Whiplash: Evidence Base for Clinical Practice by Michele Sterli
Upcoming SlideShare
Loading in...5

Like this? Share it with your network


Whiplash: Evidence Base for Clinical Practice by Michele Sterli



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 ...

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.



Total Views
Views on SlideShare
Embed Views



1 Embed 1

http://www.slideshare.net 1


Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

Whiplash: Evidence Base for Clinical Practice by Michele Sterli Document Transcript

  • 1. WHIPLASH evidence base for clinical practice Michele Sterling | Justin Kenardy
  • 2. ContentsForeword vii Chapter 5 Pain-processing mechanisms in whiplash associated disorders 40Contributor list ix Michele Curatolo, Michele SterlingReviewer list xi Introduction 40 Mechanisms for post-injury centralAcknowledgments xi hyperexcitability 40Introduction xiii Evidence for central hyperexcitability Michele Sterling, Justin Kenardy in chronic WAD 41 Evidence for central hyperexcitability in acuteChapter 1 Epidemiology of whiplash associated WAD and in the transition to chronicity 42 disorders 1 Relationships between sensory hypersensitivity Lena Holm and psychological distress 44 Definitions 1 Implications for clinical management Cumulative incidence of and risk factors of whiplash 45 for WAD 1 Conclusion 47 Course and prognosis of WAD after a motor vehicle crash 2 Chapter 6 Neuromuscular dysfunction in An epidemiological approach to aetiology 4 whiplash associated disorders 52 The economic burden of WAD 5 Deborah Falla, James Elliott, Gwendolen Jull Summary 5 Changes in the properties of the cervical muscles 52Chapter 2 Clinical presentation of whiplash Altered neuromuscular control in WAD 54 associated disorders 9 Implications for the management of the patient Michele Sterling with whiplash 60 Patterns of recovery 9 Conclusion 63 Physical and psychological characteristics 10 Classification systems for WAD 11 Chapter 7 Dizziness, visual and sensorimotor Conclusions 12 control disturbances following whiplash injury 69 Julia TreleavenChapter 3 Mechanism of injury 16 Aetiology of dizziness, visual disturbances and Brian D. Stemper, Narayan Yoganandan, sensorimotor control disturbances in whiplash Frank A. Pintar, Dennis J. Maiman associated disorders 69 Head–neck kinematics: global and Signs and symptoms of sensorimotor disturbance segmental 16 following a whiplash injury 76 Injury theories 16 Implications for assessment 78 Injury metrics 20 Implications for management 78 Influencing factors for injury potential 22 Conclusion 79 Summary 24 Chapter 8 Psychological aspects of whiplashChapter 4 The evidence for pathoanatomical associated disorders 85 lesions 29 Jan Buitenhuis, Peter de Jong, Jan Jaspers, James Elliott Justin Kenardy Introduction 29 Accident-related psychological factors 85 Pathomechanics of whiplash injury 29 Coping 87 Pathological lesions in whiplash injury 30 Catastrophising and kinesiophobia 87 Conclusion 35 v
  • 3. vi Contents Attributions, beliefs and expectations 88 Evidence-based practice 138 Conclusion 89 Remaining issues and future prospects 141 Conclusion 142Chapter 9 Potential role of stress systems in the pathogenesis of whiplash associated Chapter 14 Compensation and health disorders 93 outcomes 144 Samuel McLean Luke B. Connelly, Natalie Spearing Sympathetic nervous system 93 Introduction 144 Neuropeptide Y 95 Compensation and related concepts 145 Serotonin 96 Compensation: empirical considerations 147 Clinical implications 96 Health: the concept and its measurement 150 Current research needs and future research Conclusions 153 directions 96 Chapter 15 Whiplash and the law 157Chapter 10 Prognostic indicators of non-recovery Ian Freckelton, S.C. following whiplash injury 101 The test for compensability 157 Michele Sterling Canadian Transport Accident Compensation 161 Prognostic factors for non-recovery 101 Conclusions 166 Prediction of outcomes other than pain and disability 104 Chapter 16 Malingering and symptom magnification Clinical implications 104 in whiplash associated disorders 168 Conclusion 105 Brian McGuire Why study malingering in the areaChapter 11 Primary care management of acute of whiplash? 168 whiplash injury 108 What is meant by ‘malingering’? 169 Michele Sterling, Justin Kenardy Approaches to detection of malingering 170 Current evidence for the management of acute Differential diagnosis of psychological WAD 108 disorders where symptom production or The provision of advice and education 109 magnification is a feature 171 Is pain control important? 