Editorial - Springer Link

Eur Spine J (2008) 17 (Suppl 3):S359–S416 DOI 10.1007/s00586-007-0484-x

Editorial

Springer-Verlag 2007

Whiplash injuries and associated disorders: new insights into an old problem The term ‘‘whiplash’’ dates back to 1928 when the American physician H.E. Crowe used this term at a symposium on traffic accidents held in San Francisco. Crowe did not refer to the injury as such, but the motion that the head and neck underwent in conjunction with a collision. Already around the turn of the century 1900 researchers had debated about the risk for neck- and back injuries and the term ‘‘railway spine’’ was used to describe such problems. Nowadays the term whiplash is common knowledge, but still there is controversy regarding e.g. definition and diagnostic criteria. In many countries the number of whiplash injuries has increased during the last decades and such injuries represent the largest part of all road traffic injuries, leading to considerable human suffering and large costs for individuals, insurance companies and society. Between 60% and 85% of all reported road traffic injuries have in different studies been found to be whiplash injuries. It is difficult to compare the occurrence of short- and long-term whiplash related symptoms between countries, due to international variations in e.g. diagnostic criteria, insurance system, traffic intensity as well as the knowledge about whiplash related problems among the population at large (2). In 1995 the Quebec Task Force presented its report Scientific monograph of the Quebec Task Force on WhiplashConflict of interest statement This work was financially supported by the Whiplash Commission in Sweden, which in turn was financially supported by the four major non-life insurance companies in Sweden. B. Rydevik (&) M. Szpalski M. Aebi R. Gunzburg Department of Orthopaedics, Sahlgrenska University Hospital, 41345 Gothenburg, Sweden e-mail: [email protected]

Associated Disorders: redefining ‘‘whiplash’’ and its management (4). During the period after 1995 a large number of scientific investigations have been published on the medical aspects of whiplash injuries. Meetings and books (3) have extensively discussed the matters and the numerous controversial issues associated, specifically those related to the psychosocial and medico-legal aspects. The evolution of automobile safety techniques is also playing a role in whiplash mechanisms (1). These facts, together with the gradual increase in whiplash injuries during the last decades, motivate a review of the scientific literature in this field. The so called ‘‘Whiplash Commission’’ in Sweden was appointed in the summer of 2002 (5) following an initiative of Sweden’s four big non-life insurance companies. The background to its inception was that there had been a rapid increase in the number of whiplash related injuries reported during the 1990’s. These problems are common to many countries around the world. The mandate of the Commission was formulated as an examination of the problems of whiplash-related road accident injuries from the road safety, medical care and insurance aspect. The proposals presented in the Commission’s final report are based on scientifically established knowledge in these areas and on extensive discussions that the commission has conducted with interest groups and the public. In spring 2004, the Swedish Society of Medicine appointed, in collaboration with the Whiplash Commission, a medical task force comprising representatives from nine sections of the Swedish Society of Medicine, namely General Medicine, Neurology, Orthopaedics, Psychiatry, Radiology, Rehabilitation Medicine, Anaesthesia/Pain Management, Social Medicine and Oto-Rhino-Laryngology. This medical task force has developed the present consensus document hereby published as supplement of the European Spine Journal.

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Eur Spine J (2008) 17 (Suppl 3):S359–S416

In this supplement ‘‘Whiplash injuries: diagnosis and early management’’ relevant scientific literature in the field is summarized, evaluating it based on the experience within the group concerning research in the field and the diagnosis and management of patient with whiplash associated disorders. The supplement comprises ten sections on different medical aspects of whiplash injuries. The aim of this consensus document that it will foster improved understanding of the medical problems involved in whiplash-associated disorders and to facilitate the diagnosis and early management of patients with whiplash injuries.

2.

3. 4.

