symptoms. Cervical pain with radiation into the occipital region of the skull, shoulder girdle or upper extremities were reported as common symptoms, but irritability, poor concentration and subjective vertigo were also described.

People who are exposed to energy transfer to the neck, in sports, falls or other mishaps, may also experience cervical pain.³^–⁵ After such events, however, it is less common that the injury is labelled ‘whiplash’, but instead other terms, such as neck strain, neck sprain or simply neck injury, are used. The term whiplash associated disorder (WAD) was introduced in 1995 by the Quebec Task Force (QTF), who published the first systematic review on whiplash injuries.⁶ The term was intended to reflect that whiplash is an injury mechanism, and the consequences of the mechanism were the spectrum of symptoms (disorders). The QTF formulated the following conceptual definition:

Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during diving or other mishaps. The impact may result in bony or soft-tissue injuries (whiplash injury) which in turn may lead to a variety of clinical manifestations (whiplash-associated disorders).⁶

The reason for excluding frontal collisions from the definition is not discussed in the report and is likely to be an error, since it is known that 25–30% of whiplash injury occurs in such impact direction.⁷^–⁹

The QTF also suggested a classification of WAD into five categories based on clinical signs and symptoms (see Chapter 2). This classification is mostly used to classify WAD in the acute phase.

Since the publication of the QTF findings, the term WAD has been increasingly used in the medical literature, and it is also a frequently used term in insurance medicine.

Cumulative incidence of and risk factors for WAD

Cumulative incidence

The cumulative incidence is the number of new cases of an event or outcome occurring in a population over a certain time period. Some evidence from the literature indicates that the incidence of WAD differs between countries. There is also some evidence that the incidence of WAD has increased from the beginning of the 1990s to after the year 2000, with the annual incidence for the latter period being about 300 per 100,000 inhabitants in studies where emergency setting visits are used. In some instances, the increase is between three and tenfold.¹⁰^–¹² It is not known if this increase is partly due to a change in care-seeking behaviour.

There are also some indications from administrative insurance claims databases in different European countries (e.g. Norway, the Netherlands and Sweden) of a reduction in the number of WAD claims, whereas such decreases have not been seen in Denmark or the United Kingdom. Sweden, for instance, has seen a 33% decrease in personal motor vehicle crash (MVC) injury claims between 2002 and 2008. The relative decrease is similar between the incidence of WAD and other types of injuries, with WAD constituting about 50% of all MVC injury claims. This decrease is not due to a reduction in the number of MVCs, and nor has the insurance system in Sweden changed. Instead, this decrease is likely to be due to a combination of reasons. For example, some car manufacturers have developed whiplash-protection devices for new car models, which presumably will result in fewer cases of WAD as a result of rear-end collisions. Secondly, during the second half of the 1990s, police personnel in Sweden showed an increased awareness that there is no need to advise car occupants to seek healthcare if no symptoms are present. Thirdly, the mass media focus in Sweden on whiplash has decreased substantially from over 800 articles in the beginning of the 2000s to only about 200 articles in 2008.

Incidence calculation through insurance claims may be prone to other forms of bias. For instance, insurance systems where there are no benefits for the person responsible for a collision may underestimate the frequency of injuries, since fewer claims would be reported. This would also happen with insurance systems where insurance claim access is limited, or where payments for compensation result in a significant increase in the insurance premium. On the other hand, healthcare data may also be prone to bias, since such data only captures those who seek the type of healthcare utilisation in question (e.g. emergency care).

Risk factors for onset of WAD

A risk factor for an outcome (i.e. disease/injury) is a factor that is independently associated with the outcome or condition in question. Knowledge of the aetiology (cause) of WAD is limited. One reason for this is the difficulty in obtaining accurate and appropriate denominators to calculate risks. Rather than using persons exposed to collisions as the denominator, researchers have used proxies, such as registered licensed drivers,⁶ population censuses,^13,¹⁴ or persons involved in collisions where at least one person was injured.⁹ Some studies have adjusted for possible confounding factors, while others have not. A confounding factor is an independent risk factor for the outcome and is also associated with the exposure/risk factor of interest. Examples of possible confounding factors include gender, age, pre-collision physical and mental health, and severity and direction of crash impact.

Risk factors for WAD reported in published studies include presence of neck pain prior to the collision,^15,¹⁶ being the driver or the front-seat passenger (compared to rear-seat passenger), and being exposed to a rear-end collision or frontal collision rather than a side collision.⁹ Female gender has been suggested to be associated with a slightly higher incidence of WAD in some studies,^9, ^{6, 13} but other studies have found no gender differences.^11,¹⁴ All these studies have weaknesses, primarily, the lack of ‘true’ denominators and/or the limited possibility to control for potential confounding factors.