110 Empirical studies of malingering and symptom Physical characteristics of acute WAD magnification in pain 172 and implications for management 110 A decision-making template for possible Psychological characteristics of acute and probable malingering 175 WAD and implications for management 113 Early multidisciplinary management 115 Chapter 17 Case descriptions 180 Summary 116 Michele Sterling, Trudy Rebbeck, Justin Kenardy Case description 1: acute whiplash 180Chapter 12 Evidence-based management Case description 2: acute whiplash 181 of chronic whiplash associated disorders 120 Summary of cases 1 and 2 183 Trudy Rebbeck Case description 3: chronic whiplash 183 Evidence base for management of chronic Conclusion 185 whiplash 120 Evidence for physical interventions 120 Chapter 18 Future directions 187 Evidence for psychological interventions 127 Michele Sterling, Justin Kenardy Evidence for medical interventions 128 Intervention trials 187 Implementation of evidence in clinical Do some patients have a pre-existing risk practice 129 of developing chronic pain after whiplash Summary 132 injury? 188 Improving prognostic models 188Chapter 13 Psychological management Identification of a peripheral lesion 189 of chronic whiplash associated disorders 135 Conclusion 189 Jan Jaspers, Jan Buitenhuis, Gerbrig Versteegen, Peter de Jong Index 193 Theory-derived psychological interventions 135
  • 4. CHAPTER 1 Epidemiology of whiplash associated disorders Lena HolmDEFINITIONS The reason for excluding frontal collisions fromThe term whiplash injury has been used since the the definition is not discussed in the report and islate 1920s, when H. E. Crowe coined the term at a likely to be an error, since it is known that 25–30%medical meeting in San Francisco.1 It was originally of whiplash injury occurs in such impact direction.7–9described as an injury mechanism to the neck, but The QTF also suggested a classification of WADwas later also used to define the actual symptoms into five categories based on clinical signs and symp-after such an event. The first known case report was toms (see Chapter 2). This classification is mostlypublished in the Journal of the American Medical used to classify WAD in the acute phase.Association in 1953, when Gay and Abbot described Since the publication of the QTF findings, the term50 patients who had been exposed to whiplash WAD has been increasingly used in the medical lit-mechanism in car collisions.2 It was reported that the erature, and it is also a frequently used term in insur-majority had been exposed to rear-end collisions and ance medicine.that the majority were also examined between oneand 24 months after the collision, thus representing CUMULATIVE INCIDENCE OF ANDa mix of patients with acute or persistent symptoms. RISK FACTORS FOR WADCervical pain with radiation into the occipital regionof the skull, shoulder girdle or upper extremities Cumulative incidencewere reported as common symptoms, but irritability, The cumulative incidence is the number of new casespoor concentration and subjective vertigo were also of an event or outcome occurring in a populationdescribed. over a certain time period. Some evidence from the People who are exposed to energy transfer to the literature indicates that the incidence of WAD differsneck, in sports, falls or other mishaps, may also expe- between countries. There is also some evidence thatrience cervical pain.3–5 After such events, however, the incidence of WAD has increased from the begin-it is less common that the injury is labelled ‘whip- ning of the 1990s to after the year 2000, with thelash’, but instead other terms, such as neck strain, annual incidence for the latter period being about 300neck sprain or simply neck injury, are used. The term per 100,000 inhabitants in studies where emergencywhiplash associated disorder (WAD) was introduced setting visits are used. In some instances, the increasein 1995 by the Quebec Task Force (QTF), who pub- is between three and tenfold.10–12 It is not known iflished the first systematic review on whiplash inju- this increase is partly due to a change in care-seekingries.6 The term was intended to reflect that whiplash behaviour.is an injury mechanism, and the consequences of the There are also some indications from administra-mechanism were the spectrum of symptoms (disor- tive insurance claims databases in different Europeanders). The QTF formulated the following conceptual countries (e.g. Norway, the Netherlands and Sweden)definition: of a reduction in the number of WAD claims, whereas such decreases have not been seen in Denmark or the Whiplash is an acceleration-deceleration mecha- United Kingdom. Sweden, for instance, has seen a nism of energy transfer to the neck. It may result 33% decrease in personal motor vehicle crash (MVC) from rear-end or side-impact motor vehicle colli- injury claims between 2002 and 2008. The relative sions, but can also occur during diving or other mis- decrease is similar between the incidence of WAD and haps. The impact may result in bony or soft-tissue other types of injuries, with WAD constituting about injuries (whiplash injury) which in turn may lead 50% of all MVC injury claims. This decrease is not to a variety of clinical manifestations (whiplash- due to a reduction in the number of MVCs, and nor associated disorders).6 has the insurance system in Sweden changed. Instead, 1