5. References 1.

Farmer CM, Wells JK, Lund AK (2003) Effects of head restraint and seat redesign on neck injury risk in rear-end crashes. Traffic Inj Prev 4:83–90

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Ferrari R, Obelieniene D, Russell A, Darlington P, Gervais R, Green P (2002) Laypersons’ expectation of the sequelae of whiplash injury. A cross-cultural comparative study between Canada and Lithuania. Med Sci Monit 8:728–734 Gunzburg R., Szpalski M.(Eds) (1998) Whiplash injuries. Lippincott-Raven, Philadelphia Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, Zeiss E (1995) Scientific monograph of the Quebec Task Force on WhiplashAssociated Disorders: redefining ‘‘whiplash’’ and its management. Spine 15; (8 Suppl):1S–73S www.whiplashkommissionen.se


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Summary

The Medical Task Force of the Swedish Society of Medicine and the Whiplash Commission has come to the following main conclusions: The term ‘‘whiplash’’ is so generally accepted that it should continue to be used, but the term ‘‘whiplash trauma’’ should only be used to refer to indirect cervical spine trauma. By deleting WAD grades 0 and IV from the classification system introduced in 1995 by the Quebec Task Force (QTF), the diagnosis of whiplash injury will be more exact and more realistically defined, which will reduce the risk of misunderstanding. The reported incidence of whiplash injuries in Sweden varies depending on the particular investigation cited, and ranges between 1.0 and 3.2/1000 per year. Whiplash injuries represent approximately 1/3 of all claims submitted after traffic injuries to insurance companies in Sweden, and give rise to a medical disability rate of 10% or more. Various studies of how the possibility of an insurance claim influences the course of a whiplash injury have produced quite different results, but generally there is no evidence of significant differences in outcome between those who have and have not sought claim. Ligament injuries can rarely be demonstrated acutely after whiplash trauma, and radiologically verified instability later in the course of the injury is also rare. Experimental studies have shown that whiplash trauma can lead to loads on discs and facet joints that might result in injury of these structures, but there is no scientific evidence to verify such injuries in patients with whiplash injury. Certain studies indicate that a dysfunction in the nervous system may exist in a small proportion of patients with whiplash injury. A series of physiological changes occurs in both the peripheral and the central nervous systems after whiplash injury, comprising peripheral as well as central sensitisation. There is no scientific evidence that such physiological changes are specific to the pain associated with whiplash

injury; similar changes have been shown to occur in association with various other pain conditions, acute as well as long-term. It is likely that any previous mental ill-health and the patient’s current mental state are both important for the clinical development and course of whiplash injury. To minimise the risk of long-term problems among people with acute whiplash injury, concurrently occurring acute stress disorder (ASD) and/or post-traumatic stress disorder (PTSD) should be diagnosed and treated. It is also important to diagnose and adequately treat possible sleep disorder, depression, or anxiety among people with whiplash injury. Neck problems in terms of pain and stiffness, either with or without objective clinical findings such as decreased range of motion and tenderness at palpation (WAD grades I and II), are most common. Symptoms usually appear within the first day and up to a few days after whiplash trauma. Headache commonly occurs, along with pain in the shoulders and the thoracic spine. Neurological symptoms are present in approximately 20% of patients, though only 3–4% display objective neurological findings (WAD grade III). Symptoms such as sleep disorder, memory and concentration difficulties, and signs of stress are reported in approximately 25% of cases. The prognosis after whiplash injury is usually favourable, and 90–95% of patients recover completely or experience only minor ongoing problems. Risk factors can often be identified early, high pain intensity and a high grade of WAD being warning signs. Fear or avoidance of motion and other psychiatric reactions should be identified early on. Patients with whiplash injuries comprise a heterogeneous group in terms of severity, clinical problems, and objective findings, so treatment should be individualised. If a patient complains of vertigo that has occurred acutely after whiplash injury, benign positional vertigo

