evidence base for clinical practice

Michele Sterling | Justin Kenardy

WHIPLASH

ISBN 978-0-7295-3946-3

9

780729 539463feedback@elsevier.com.au

Whiplash is one of the most debated and controversial musculoskeletal conditions. This is, in part, due to the often compensable nature of the injury and the fact that a precise pathoanatomical diagnosis is not usually achievable.

Whiplash: Evidence base for clinical practice presents the evidence underpinning the complexity of whiplash associated disorders (WADs), from the specifics of current physiological and psychological manifestations of the condition to broader issues such as compensation and litigation.

This new text will be essential reading for physiotherapy, chiropractic, osteopathy, occupational therapy and health psychology practitioners and postgraduate students, as well as practitioners in rehabilitation therapies and primary care.

Features• discrete chapters on litigation, and the role of compensation • case studies on acute and chronic whiplash conditions• covers the spectrum of the current evidence base for whiplash • includes perspectives from a wide range of disciplines

All professions involved in the management of patients with whiplash, from clinicians to policy makers will find this an invaluable resource.

About the authorsMichele Sterling PhD, MPhty, BPhty, Grad Dip Manip Physio, FACP Associate Professor, Schools of Medicine and Health and Rehabilitation Science; Chief Investigator, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health; Associate Director, Centre of National Research on Disability and Rehabilitation Medicine, University of Queensland, Brisbane, Australia

Justin Kenardy PhD, BSc(Hons), FAPSProfessor, Schools of Psychology and Medicine; Deputy Director, Centre of National Research on Disability and Rehabilitation Medicine; Chief Investigator, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, University of Queensland, Brisbane, Australia

WHIPLASHevidence base for clinical practice

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: Evidence base for clinical practiceSterling | Kenardy

v

Foreword vii

Contributor list ix

Reviewer list xi

Acknowledgments xi

Introduction xiiiMichele Sterling, Justin Kenardy

Chapter 1 Epidemiology of whiplash associated disorders 1Lena HolmDefi nitions 1Cumulative incidence of and risk factors

for WAD 1Course and prognosis of WAD after a motor

vehicle crash 2An epidemiological approach to aetiology 4The economic burden of WAD 5Summary 5

Chapter 2 Clinical presentation of whiplash associated disorders 9Michele SterlingPatterns of recovery 9Physical and psychological characteristics 10Classifi cation systems for WAD 11Conclusions 12

Chapter 3 Mechanism of injury 16Brian D. Stemper, Narayan Yoganandan,

Frank A. Pintar, Dennis J. MaimanHead–neck kinematics: global and

segmental 16Injury theories 16Injury metrics 20Infl uencing factors for injury potential 22Summary 24

Chapter 4 The evidence for pathoanatomical lesions 29James ElliottIntroduction 29Pathomechanics of whiplash injury 29Pathological lesions in whiplash injury 30Conclusion 35

Chapter 5 Pain-processing mechanisms in whiplash associated disorders 40Michele Curatolo, Michele SterlingIntroduction 40Mechanisms for post-injury central

hyperexcitability 40Evidence for central hyperexcitability

in chronic WAD 41Evidence for central hyperexcitability in acute

WAD and in the transition to chronicity 42Relationships between sensory hypersensitivity

and psychological distress 44Implications for clinical management

of whiplash 45Conclusion 47

Chapter 6 Neuromuscular dysfunction in whiplash associated disorders 52Deborah Falla, James Elliott, Gwendolen JullChanges in the properties of the cervical

muscles 52Altered neuromuscular control in WAD 54Implications for the management of the patient

with whiplash 60Conclusion 63

Chapter 7 Dizziness, visual and sensorimotor control disturbances following whiplash injury 69Julia TreleavenAetiology of dizziness, visual disturbances and

sensorimotor control disturbances in whiplash associated disorders 69

Signs and symptoms of sensorimotor disturbance following a whiplash injury 76

Implications for assessment 78Implications for management 78Conclusion 79

Chapter 8 Psychological aspects of whiplash associated disorders 85Jan Buitenhuis, Peter de Jong, Jan Jaspers,

Justin KenardyAccident-related psychological factors 85Coping 87Catastrophising and kinesiophobia 87

