WHIPLASH. evidence base for clinical practice. Michele Sterling Justin Kenardy

Transcription

1 WHIPLASH evidence base for clinical practice Michele Sterling Justin Kenardy

2 Contents Foreword vii Contributor list ix Reviewer list xi Acknowledgments xi Introduction xiii Michele Sterling, Justin Kenardy Chapter 1 Epidemiology of whiplash associated disorders 1 Lena Holm Definitions 1 Cumulative incidence of and risk factors for WAD 1 Course and prognosis of WAD after a motor vehicle crash 2 An epidemiological approach to aetiology 4 The economic burden of WAD 5 Summary 5 Chapter 2 Clinical presentation of whiplash associated disorders 9 Michele Sterling Patterns of recovery 9 Physical and psychological characteristics 10 Classification systems for WAD 11 Conclusions 12 Chapter 3 Mechanism of injury 16 Brian D. Stemper, Narayan Yoganandan, Frank A. Pintar, Dennis J. Maiman Head neck kinematics: global and segmental 16 Injury theories 16 Injury metrics 20 Influencing factors for injury potential 22 Summary 24 Chapter 4 The evidence for pathoanatomical lesions 29 James Elliott Introduction 29 Pathomechanics of whiplash injury 29 Pathological lesions in whiplash injury 30 Conclusion 35 Chapter 5 Pain-processing mechanisms in whiplash associated disorders 40 Michele Curatolo, Michele Sterling Introduction 40 Mechanisms for post-injury central hyperexcitability 40 Evidence for central hyperexcitability in chronic WAD 41 Evidence for central hyperexcitability in acute WAD and in the transition to chronicity 42 Relationships between sensory hypersensitivity and psychological distress 44 Implications for clinical management of whiplash 45 Conclusion 47 Chapter 6 Neuromuscular dysfunction in whiplash associated disorders 52 Deborah Falla, James Elliott, Gwendolen Jull Changes in the properties of the cervical muscles 52 Altered neuromuscular control in WAD 54 Implications for the management of the patient with whiplash 60 Conclusion 63 Chapter 7 Dizziness, visual and sensorimotor control disturbances following whiplash injury 69 Julia Treleaven Aetiology 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 78 Implications for management 78 Conclusion 79 Chapter 8 Psychological aspects of whiplash associated disorders 85 Jan Buitenhuis, Peter de Jong, Jan Jaspers, Justin Kenardy Accident-related psychological factors 85 Coping 87 Catastrophising and kinesiophobia 87 v

3 vi Contents Attributions, beliefs and expectations 88 Conclusion 89 Chapter 9 Potential role of stress systems in the pathogenesis of whiplash associated disorders 93 Samuel McLean Sympathetic nervous system 93 Neuropeptide Y 95 Serotonin 96 Clinical implications 96 Current research needs and future research directions 96 Chapter 10 Prognostic indicators of non-recovery following whiplash injury 101 Michele Sterling Prognostic factors for non-recovery 101 Prediction of outcomes other than pain and disability 104 Clinical implications 104 Conclusion 105 Chapter 11 Primary care management of acute whiplash injury 108 Michele Sterling, Justin Kenardy Current evidence for the management of acute WAD 108 The provision of advice and education 109 Is pain control important? 110 Physical characteristics of acute WAD and implications for management 110 Psychological characteristics of acute WAD and implications for management 113 Early multidisciplinary management 115 Summary 116 Chapter 12 Evidence-based management of chronic whiplash associated disorders 120 Trudy Rebbeck Evidence base for management of chronic whiplash 120 Evidence for physical interventions 120 Evidence for psychological interventions 127 Evidence for medical interventions 128 Implementation of evidence in clinical practice 129 Summary 132 Chapter 13 Psychological management of chronic whiplash associated disorders 135 Jan Jaspers, Jan Buitenhuis, Gerbrig Versteegen, Peter de Jong Theory-derived psychological interventions 135 Evidence-based practice 138 Remaining issues and future prospects 141 Conclusion 142 Chapter 14 Compensation and health outcomes 144 Luke B. Connelly, Natalie Spearing Introduction 144 Compensation and related concepts 145 Compensation: empirical considerations 147 Health: the concept and its measurement 150 Conclusions 153 Chapter 15 Whiplash and the law 157 Ian Freckelton, S.C. The test for compensability 157 Canadian Transport Accident Compensation 161 Conclusions 166 Chapter 16 Malingering and symptom magnification in whiplash associated disorders 168 Brian McGuire Why study malingering in the area of whiplash? 168 What is meant by malingering? 169 Approaches to detection of malingering 170 Differential diagnosis of psychological disorders where symptom production or magnification is a feature 171 Empirical studies of malingering and symptom magnification in pain 172 A decision-making template for possible and probable malingering 175 Chapter 17 Case descriptions 180 Michele Sterling, Trudy Rebbeck, Justin Kenardy Case description 1: acute whiplash 180 Case description 2: acute whiplash 181 Summary of cases 1 and Case description 3: chronic whiplash 183 Conclusion 185 Chapter 18 Future directions 187 Michele Sterling, Justin Kenardy Intervention trials 187 Do some patients have a pre-existing risk of developing chronic pain after whiplash injury? 188 Improving prognostic models 188 Identification of a peripheral lesion 189 Conclusion 189 Index 193

4 CHAPTER 1 Epidemiology of whiplash associated disorders Lena Holm 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 (whiplashassociated 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 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 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, 1

5 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 substantially from over 800 articles in the beginning of the 2000s to only about 200 articles in 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 selflimiting, 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 preand post-psychosocial factors are not relevant in recovery 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 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 psychocultural 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 2

6 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 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 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 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 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 neurophysiological 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 widespread 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 widespread pain is probably complex and multifactorial, but there are no indications that it would be specific 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 symptoms and illness behaviour may increase the risk of development of widespread pain Thus, it seems that biological as well as psychological and social 3

7 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 conservative definition 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 gender, poor prior health, greater initial symptomatology (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 traffic 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 figure (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 association between degree of manual labour ( blue or white collar work) or education level and not returning 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 suffi cient cause represents one of presumably several alternative routes leading to recovery. The interactions 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 examples given in Figure 1.1 represent both biological, psychological and social factors. The other B s, P s and S in the figure represent other factors that are important for the prognosis. In real life, of course, different 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 identified. Instead, several contributing causes (i.e. factors that affect the causes for recovery) have been found. When linking this pie model to the evidence of prognostic factors in WAD, numerous sets of possible individual pies become obvious. In summary, 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 discussing empirical results on risk and prognosis. A single contributing cause may otherwise be confused for a suffi cient cause. The whole picture of specific 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 simultaneously. 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 perception and behaviour (positively or negatively). In other instances, pain intensity may cause depressed mood, or depressed mood may cause more pain (bidirectional). Nevertheless, this component cause model is 4

8 1 Epidemiology of whiplash associated disorders One contributing cause High recovery expectations Minor neurophysiological disturbance Minor tissue damage P P Absence of depressive mood S Sufficient social support B B Low financial incentives One sufficient cause One sufficient cause B = Biological, P = Psychological, S = Social Figure 1.1 The pie model examples of factors related to recovery from WAD. 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 economic 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 independent 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 conclusions of the final report was that the yearly cost for society and for the insurance industry was approximately SEK 1.5 billion (US$201 million), while projected 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 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 injuries, factors that are involved in the risk or prognosis of WAD are multifactorial and constitute a web of biological, psychological and social components. 5

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