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should be the primary differential diagnosis and tests for this condition should be performed. Vertigo characterised by instability is not uncommon in association with late whiplash-related problems, but the background to such vertigo is often unclear and diagnostic tests that can relate the vertigo problems to the whiplash trauma are lacking. If considerable hearing impairment or tinnitus occurs during the acute phase after whiplash injury, a hearing examination should be performed. Early management of people with whiplash injury should include documentation of pain intensity and possible neurological symptoms and findings, as well as of possible stress, fear, and anxiety. The grade of WAD should be determined. Appropriate treatment initiatives are dependent on pain intensity and grade of WAD, and should take account of the patient’s entire circumstance in cases of delayed recovery. Information and advice should be directed towards a rapid return to normal activity, since most people do recover. Patients’ own active, adaptive strategies, such as daily, regular head and shoulder movements to the pain threshold, relaxation exercises, and walks should be encouraged. Use of a cervical collar, however, has no role in treatment. Any pharmacological or other treatment should be regular, temporary, and followed up. In cases of persistent pain after one month and difficulties with work and daily activities, coordinated evaluation at a primary care unit, or alternatively at a pain specialist unit, is recommended.

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In the acute phase there is no need for the x-ray examination of patients under age 65 with WAD grade I complaints, except for those with concurrent skeletal disease, such as Bechterew’s disease (ankylosing spondylitis) and rheumatoid arthritis. In cases of WAD grade II, plain x-ray or computerised tomography (CT) is recommended. If there are symptoms indicating spinal nerve root or spinal cord involvement, CT is recommended. In cases of WAD grade III with objective neurological findings, CT is the primary investigative modality and additional investigation with magnetic resonance imaging (MRI) is often indicated. Neurophysiological examinations such as eye movement tests, neck torsion tests, cervical kinaesthesia/joint position error, and posturography should not be used in routine care, since these investigations are of no documented diagnostic value with regard to whiplash injuries. These tests should be reserved for use in association with clinical research. There is a need for improved knowledge in all the areas covered in this document; ongoing research into, for example, injury causes, pain mechanisms, and the background to functional impairment associated with whiplash injury is therefore crucial. We also need continued research into diagnosis and treatment, as well as medical insurance aspects. Through continued basic and clinical research, a platform can be created for improved diagnostic methods and treatment modalities in association with whiplash injury.


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1 Classification and definitions

The term ‘‘whiplash’’ was introduced in 1928 by Crowe to describe a clinical picture occurring in some patients who had been exposed to indirect trauma of the cervical spine in association with motor vehicle accidents [47]. Since the mechanism of indirect cervical spine trauma resembles that of a whip lash, namely, a relatively minor force at the handle of the whip leading to a much larger and more rapid movement at the end of the whip, the term whiplash is used also to describe both the motion pattern and injury mechanism associated with indirect cervical spine trauma. However, there is one considerable difference between the motion and forces associated with an actual whip and the situation regarding ‘‘whiplash’’ injury of the cervical spine, namely, the weight of the head (approximately 3–4 kg), which enhances the forces affecting the cervical spine and the head. The term whiplash was originally introduced to refer to cervical spine injuries, but since then the term has gradually become expanded in application, and many use it to describe both the injury mechanisms and clinical symptoms. Several authors also use the term whiplash to refer to direct cervical spine trauma either with or without fractures. In public debate, the term is often used in contexts implying that whiplash is a type of injury that is difficult to treat and has a poor prognosis. In the classification of injuries and health problems of the Swedish National Board of Health and Welfare, whiplash injury is referred to as the distortion of the cervical column (S13.4 according to ICD-10). The vague definition of the term whiplash has led to a wide range of interpretations, which has probably caused considerable misunderstanding with consequent negative effects for patients. We suggest the following definitions: Whiplash trauma Mechanical insult to structures of the cervical spine and the head that occurs when an acceleration-deceleration movement transfers forces to these structures without the existence of direct trauma to the head or the cervical spine.