Contents

vi Contents

Attributions, beliefs and expectations 88Conclusion 89

Chapter 9 Potential role of stress systems in the pathogenesis of whiplash associated disorders 93Samuel McLeanSympathetic nervous system 93Neuropeptide Y 95Serotonin 96Clinical implications 96Current research needs and future research

directions 96

Chapter 10 Prognostic indicators of non-recovery following whiplash injury 101Michele SterlingPrognostic factors for non-recovery 101Prediction of outcomes other than pain and

disability 104Clinical implications 104Conclusion 105

Chapter 11 Primary care management of acute whiplash injury 108Michele Sterling, Justin KenardyCurrent evidence for the management of acute

WAD 108The provision of advice and education 109Is pain control important? 110Physical characteristics of acute WAD

and implications for management 110Psychological characteristics of acute

WAD and implications for management 113Early multidisciplinary management 115Summary 116

Chapter 12 Evidence-based management of chronic whiplash associated disorders 120Trudy RebbeckEvidence base for management of chronic

whiplash 120Evidence for physical interventions 120Evidence for psychological interventions 127Evidence for medical interventions 128Implementation of evidence in clinical

practice 129Summary 132

Chapter 13 Psychological management of chronic whiplash associated disorders 135Jan Jaspers, Jan Buitenhuis, Gerbrig Versteegen,

Peter de JongTheory-derived psychological interventions 135

Evidence-based practice 138Remaining issues and future prospects 141Conclusion 142

Chapter 14 Compensation and health outcomes 144Luke B. Connelly, Natalie SpearingIntroduction 144Compensation and related concepts 145Compensation: empirical considerations 147Health: the concept and its measurement 150Conclusions 153

Chapter 15 Whiplash and the law 157Ian Freckelton, S.C.The test for compensability 157Canadian Transport Accident Compensation 161Conclusions 166

Chapter 16 Malingering and symptom magnifi cation in whiplash associated disorders 168Brian McGuireWhy study malingering in the area

of whiplash? 168What is meant by ‘malingering’? 169Approaches to detection of malingering 170Differential diagnosis of psychological

disorders where symptom production or magnifi cation is a feature 171

Empirical studies of malingering and symptom magnifi cation in pain 172

A decision-making template for possible and probable malingering 175

Chapter 17 Case descriptions 180Michele Sterling, Trudy Rebbeck, Justin KenardyCase description 1: acute whiplash 180Case description 2: acute whiplash 181Summary of cases 1 and 2 183Case description 3: chronic whiplash 183Conclusion 185

Chapter 18 Future directions 187Michele Sterling, Justin KenardyIntervention trials 187Do some patients have a pre-existing risk

of developing chronic pain after whiplash injury? 188

Improving prognostic models 188Identifi cation of a peripheral lesion 189Conclusion 189

Index 193

1

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 defi ne the actual symptoms after such an event. The fi rst 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 expe-rience cervical pain. 3 – 5 After such events, however, it is less common that the injury is labelled ‘whip-lash’, 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 pub-lished the fi rst systematic review on whiplash inju-ries. 6 The term was intended to refl ect that whiplash is an injury mechanism, and the consequences of the mechanism were the spectrum of symptoms (disor-ders). The QTF formulated the following conceptual defi nition:

Whiplash is an acceleration-deceleration mecha-nism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle colli-sions, but can also occur during diving or other mis-haps. 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 defi nition 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 classifi cation of WAD into fi ve categories based on clinical signs and symp-toms (see Chapter 2). This classifi cation is mostly used to classify WAD in the acute phase.

Since the publication of the QTF fi ndings, the term WAD has been increasingly used in the medical lit-erature, and it is also a frequently used term in insur-ance 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 begin-ning 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 administra-tive 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,

CHAPTER 1 Epidemiology of whiplash associated disorders

Lena Holm

2

WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICE

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 substan-tially 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 benefi ts 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 signifi -cant 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 diffi culty in obtaining accurate and appro-priate denominators to calculate risks. Rather than using persons exposed to collisions as the denomina-tor, researchers have used proxies, such as registered licensed drivers, 6 population censuses, 13, 14 or per-sons involved in collisions where at least one person was injured. 9 Some studies have adjusted for possible confounding factors, while others have not. A con-founding 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 stud-ies include presence of neck pain prior to the colli-sion, 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’ denom-inators 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 differ-ent crash types. Car occupant acceleration, velocity and rebound are all factors that should be consid-ered. 17 In much of the research, a major focus is on rear-end injury mechanisms despite consistent fi nd-ings 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 fi rm conclusions about the magnitude of such preventive interventions can be drawn, larger studies with well-defi ned 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 stud-ies 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 coun-tries report that 2% or less of study participants report long-lasting symptoms after car collisions. 15, 27 How-ever, drawing fi rm conclusions based on the fi ndings of these studies is inappropriate, since ‘psycho-cultural’ factors were not studied per se. Neverthe-less, 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