  • 5. WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICEthis decrease is likely to be due to a combination of found no gender differences.11, 14 All these studiesreasons. For example, some car manufacturers have have weaknesses, primarily, the lack of ‘true’ denom-developed whiplash-protection devices for new car inators and/or the limited possibility to control formodels, which presumably will result in fewer cases potential confounding factors.of WAD as a result of rear-end collisions. Secondly, One possible risk factor for WAD is the severityduring the second half of the 1990s, police personnel of the crash (impact). The biomechanical research onin Sweden showed an increased awareness that there WAD is mainly based on experimental studies usingis no need to advise car occupants to seek healthcare cadavers, volunteers and simulation experiments. Soif no symptoms are present. Thirdly, the mass media far, the injury mechanism has not been established asfocus in Sweden on whiplash has decreased substan- a known risk factor. Reasons for this may be that theretially from over 800 articles in the beginning of the are different injury mechanisms occurring with differ-2000s to only about 200 articles in 2008. ent crash types. Car occupant acceleration, velocity Incidence calculation through insurance claims and rebound are all factors that should be consid-may be prone to other forms of bias. For instance, ered.17 In much of the research, a major focus is oninsurance systems where there are no benefits for the rear-end injury mechanisms despite consistent find-person responsible for a collision may underestimate ings that rear-end collisions are only responsible forthe frequency of injuries, since fewer claims would 40–55% of all cases of WAD in MVCs.8, 18 However,be reported. This would also happen with insurance there are some promising results from actual rear-endsystems where insurance claim access is limited, or collisions in that the redesign of headrests and seatswhere payments for compensation result in a signifi- so that head/neck extension is limited in rear-endcant increase in the insurance premium. On the other collisions has reduced the incidence of WAD.19, 20hand, healthcare data may also be prone to bias, since Before firm conclusions about the magnitude of suchsuch data only captures those who seek the type of preventive interventions can be drawn, larger studieshealthcare utilisation in question (e.g. emergency with well-defined outcome measures and controls forcare). potential confounding factors are needed.Risk factors for onset of WAD COURSE AND PROGNOSIS OF WADA risk factor for an outcome (i.e. disease/injury) is AFTER A MOTOR VEHICLE CRASHa factor that is independently associated with theoutcome or condition in question. Knowledge of the Course of recoveryaetiology (cause) of WAD is limited. One reason for Understanding the course and prognosis in WADthis is the difficulty in obtaining accurate and appro- is critical. Will people recover from this commonpriate denominators to calculate risks. Rather than injury? If so, when? If the injury is transient and self-using persons exposed to collisions as the denomina- limiting, there would be no need for major preventiontor, researchers have used proxies, such as registered and intervention strategies. The natural course andlicensed drivers,6 population censuses,13, 14 or per- prognosis of WAD has been a controversial matter.sons involved in collisions where at least one person Some claim that the prognosis is solely determinedwas injured.9 Some studies have adjusted for possible by the physical injury and its severity, and that pre-confounding factors, while others have not. A con- and post-psychosocial factors are not relevant infounding factor is an independent risk factor for the recovery.21–23 Others claim that persistent WAD isoutcome and is also associated with the exposure/risk mainly a ‘psycho-cultural’ illness, and refer to stud-factor of interest. Examples of possible confounding ies from Lithuania and Greece where there is no orfactors include gender, age, pre-collision physical little awareness or reporting of WAD resulting fromand mental health, and severity and direction of crash a whiplash mechanism.24–26 Studies from these coun-impact. tries report that 2% or less of study participants report Risk factors for WAD reported in published stud- long-lasting symptoms after car collisions.15, 27 How-ies include presence of neck pain prior to the colli- ever, drawing firm conclusions based on the findingssion,15, 16 being the driver or the front-seat passenger of these studies is inappropriate, since ‘psycho-(compared to rear-seat passenger), and being exposed cultural’ factors were not studied per se. Neverthe-to a rear-end collision or frontal collision rather than less, when persons who do not experience neck paina side collision.9 Female gender has been suggested following a car collision have been asked to reportto be associated with a slightly higher incidence of on which symptoms they would expect after neckWAD in some studies,9, 6, 13 but other studies have injury or minor head injury, those from Lithuania and2