Whiplash injury Injury or functional impairment that occurs in association with whiplash trauma. Whiplash injury, as defined above, is synonymous with whiplash-associated disorders (WAD) according to the nomenclature of the Quebec Task Force (QTF) [242]. In most patients who present symptoms after a whiplash trauma, such symptoms occur in close association with the trauma [99, 250]. In certain contexts, it has even been stated that the onset of symptoms must be within 72 hours of the injury for the symptomatology to be regarded as connected with whiplash trauma. Though there is no scientific evidence for a definitive time limit, it is reasonable that symptoms and clinical findings should occur within a few days of the trauma to be related to a whiplash trauma. The Quebec Task Force (QTF) [242] published a monograph about whiplash-associated disorders in which a definition of whiplash and a classification of whiplash injuries were presented (Fig. 1). The monograph gained considerable publicity and had a major impact, facilitating increased general awareness of the field and improved scientific debate through the application of the structured view of the symptoms and clinical findings as classified. While these benefits should continue to be safeguarded, certain weaknesses in the definition and in the classification system should be addressed. For this reason, changes to the QTF classification are suggested (Fig. 2). The QTF classification covers a broad spectrum of cervical spine injuries, ranging from those of individuals lacking symptoms or findings at clinical examination (WAD grade 0) to fractures and dislocations of the cervical spine (WAD grade IV). Why the classification includes such a broad range of injuries is unclear, since WAD grades 0 and IV are not covered in the QTF monograph. Individuals who do not present symptoms or clinical findings at examination cannot be regarded as having any cervical spine injury and thus should not be provided with a trauma diagnosis; instead they should be classified

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Eur Spine J (2008) 17 (Suppl 3):S359–S416 THE QUEBEC TASK FORCE OF WHIPLASH-ASSOCIATED DISORDERS

Grade Clinical Presentation 0

No complaint about the neck No physical sign(s)

I

Neck complaint of pain, stiffness or tenderness only No physical sign(s)

II

Neck complaint a AND Musculoskeletal sign(s)

III

Neck complaint b AND Neurological sign(s)

IV

Neck complaint AND Fracture or dislocation a

Musculoskeletal signs include decreased range of motion and point tenderness

b

Neurological signs include decreased or absent deep tendon reflexes, weakness and sensory deficits

Symptoms and disorders can be manifested in all grades include deafness, dizziness, tinnitus, headache, memory loss, dysphagia and temporomandibular joint pain.

• Fig. 1 QTF classification of whiplash injuries [242]. The Quebec Task Force 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 driving or other mishaps. The impact may result in bony or soft-tissue injuries (whiplash injury), which in turn can lead to a variety of clinical manifestations (Whiplash-Associated Disorders, WAD)’’

Cervical spine trauma

Indirect (whiplash)

No symptoms and normal physical findings Investigation and observation after transportation injuries Z04.1 Investigation and observation after other trauma Z04.3

Direct

WAD I, II, III Neck symptoms: as in grade

S13.4

Fracture, dislocation, ligament rupture Morphological diagnosis

WAD

Symtoms

Physical findings

Grade I:

Neck symptoms: pain, subjective stiffness

Normal

Grade II:

Neck symptoms: as in grade Musculoskeletal findings: decreased range of motion, I + possible neurological palpation tenderness symptoms

Grade III:

As in grade II + neurological As in grade II + neurological symptoms findings (e.g. weakened tendon reflexes, decreased muscle strength, decreased sensibility.

Fig. 2 Modified classification of whiplash injuries. This classification differs from the QTF classification in that WAD grade 0 (no symptoms and normal physical findings) and WAD grade IV (fracture, dislocation or ligament rupture) are not part of the classification. Moreover, it is emphasised that the injury should have been caused by indirect trauma to the cervical spine