One possible risk factor for WAD is the severity of the crash (impact). The biomechanical research on WAD is mainly based on experimental studies using cadavers, volunteers and simulation experiments. So far, the injury mechanism has not been established as a known risk factor. Reasons for this may be that there are different injury mechanisms occurring with different crash types. Car occupant acceleration, velocity and rebound are all factors that should be considered.¹⁷ In much of the research, a major focus is on rear-end injury mechanisms despite consistent findings that rear-end collisions are only responsible for 40–55% of all cases of WAD in MVCs.^8,¹⁸ However, there are some promising results from actual rear-end collisions in that the redesign of headrests and seats so that head/neck extension is limited in rear-end collisions has reduced the incidence of WAD.^19,²⁰ Before firm conclusions about the magnitude of such preventive interventions can be drawn, larger studies with well-defined outcome measures and controls for potential confounding factors are needed.

Course and prognosis of WAD after a motor vehicle crash

Course of recovery

Understanding the course and prognosis in WAD is critical. Will people recover from this common injury? If so, when? If the injury is transient and self-limiting, there would be no need for major prevention and intervention strategies. The natural course and prognosis of WAD has been a controversial matter. Some claim that the prognosis is solely determined by the physical injury and its severity, and that pre- and post-psychosocial factors are not relevant in recovery.²¹^–²³ Others claim that persistent WAD is mainly a ‘psycho-cultural’ illness, and refer to studies from Lithuania and Greece where there is no or little awareness or reporting of WAD resulting from a whiplash mechanism.²⁴^–²⁶ Studies from these countries report that 2% or less of study participants report long-lasting symptoms after car collisions.^15,²⁷ However, drawing firm conclusions based on the findings of these studies is inappropriate, since ‘psycho-cultural’ factors were not studied per se. Nevertheless, when persons who do not experience neck pain following a car collision have been asked to report on which symptoms they would expect after neck injury or minor head injury, those from Lithuania and Greece do not expect to have as many symptoms or do not have as long-lasting symptoms compared to persons in Canada.²⁸^–³⁰

In the majority of studies, the recovery rate is substantially lower than recovery rates reported in Greece and Lithuania. Some report a 66–68% recovery rate at one year after the injury,^31,³² whereas others report a less than 40% recovery rate at a similar time point.^33,³⁴ Differences in recovery rates are at least partially due to selection bias. For instance, in the study by Miettinen et al., only 58% of the invited study population was followed up 12 months post injury, so it was unknown what the recovery rate was for the 42% of participants who could not be contacted at follow-up.³³

Prognostic factors

A prognostic factor is a factor that is independently associated with the prognosis, and which can contribute to or work against recovery from a condition. Some factors known to contribute to a poor prognosis in WAD are similar to those for other forms of persistent neck pain. These factors include, among others, passive coping strategies, poor mental health, high level of stress, high pain intensity and more ‘associated’ symptoms, such as arm pain, headache and nausea.³⁵^–⁴⁰ Similar to the literature on neck pain in the general population, gender does not seem to be a clear prognostic factor in WAD, after adjustments have been made for psychosocial factors.⁴¹ This suggests that the observed poor prognosis in females in some studies might be explained in terms of the psychosocial factors rather than the biological factors of gender. Furthermore, societal factors, such as insurance systems with possibilities to claim for pain and suffering,³⁷ and extensive healthcare utilisation in the early stage of the injury,⁴² have been suggested to be associated with delayed recovery in WAD.

Surprisingly, the bulk of evidence suggests that crash-related factors (e.g. impact direction, awareness of collision, head position) are not associated with the prognosis.⁴¹

There is evidence that people’s lowered expectations of recovery and return to work, assessed early in the process of recovery, are an important predictor for long-lasting WAD, even after controlling for other factors, such as prior health, pain intensity, pain areas and acute post-traumatic stress symptoms.⁴³^–⁴⁵ An expectation is defined as a degree of belief that some event will occur,⁴⁶ and is also explained by some as being tied to an outcome, such as a recovery state or return to work, rather than the individual behaviours required to achieve that outcome (self-efficacy expectations).⁴⁷ It is believed to be influenced by personal and psychological features, such as anxiety, self-efficacy, coping abilities and fear, and recent studies have demonstrated that in those with WAD, initial pain, depressive symptomatology, and some crash and demographic factors were associated with recovery and return-to-work expectation.⁴⁸

Health expectations are postulated to be primarily learned from the cultural environment, and based on ‘prior knowledge’. The mechanism by which expectations influence emotional and physical reactions may also actually affect the autonomic nervous system, involving biochemical processes, which may explain some of the power observed in studies of the placebo and nocebo effect.^49,⁵⁰ These mechanisms help to explain why persons who strongly anticipate they will recover really do, and why strong expectations about bad health actually lead to bad health. A concept that is closely related to expectations is a person’s belief—the lens through which a person views the world—which is shaped by the environment. In a study where injured persons were asked about their belief of the origin of their neck pain (causal belief), those who believed that something serious had happened to their neck had greater perceived disability during follow-up compared to those who did not have such beliefs.⁵¹

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