  • 6. 1 Epidemiology of whiplash associated disordersGreece do not expect to have as many symptoms or expectations).47 It is believed to be influenced bydo not have as long-lasting symptoms compared to personal and psychological features, such as anxi-persons in Canada.28–30 ety, self-efficacy, coping abilities and fear, and recent In the majority of studies, the recovery rate is studies have demonstrated that in those with WAD,substantially lower than recovery rates reported in initial pain, depressive symptomatology, and someGreece and Lithuania. Some report a 66–68% recov- crash and demographic factors were associated withery rate at one year after the injury,31, 32 whereas oth- recovery and return-to-work expectation.48ers report a less than 40% recovery rate at a similar Health expectations are postulated to be primar-time point.33, 34 Differences in recovery rates are at ily learned from the cultural environment, and basedleast partially due to selection bias. For instance, in on ‘prior knowledge’. The mechanism by whichthe study by Miettinen et al., only 58% of the invited expectations influence emotional and physical reac-study population was followed up 12 months post tions may also actually affect the autonomic nervousinjury, so it was unknown what the recovery rate was system, involving biochemical processes, which mayfor the 42% of participants who could not be con- explain some of the power observed in studies of thetacted at follow-up.33 placebo and nocebo effect.49, 50 These mechanisms help to explain why persons who strongly anticipatePrognostic factors they will recover really do, and why strong expecta-A prognostic factor is a factor that is independently tions about bad health actually lead to bad health. Aassociated with the prognosis, and which can con- concept that is closely related to expectations is a per-tribute to or work against recovery from a condition. son’s belief—the lens through which a person viewsSome factors known to contribute to a poor prognosis the world—which is shaped by the environment. In ain WAD are similar to those for other forms of persis- study where injured persons were asked about theirtent neck pain. These factors include, among others, belief of the origin of their neck pain (causal belief),passive coping strategies, poor mental health, high those who believed that something serious had hap-level of stress, high pain intensity and more ‘asso- pened to their neck had greater perceived disabilityciated’ symptoms, such as arm pain, headache and during follow-up compared to those who did not havenausea.35–40 Similar to the literature on neck pain in such beliefs.51the general population, gender does not seem to bea clear prognostic factor in WAD, after adjustments WAD and widespread painhave been made for psychosocial factors.41 This sug- One important aspect about the course of recoverygests that the observed poor prognosis in females in from WAD is whether the neck injury is a triggersome studies might be explained in terms of the psy- for subsequent widespread body pain. This has beenchosocial factors rather than the biological factors of suggested from cross-sectional studies, but knowinggender. Furthermore, societal factors, such as insur- whether widespread pain came before the neck injuryance systems with possibilities to claim for pain and remains unclear from this type of study design.52, 53suffering,37 and extensive healthcare utilisation in the A potential aetiological explanation is a neurophysi-early stage of the injury,42 have been suggested to be ological disturbance in the peripheral and centralassociated with delayed recovery in WAD. nervous system, which, in some instances, leads to Surprisingly, the bulk of evidence suggests that an increased sensitivity to pain in other ‘uninjured’crash-related factors (e.g. impact direction, aware- areas.54, 55 Another possible explanation for wide-ness of collision, head position) are not associated spread pain is that new tissue damage may resultwith the prognosis.41 from an altered pattern of movement in the body There is evidence that people’s lowered expecta- due to the neck pain. The exact aetiology of wide-tions of recovery and return to work, assessed