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according to ICD-10 as ‘‘investigation and observation after transportation injuries, Z04.1’’. If it is not a matter of injury in a motor vehicle accident but another type of trauma, then one should use the diagnosis ‘‘investigation and observation after other trauma, Z04.3’’. On the other hand, fractures and dislocations are very rare after indirect cervical spine trauma. Such injuries are best classified according to established classification symptoms or according to a strict morphological classification, the method most commonly used in clinical work. According to the classification by the Swedish National Board of Health and Welfare, whiplash injury is part of the diagnosis ‘‘distortion of the cervical spine, S13.4’’. Joint efforts are ongoing to evaluate whether whiplash injury can be classified in more specific terms. Acute neurological symptoms are important to note, since these often occur in patients who have been exposed to severe whiplash trauma and can yield information that is important for treatment and prognosis. Neurological symptoms can occur both with and without objective neurological findings at neurological examination. Minor deviations from normal findings at acute clinic evaluation can easily be neglected. By paying close attention to the patient’s own description of his or her symptoms, the risk of important information being missed will probably be reduced. The QTF classification states: ‘‘Symptoms and disorders that can be manifested in all grades include deafness, dizziness, tinnitus, headache, memory loss, dysphagia, and temporomandibular joint pain’’. Our opinion is that the majority of these symptoms are more likely to occur in patients with more pronounced symptomatologies, and not in association with WAD grades 0 and I. For example, acute deafness is rare after whiplash trauma, but in cases where deafness does occur, it is both a symptom and a clinical finding and should thus be classified as WAD grade III. The QTF classification also contains a time axis to indicate the time of classification. Our general impression is that time of classification is not so commonly used in either clinical work or clinical research. The QTF classification was mainly intended for use in acute evaluation and to aid prognostication, which is consistent with our opinion that classification should be made in association with acute management. One should, however, be aware that a classification made shortly after a trauma can be reassessed at follow-up examination one or several days later, since symptomatology and clinical findings can change. A classification made later in the course among patients with long-term problems after whiplash trauma is of very limited clinical value, since a classification made at that time cannot serve as a basis for prognosis or treatment.


Other classifications Radanov et al. [210] presented a classification system based on symptomatology. These authors separated the clinical problems into two syndromes: lower cervical spine syndrome (LCS) and cervicoencephalic syndrome (CES). LCS was characterised by cervical and cervicobrachial problems, while CES was characterised by headache, fatigue, impaired concentration, and visual problems. Gerdle et al. [74] suggested a classification system in which symptoms and clinical findings are based on the anatomical regions considered to be involved as well as on the time course and duration of symptoms. An expansion of the QTF classification system has been suggested [245], in which WAD grade II is divided into three subgroups. This system would require considerable investigation of motor and sensory function, including the determination of pain thresholds for both heat and cold. Furthermore, psychological stress and fear are included in this proposed expanded classification. Such a classification system would probably have advantages when used in clinical research,

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but would require much too detailed investigations to be used in clinical practice; the prognostic value of this expanded classification has not yet been examined. Recently it has been suggested to use the Multidemensional Pain Inventory (MPI) in addition to classification based on medical conditions in order to identify subgroups that differ on the basis of psychological and behavioural factors [241]. Conclusions • The term whiplash is generally accepted and should continue to be used. • To better reflect the trauma mechanism associated with whiplash trauma, the definition should be clarified so that the term whiplash trauma is only used for indirect cervical spine trauma. • By deleting WAD grades 0 and IV from the QTF classification and instead using specific diagnoses for these conditions, the diagnosis of whiplash injury will acquire a more exact and realistic meaning, which will reduce the risks of misunderstanding and overly broad interpretation.

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2 Epidemiology, health economics and sociomedical implications

Epidemiological data regarding whiplash injuries are limited [183]. The most common sources consulted when estimating the number of whiplash injuries are police reports, emergency ward visits at hospitals, and insurance claims regarding such injuries. However, no data compilations are available from these sources. In Sweden, whiplash injuries attracted considerable attention as a result ˚ ke Nygren [184]; this author noted of a doctoral thesis by A that of the 70 000 rear-impact collisions registered per year in Sweden, approximately 10% had led to reports of neck injury and of these, approximately 10% resulted in persistent disability. It has been estimated that 14–42% of whiplash trauma progresses to a chronic WAD and approximately 10% of the patients report constant severe pain [9]. In a study of 586 patients diagnosed with whiplash injury, 7% did not return to work [79]. Whiplash injuries are now one of the most common disabling disorders following traffic accidents in several western countries as shown by insurance statistics [242, 263]