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1 Epidemiology of whiplash associated disorders

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% recov-ery rate at one year after the injury, 31, 32 whereas oth-ers 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 con-tacted at follow-up. 33

Prognostic factors A prognostic factor is a factor that is independently associated with the prognosis, and which can con-tribute 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 persis-tent neck pain. These factors include, among others, passive coping strategies, poor mental health, high level of stress, high pain intensity and more ‘asso-ciated’ 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 sug-gests that the observed poor prognosis in females in some studies might be explained in terms of the psy-chosocial factors rather than the biological factors of gender. Furthermore, societal factors, such as insur-ance 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, aware-ness of collision, head position) are not associated with the prognosis. 41

There is evidence that people’s lowered expecta-tions 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 defi ned 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 behav-iours required to achieve that outcome (self-effi cacy

expectations). 47 It is believed to be infl uenced by personal and psychological features, such as anxi-ety, self-effi cacy, 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 primar-ily learned from the cultural environment, and based on ‘prior knowledge’. The mechanism by which expectations infl uence emotional and physical reac-tions 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 expecta-tions about bad health actually lead to bad health. A concept that is closely related to expectations is a per-son’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 hap-pened to their neck had greater perceived disability during follow-up compared to those who did not have such beliefs. 51

WAD and widespread pain One important aspect about the course of recovery from WAD is whether the neck injury is a trigger for subsequent widespread body pain. This has been suggested from cross-sectional studies, but knowing whether widespread pain came before the neck injury remains unclear from this type of study design. 52, 53 A potential aetiological explanation is a neurophysi-ological disturbance in the peripheral and central nervous system, which, in some instances, leads to an increased sensitivity to pain in other ‘uninjured’ areas. 54, 55 Another possible explanation for wide-spread pain is that new tissue damage may result from an altered pattern of movement in the body due to the neck pain. The exact aetiology of wide-spread pain is probably complex and multifactorial, but there are no indications that it would be specifi c to WAD. It can also occur after surgical intervention or any tissue damage. 54 In addition, large prospective studies on pain of other aetiology have demonstrated that psychosocial factors at work, repetitive strains or other physical strains at work, awareness of symp-toms and illness behaviour may increase the risk of development of widespread pain. 56 – 58 Thus, it seems that biological as well as psychological and social

4

WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICE

factors contribute to the development of widespread pain.

Prospective studies on WAD and its association with widespread pain are sparse and the evidence is not clear. The results from one study suggest a relationship between the onset of neck pain or other associated symptoms as well as self-perceived injury severity, after an MVC, and subsequent widespread pain. 59 However, age, gender, health behaviour and somatic symptoms prior to collision were at least as important. Another study investigated the incidence of onset of more extensive pain during 12 months follow-up of WAD claimants, and associated factors with such an outcome. 60 In that study, a less conser-vative defi nition of widespread pain was used and would probably have resulted in a higher incidence. The main conclusions were that widespread pain was common over a 12-month period (21%), but most improved over the follow-up period. Female gen-der, poor prior health, greater initial symptomatol-ogy (including pain intensity) and more depressive symptoms were associated with the development of extensive pain. The authors also found that local neck/spinal pain was rare after a traffi c collision—only 11% of eligible WAD claimants had local neck/back pain, raising the question of the potential cause of widespread pain in other studies.

Work absenteeism and work disability Many persons with acute WAD also have some absence from work, and no clear difference occurs between ‘blue’ and ‘white’ collar workers. In one population-based study, 46% of persons had been off work due to the injury. 8 A similar fi gure (49%) was seen in a Dutch study. 61 The majority of people returned to work within a few days and only 4 – 9% were reported to be off work at six months post injury. 32, 62 In a study from the Netherlands, factors associated with not returning to work were older age and concentration problems. 63 There was no asso-ciation between degree of manual labour (‘blue’ or ‘white’ collar work) or education level and not return-ing to work.

AN EPIDEMIOLOGICAL APPROACH TO AETIOLOGY In epidemiology, one of the aims is to assess the independent association between a potential risk or prognostic factor. It is, however, extremely important to keep in mind that in most diseases and injuries, a multifactorial causal model is needed to understand the onset and prognosis.