early spread pain is probably complex and multifactorial,in the process of recovery, are an important predictor but there are no indications that it would be specificfor long-lasting WAD, even after controlling for other to WAD. It can also occur after surgical interventionfactors, such as prior health, pain intensity, pain areas or any tissue damage.54 In addition, large prospectiveand acute post-traumatic stress symptoms.43–45 An studies on pain of other aetiology have demonstratedexpectation is defined as a degree of belief that some that psychosocial factors at work, repetitive strainsevent will occur,46 and is also explained by some as or other physical strains at work, awareness of symp-being tied to an outcome, such as a recovery state toms and illness behaviour may increase the risk ofor return to work, rather than the individual behav- development of widespread pain.56–58 Thus, it seemsiours required to achieve that outcome (self-efficacy that biological as well as psychological and social 3
  • 7. WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICEfactors contribute to the development of widespread This can effectively be discussed using the ‘pie’pain. model, or the component cause model, introduced to Prospective studies on WAD and its association epidemiologists by Rothman.64 In Figure 1.1, somewith widespread pain are sparse and the evidence prognostic factors that may be involved in recoveryis not clear. The results from one study suggest a from WAD are introduced in two different ‘pie’ models.relationship between the onset of neck pain or other According to the ‘pie’ model, all contributingassociated symptoms as well as self-perceived injury causes in one of the sufficient causes, or ‘pie’, areseverity, after an MVC, and subsequent widespread needed, in order to recover from WAD. Each suf-pain.59 However, age, gender, health behaviour and ficient cause represents one of presumably severalsomatic symptoms prior to collision were at least as alternative routes leading to recovery. The interac-important. Another study investigated the incidence tions between contributing causes are illustrated asof onset of more extensive pain during 12 months separate ‘pie slices’ included in the same ‘pie’. Slicesfollow-up of WAD claimants, and associated factors in one ‘pie’ are said to interact, because it is their jointwith such an outcome.60 In that study, a less conser- action that leads to recovery. The six outlined exam-vative definition of widespread pain was used and ples given in Figure 1.1 represent both ‘biological’,would probably have resulted in a higher incidence. ‘psychological’ and ‘social’ factors. The other B’s,The main conclusions were that widespread pain was P’s and S in the figure represent other factors that arecommon over a 12-month period (21%), but most important for the prognosis. In real life, of course, dif-improved over the follow-up period. Female gen- ferent distributions of biological, psychological andder, poor prior health, greater initial symptomatol- social factors occur among different people.ogy (including pain intensity) and more depressive In the literature, there is no recognised singlesymptoms were associated with the development contributing cause that is considered necessary forof extensive pain. The authors also found that local recovery from WAD. Neither has any sufficient causeneck/spinal pain was rare after a traffic collision— been identified. Instead, several contributing causesonly 11% of eligible WAD claimants had local neck/ (i.e. factors that affect the causes for recovery) haveback pain, raising the question of the potential cause been found. When linking this ‘pie’ model to the evi-of widespread pain in other studies. dence of prognostic factors in WAD, numerous sets of possible ‘individual pies’ become obvious. In sum-Work absenteeism and work disability mary, several different sufficient causes for recoveryMany persons with acute WAD also have some from WAD exist; in other words, several alternativeabsence from work, and no clear difference occurs routes lead to recovery.between ‘blue’ and ‘white’ collar workers. In one In research, the effect of individual contributingpopulation-based study, 46% of persons had been causes, or risk factors, are usually investigated foroff work due to the injury.8 A similar figure (49%) the condition in question. Complete sufficient causeswas seen in a Dutch study.61 The majority of people usually do not lend themselves to studies because fewreturned to work within a few days and only 4–9% of these scenarios actually exist (exceptions includewere reported to be off work at six months post bacterial infection). Still, it is important to keep theinjury.32, 62 In a study from the Netherlands, factors ‘pie’ model in mind when interpreting and discuss-associated with not returning to