Incidence The incidence of whiplash injuries has been estimated to be 1/1000 people per year in the western world [9], and has increased dramatically over recent decades. In Swedish studies, which mainly refer to emergency ward data, the reported incidence ranges from 1.0 to 3.2/1000, the higher incidence being reported in data from the late 1990s [18, 25, 32, 96, 250]. Bylund and Bjo¨rnstig [32] report a slightly higher incidence among women (1.7/1000) than among men (1.2/1000). Between January 1997 and February 1998, Sterner studied every person (aged 16–64 years) who sought medical treatment at a hospital emergency ward or general practitioner after whiplash trauma associated with a car or bus accident in the city of Umea˚, Sweden [250]. The population in the area in the examined age group amounted

to 80 000 people, and 356 cases fulfilled the criteria for inclusion in the study. The incidence of WAD grades I–III was estimated at 3.2/1000, and no gender differences in incidence were found. Studies in Canada and the USA have found an incidence ranging between 1.0 and 7.0/1000 people [208, 242]. In Suffolk County, New York, the incidence was estimated at 3.6/1 000, based on those visiting hospital emergency wards [8]. In the USA, the incidence was estimated at 3.9/ 1000 in 1992, while in England in 1995–1996 it was 4.2/ 1000.

Prevalence With an incidence of 1/1000, assuming that 25% of patients will experience long-term problems and 10% disabling problems, the prevalence in Sweden over a cumulative 40-year period is 1 and 0.4%, respectively [150]. The reported prevalence of long-term problems after whiplash injury ranges from 14 to 67% according to an overview by Bring [24]. Since definitions of whiplash injury, the inclusion criteria, and what is meant by residual symptoms following injury vary between studies, it is difficult to obtain a clear estimate of the true prevalence.

Prevalence of neck pain in the population The one-month prevalence of neck pain was found to be 41.1% in a Finnish study [176]. One Swedish study reported that 22% of women and 16% of men experience long-term pain, i.e., pain lasting over six months [82]. Another Swedish study demonstrated that 23% of women and 15% of men aged 20–74 years reported experiencing, in the last 12 months, continuous or regularly recurring neck pain lasting at least three months [12].

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Health economics Although the costs to society of whiplash injuries are considerable, they are difficult to calculate because of an almost complete absence of research in the field. Bylund and Bjo¨rnstig [32], however, have estimated the costs related to those injured in traffic accidents in the city of Umea˚ in 1990 and 1991. A total of 275 injured car drivers, 255 of whom were aged 16–64 years, were affected to such a degree that they went to the hospital. Of the 255, 141 had whiplash injuries, and three out of four of those in the group who were on long-term sick leave had a whiplash injury. In 1996 nine members of the original study group were on disability pension as a result of whiplash injury and nine people were still on sick leave, seven as a result of whiplash injury. Trauma researchers have estimated the costs of sick leave and disability pension related to traffic accidents in Umea˚ to be between SEK 8 and 25 million per year. Assuming that whiplash injuries account for 75% of these costs, then such injuries cost SEK 6–19 million per year just for Umea˚. Bjo¨rnstig et al. [18] investigated 139 patients at the emergency ward of Umea˚ University Hospital presenting soft tissue injuries in the neck. Of these injuries, 69% were from traffic accidents and 30 of these led to sick leave; in four of the cases, sick leave lasted for over one year. The median length of sick leave was 31 days at a cost of SEK 422 000; in addition, the costs of related hospital care amounted to SEK 203 000. Despite these precise cost estimates, it is difficult to calculate the total cost. The city of Umea˚ is probably especially affected by whiplash injuries, since two major roads run through central parts of the city. The trauma group in Umea˚ has also found [19] that rear-impact injuries were especially common at traffic light intersections of these major roads. A comparison of the traffic injury situation between the cities of Umea˚ and Hudiksvall, based on health care statistics [33], found that the injury incidence was higher in Umea˚, 93/10 000 inhabitants as compared to 64/10 000 in Hudiksvall. The proportion of injured car drivers with whiplash injuries is 66% in Umea˚ as compared to 18% in Hudiksvall. Such local differences make it difficult to obtain an overview of the national situation. There is also a lack of reliable data regarding the number of people on sick leave and/or disability pension due to whiplash injuries. This is because whiplash injuries are considered a sub-diagnosis of the S13.4 category, distortion in the cervical spine, which encompasses several other injuries. Similarly, T91.8 includes not only late sequels to whiplash injuries but also injuries to the thoracic spine, thoracic cage, spinal cord, and lumbar spine. There are no exact data regarding how many people obtain disability pension based on whiplash injuries that have been