This can effectively be discussed using the ‘pie’ model, or the component cause model, introduced to epidemiologists by Rothman. 64 In Figure 1.1 , some prognostic factors that may be involved in recovery from WAD are introduced in two different ‘pie’ models.

According to the ‘pie’ model, all contributing causes in one of the suffi cient causes , or ‘pie’, are needed, in order to recover from WAD. Each suf-fi cient cause represents one of presumably several alternative routes leading to recovery. The interac-tions between contributing causes are illustrated as separate ‘pie slices’ included in the same ‘pie’. Slices in one ‘pie’ are said to interact, because it is their joint action that leads to recovery. The six outlined exam-ples given in Figure 1.1 represent both ‘biological’, ‘psychological’ and ‘social’ factors. The other B’s, P’s and S in the fi gure represent other factors that are important for the prognosis. In real life, of course, dif-ferent distributions of biological, psychological and social factors occur among different people.

In the literature, there is no recognised single contributing cause that is considered necessary for recovery from WAD. Neither has any suffi cient cause been identifi ed. Instead, several contributing causes (i.e. factors that affect the causes for recovery) have been found. When linking this ‘pie’ model to the evi-dence of prognostic factors in WAD, numerous sets of possible ‘individual pies’ become obvious. In sum-mary, several different suffi cient causes for recovery from WAD exist; in other words, several alternative routes lead to recovery.

In research, the effect of individual contributing causes , or risk factors, are usually investigated for the condition in question. Complete suffi cient causes usually do not lend themselves to studies because few of these scenarios actually exist (exceptions include bacterial infection). Still, it is important to keep the ‘pie’ model in mind when interpreting and discuss-ing empirical results on risk and prognosis. A single contributing cause may otherwise be confused for a suffi cient cause . The whole picture of specifi c sets of suffi cient causes is seldom discussed in the research of WAD or in other contexts.

The causal process is more complicated than explained by the ‘pie’ model, since effects are likely to depend on other factors that happen simultane-ously. For instance, some persons in pain may call for support from family members or workmates, which in turn may change the person’s future pain percep-tion and behaviour (positively or negatively). In other instances, pain intensity may cause depressed mood, or depressed mood may cause more pain (bidirec-tional). Nevertheless, this component cause model is

5

1 Epidemiology of whiplash associated disorders

a fruitful way to conceptualise WAD as it visualises the multifactorial nature of WAD and how biological, psychological and social factors may interact.

THE ECONOMIC BURDEN OF WAD Little is known about the individual and societal eco-nomic burden of WAD. For instance, little is known about the prevalence of long-lasting work disability due to WAD, which is probably the most costly part. This burden is probably largely dependent on the legislation in different countries. In 2002, an inde-pendent and temporary Commission on Whiplash-Related Injuries was formed in Sweden, initiated by the four largest motor vehicle insurers. The mandate of the 3-year Commission was an examination of the problems of WAD from road safety, medical care, insurance and societal aspects. 65 One of the conclu-sions of the fi nal report was that the yearly cost for society and for the insurance industry was approxi-mately SEK 1.5 billion (US$201 million), while pro-jected costs (i.e. what new cases of WAD arising in a particular year will cost society and insurers by the

time the person reaches retirement age) amounted to SEK 4.6 billion (US$648 million). These calculations were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002. Since the report’s publication, the number of WAD cases have decreased dramatically to about 16,000 claims in 2008 (173 per 100,000 inhabitants), which, of course, has an impact on the overall costs.

Comparable data has not been found, but there is some evidence from a study that addressed the incidence of WAD in 10 European countries. 66 The administrative data suggest that the total claims cost in Switzerland was 500 million Swiss francs (US$467 million). Switzerland’s population is 80% that of Sweden. Expenditures in addition to the claims cost was not reported in that study.

SUMMARY In summary, as in almost all other diseases and inju-ries, factors that are involved in the risk or prognosis of WAD are multifactorial and constitute a web of biological, psychological and social components.

Highrecovery

expectations

Minorneurophysiological

disturbance

Absence ofdepressive

mood

Lowfinancial

incentivesSufficient

socialsupport

S

PP

B

B

Minor tissuedamage

One sufficient cause One sufficient cause

One contributing cause

B = Biological, P = Psychological, S = Social Figure 1.1 The ‘pie’ model—examples of factors related to recovery from WAD.

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WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICE

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