work were older age ing empirical results on risk and prognosis. A singleand concentration problems.63 There was no asso- contributing cause may otherwise be confused for aciation between degree of manual labour (‘blue’ or sufficient cause. The whole picture of specific sets of‘white’ collar work) or education level and not return- sufficient causes is seldom discussed in the researching to work. of WAD or in other contexts. The causal process is more complicated than explained by the ‘pie’ model, since effects are likelyAN EPIDEMIOLOGICAL APPROACH TO to depend on other factors that happen simultane-AETIOLOGY ously. For instance, some persons in pain may call forIn epidemiology, one of the aims is to assess the support from family members or workmates, whichindependent association between a potential risk or in turn may change the person’s future pain percep-prognostic factor. It is, however, extremely important tion and behaviour (positively or negatively). In otherto keep in mind that in most diseases and injuries, a instances, pain intensity may cause depressed mood,multifactorial causal model is needed to understand or depressed mood may cause more pain (bidirec-the onset and prognosis. tional). Nevertheless, this component cause model is4
  • 8. 1 Epidemiology of whiplash associated disorders One contributing cause High Minor recovery neurophysiological expectations disturbance Minor tissue P Absence of damage P depressive mood S B Low Sufficient B financial social incentives support One sufficient cause One sufficient causeB = Biological, P = Psychological, S = SocialFigure 1.1 The ‘pie’ model—examples of factors related to recovery from WAD.a fruitful way to conceptualise WAD as it visualises time the person reaches retirement age) amounted tothe multifactorial nature of WAD and how biological, SEK 4.6 billion (US$648 million). These calculationspsychological and social factors may interact. were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002.THE ECONOMIC BURDEN OF WAD Since the report’s publication, the number of WADLittle is known about the individual and societal eco- cases have decreased dramatically to about 16,000nomic burden of WAD. For instance, little is known claims in 2008 (173 per 100,000 inhabitants), which,about the prevalence of long-lasting work disability of course, has an impact on the overall costs.due to WAD, which is probably the most costly part. Comparable data has not been found, but thereThis burden is probably largely dependent on the is some evidence from a study that addressed thelegislation in different countries. In 2002, an inde- incidence of WAD in 10 European countries.66 Thependent and temporary Commission on Whiplash- administrative data suggest that the total claims costRelated Injuries was formed in Sweden, initiated by in Switzerland was 500 million Swiss francs (US$467the four largest motor vehicle insurers. The mandate million). Switzerland’s population is 80% that ofof the 3-year Commission was an examination of the Sweden. Expenditures in addition to the claims costproblems of WAD from road safety, medical care, was not reported in that study.insurance and societal aspects.65 One of the conclu-sions of the final report was that the yearly cost for SUMMARYsociety and for the insurance industry was approxi- In summary, as in almost all other diseases and inju-mately SEK 1.5 billion (US$201 million), while pro- ries, factors that are involved in the risk or prognosisjected costs (i.e. what new cases of WAD arising in of WAD are multifactorial and constitute a web ofa particular year will cost society and insurers by the biological, psychological and social components. 5
  • 9. WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICEReferences 17. Sendur P, Thibodeau R, Burge J, Tencer A. Parametric 1. Crowe H. A new diagnostic sign in neck injuries. Calif analysis of vehicle design influence on the four phases Med 1964;100:12–13. of whiplash motion. Traffic Inj Prev 2005;6(3):258–66. 2. Gay J, Abbott K. Common whiplash injuries of the 18. Crutebo S, Nilsson C, Skillgate E, Holm LW. The neck. JAMA 1953;152:1698–704. course of symptoms for whiplash-associated disorders 3. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. in Sweden: 6-month followup study. J Rheumatol Head and neck injuries among ice hockey players 2010;37(7):1527–33. wearing full face shields vs half face shields. JAMA 19. Farmer CM, Wells JK, Lund AK. Effects of head 1999;282(24):2328–32. restraint and seat redesign on neck injury risk in rear- 4. Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ. end crashes. Traffic Inj Prev 2003;4(2):83–90. Neck sprain not arising from car accidents: a 20. Jakobsson L, Isaksson-Hellman I, Lindman M. retrospective study covering 25 years. Eur Spine J WHIPS (Volvo cars’ Whiplash Protection System)— 1998;7(3):201–5. the development and real-world performance. Traffic 5. Lorish TR, Rizzo TD, Jr., Ilstrup DM, Scott SG. Inj Prev 2008;9(6):600–5. Injuries in adolescent and preadolescent boys at 21. Johansson B. Whiplashskador har entydig organisk two large wrestling tournaments. Am J Sports Med grund [Whiplash injuries has an unambiguous organic 1992;20(2):199–202. basis]. Läkartidningen 2001;98(25):3061–2. 6. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific 22. Freeman MD, Centeno C. “Alar, Transverse, and monograph of the Quebec Task Force on whiplash- Apical Ligament Strain Due to Head-Turned Rear associated disorders: redefining “whiplash” and its Impact” by Maak et al. Spine 2006;31(17):2030. management. Spine 1995;20(8 Suppl):1S–73S. 23. Freeman M, Croft A, Rossignol A, et al. A review 7. Holm LW, Carroll LJ, Cassidy JD, Ahlbom A. Factors and methodologic critique of the literature refuting influencing neck pain intensity in whiplash-associated whiplash syndrome. Spine 1999;24(1):86–98. disorders in Sweden. Clin J Pain 2007;23(7):591–7. 24. Ferrari R, Shorter E. From railway spine to whiplash— 8. Ferrari R, Russell AS, Carroll LJ, Cassidy JD. the recycling of nervous irritation. Med Sci Monit A re-examination of the whiplash-associated disorders 2003;9(11):HY27–37. (WAD) as a systemic illness. Ann Rheum Dis 25. Ferrari R, Kwan O, Russell AS, et al. The best approach 2005:1337–42. to the problem of whiplash? One ticket to Lithuania 9. Berglund A, Alfredsson L, Jensen I, et al. Occupant- please. Clin Exp Rheumatol 1999;17:321–6. and crash-related factors associated with the risk of 26. Ferrari R. Myths of whiplash. Surgeon 2003;1(2):99, whiplash injury. Ann Epidemiol 2003;13(1):66–72. 101–3.10. Bylund P-O, Björnstig U. Sick leave and disability 27. Partheni M, Constantoyannis C, Ferrari R, et al. pension among passenger car occupants injured in A prospective cohort study of the outcome of acute urban traffic. Spine 1998;23(9):1023–8. whiplash injury in Greece. Clin Exp Rheumatol11. Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ. 2000;18:67–70. Neck sprain in patients injured in car accidents: a 28. Ferrari R, Constantoyannis C, Papadakis N. Cross- retrospective study covering the period 1970–1994. cultural study of symptom expectation following Eur Spine J 1998;7(3):195–200. minor head injury in Canada and Greece. Clin Neurol12. Björnstig U, Hildingson C, Toolanen G. Soft-tissue Neurosurg 2001;103(4):254–9. injury of the neck in hospital based material. Spine 29. Ferrari R, Obelieniene D, Russell AS, et al. Symptoms 1990;18(4):263–7. expectation after minor head injury. A comparative13. Quinlan KP, Annest JL, Myers B, et al. Neck strains study between Canada and Lithuania. Clin Neurol and sprains among motor vehicle occupants—United Neurosurg 2001;103:184–94. States, 2000. Accid Anal Prev 2004;36(1):21–7. 30. Ferrari R, Obelieniene D, Russell A, et al. Laypersons´14. Bring G, Bjornstig U, Westman G. Gender patterns in expectation of the sequelae of whiplash injury. minor head and neck injuries: an analysis of casualty A cross-cultural comparative study between Canada register data. Accid Anal Prev 1996;28(3):359–69. and Lithuania. Med Sci Monit 2002;8(11):728–34.15. Obelieniene D, Schrader H, Bovim G, et al. Pain 31. Kivioja J, Jensen I, Lindgren U. Early coping after whiplash: a prospective controlled inception strategies do not influence the prognosis after whiplash cohort study. J Neurol Neurosurg Psychiatry injuries. Injury 2005;36(8):935–40. 1999;66:279–83. 32. Sterner Y, Toolanen G, Gerdle B, Hildingsson C.16. Wiles NJ, Jones GT, Silman AJ, Macfarlane GJ. Onset The incidence of whiplash trauma and the effect of of neck pain after a motor vehicle accident: a case- different factors on recovery. J Spinal Disord Tech control study. J Rheumatol 2005;32(8):1576–83. 2003;16(2):195–9.6
  • 10. 1 Epidemiology of whiplash associated disorders33. Miettinen T, Airaksinen O, Lindgren KA, Leino E. 47. Janzen JA, Silvius J, Jacobs S, et al. What is a health Whiplash injuries in Finland—the possibility of expectation? Developing a pragmatic conceptual some sociodemographic and psychosocial factors to model from psychological theory. Health Expect predict the outcome after one year. Disabil Rehabil 2006;9(1):37–48. 2004;26(23):1367–72. 48. Ozegovic D, Carroll L, Cassidy J. Factors associated34. Gargan MF, Bannister GC. The rate of recovery with return to work expectations in a population based following whiplash injury. Eur Spine J 1994;3(3):162–4. WAD cohort. J Rehabil Med 2010;42;66–73.35. Croft PR, Lewis M, Papageorgiou AC, et al. Risk 49. Pariente J, White P, Frackowiak RS, Lewith G. factors for neck pain: a longitudinal study in the Expectancy and belief modulate the neuronal general population. Pain 2001;93(3):317–25. substrates of pain treated by acupuncture. Neuroimage36. Bot SD, van der Waal JM, Terwee CB, et al. Predictors 2005;25(4):1161–7. of outcome in neck and shoulder symptoms: a cohort 50. Beauregard M. Effect of mind on brain activity: study in general practice. Spine 2005;30(16):E459–70. evidence from neuroimaging studies of psychotherapy37. Cassidy JD, Carroll L, Côté P, et al. Effect of and placebo effect. Nord J Psychiatry 2009;63(1):5–16. eliminating compensation for pain and suffering on the 51. Buitenhuis J, de Jong PJ, Jaspers JP, Groothoff JW. outcome of insurance claims for whiplash injury. Catastrophizing and causal beliefs in whiplash. Spine N Engl J Med 2000;342(16):1179–86. 2008;33(22):2427–33.38. Carroll LJ, Cassidy JD, Côté P. The role of pain 52. Buskila D, Neuman L, Vaisberg G, et al. Increased coping strategies in prognosis after whiplash injury: rates of fibromyalgia following cervical spine injury. passive coping predicts slowed recovery. Pain Arthritis Rheum 1997;40(3):446–52. 2006;124:18–26. 53. McLean SA, Williams DA, Clauw DJ. Fibromyalgia39. Côté P, Cassidy JD, Carroll L, et al. A systematic after motor vehicle collision: evidence and review of the prognosis of acute whiplash and a new implications. Traffic Inj Prev 2005;6(2):97–104. conceptual framework to synthesize the literature. 54. Melzack R, Coderre TJ, Katz J, Vaccarino AL. Central Spine 2001;26(19):E445–58. neuroplasticity and pathological pain. Ann N Y Acad40. Carstensen TB, Frostholm L, Oernboel E, et al. Post- Sci 2001;933:157–74. trauma ratings of pre-collision pain and psychological 55. Meeus M, Nijs J. Central sensitization: a biopsychosocial distress predict poor outcome following acute explanation for chronic widespread pain in patients whiplash trauma: a 12-month follow-up study. Pain with fibromyalgia and chronic fatigue syndrome. Clin 2008;139(2):248–59. Rheumatol 2006:465–73.41. Carroll LJ, Holm LW, Hogg-Johnson S, et al. Course 56. McBeth J, Harkness EF, Silman AJ, Macfarlane and prognostic factors for neck pain in whiplash- GJ. The role of workplace low-level mechanical associated disorders (WAD): results of the Bone and trauma, posture and environment in the onset of Joint Decade 2000-2010 Task Force on Neck Pain and chronic widespread pain. Rheumatology (Oxford) Its Associated Disorders. Eur Spine J 2008;17 2003;42(12):1486–94. (Suppl 1):S83–92. 57. McBeth J, Macfarlane GJ, Benjamin S, Silman AJ.42. Côté P, Hogg-Johnson S, Cassidy JD, et al. Initial Features of somatization predict the onset of chronic patterns of clinical care and recovery from whiplash widespread pain. Arthritis Rheum 2001;44(4):940–6. injuries: a population-based cohort study. Arch Intern 58. Harkness EF, Macfarlane GJ, Nahit E, et al. Med 2005;165(19):2257–63. Mechanical injury and psychosocial factors in the43. Holm LW, Carroll LJ, Cassidy JD, et al. Expectations work place predict the onset of widespread body pain: for recovery important in the prognosis of whiplash a two-year prospective study among cohorts of newly injuries. PLoS Med 2008;5(5):e105. employed workers. Arthritis Rheum 2004;50(5):44. Carroll LJ, Holm LW, Ferrari R, et al. Recovery in 1655–64. whiplash-associated disorders: do you get what you 59. Wynne-Jones G, Jones GT, Wiles NJ, et al. Predicting expect? J Rheumatol 2009;36(5):1063–70. new onset of widespread pain following a motor45. Ozegovic D, Carroll LJ, David Cassidy J. Does vehicle collision. J Rheumatol 2006;33(5):968–74. expecting mean achieving? The association between 60. Holm LW, Carroll LJ, Cassidy JD, et al. Widespread expecting to return to work and recovery in whiplash pain following whiplash-associated disorders: associated disorders: a population-based prospective incidence, course, and risk factors. J Rheumatol cohort study. Eur Spine J 2009;18(6):893–9. 2006;34(1):193–200.46. Kirsch I. How expectancies shape experience. 61. Hendriks EJ, Scholten-Peeters GG, van der Windt DA, Washington, DC: The American Psychology et al. Prognostic factors for poor recovery in acute Association, 1999. whiplash patients. Pain 2005;114(3):408–16. 7
  • 11. WHIPLASH: EVIDENCE BASE FOR CLINICAL PRACTICE62. Kasch, H, Bach F, Jensen T. Handicap after acute 65. The Swedish Commission on Whiplash-Related whiplash injury: a 1-year prospective study of risk Injuries. The Whiplash Commission Final Report, 2009. factors. Neurology 2001;56(12):1637–43. Online. Available at: http://www.whiplashkommissionen.63. Buitenhuis J, de Jong PJ, Jaspers JP, Groothoff JW. se/english/english.htm, viewed 20 August 2010. Work disability after whiplash: a prospective cohort 66. Chappuis G, Soltermann B. Number and cost of study. Spine 2009;34(3):262–7. claims linked to minor cervical trauma in Europe:64. Rothman K. Epidemiology: an introduction. New results from the comparative study by CEA, AREDOC York: Oxford University Press, 2002. and CEREDOC. Eur Spine J 2008;17(10):1350–7.8