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approved as work-related; thus it is very difficult to calculate these costs reliably. As well, the costs of health care and loss of production are difficult to determine. According to the Quebec Task Force [242], the costs of whiplash injuries were USD 29 billion per year in the USA. Whiplash is the most common injury in motor vehicle accidents and a common cause of long-term disability [44].

Medical insurance aspects In Sweden, whiplash injuries account for approximately 1/3 of all insurance claims made after motor vehicle accidents, and produce a medical disability rate of 10% or more. Between 1989 and 1994 the number of traffic accidents leading to insurance claims increased from 16 to 28% [105]. In Scandinavian countries, the number of people injured in traffic decreased by 50% between 1970 and 1995 (for example from 19.3 to 8.1 killed per 100 000), despite the increase in traffic [65]. Over the same period, statistics from Norway show a doubling in the number of whiplash cases after rear-impact accidents [243]. Mayou [164] investigated three different groups in Oxford, namely whiplash injuries, multiple road traffic injuries involving cars and road traffic injuries involving motorcycles at three different time points—the time of the accident and then three months and twelve months after the accident. The study showed that initial acute stress symptoms were highly predictive of later problems, in terms of both emotional stress and post-traumatic symptoms. The accidents often led to great problems in daily life, considerably reduced activity, and financial problems. The compensation awarded to the injured party was usually lower than one would expect and was often delayed. It often took a long time to obtain financial compensation, which meant that the applicants did not have the awarded money when they needed it the most. In contrast to the common assumption that the motivation to seek financial awards would be high, many of the injured were reluctant to launch legal claims or had difficulties pursuing them in such a way as to obtain maximal financial awards. Compensation for outright financial losses was the most common reason for seeking compensation, but a desire for official, legal recognition of suffering and of a person’s innocence were also cited [164]. Some of those who would probably have been entitled to financial compensation did not seek it because they either could not be bothered to do so or thought it would be too difficult. Some of those who applied for financial compensation accepted small amounts of compensation very early on in the process since they did not want to become involved in protracted and frustrating legal disputes.


In summary, no significant differences in terms of recovery were found between those who did and did not apply for compensation [164]. Moreover, there were no obvious differences between those who had received compensation early on and those who received it only after a longer period. The results indicate that the health complaints of those who had settled their claims improved somewhat, as compared to those who had not, though this could be because those who had settled their claims experienced milder symptoms than did those who had not. Mayou’s prospective study provides new evidence regarding the role of compensation in the prognosis of certain health complaints stemming from car accidents. The findings indicate that the psychological and social consequences of such complaints largely resemble those of other major physical complaints but that specific posttraumatic problems also occur in many cases. Physical complications and psychologically related consequences are often considerable, and daily life may be more affected than was realised, even in the case of minor injuries. The results of this study [164] of a non-selected population differ markedly from those of studies of people involved in legal processes. Notably, many published studies of those who seek compensation after injury are based on a remarkably small and possibly unrepresentative patient sample. The results of such studies thus do not truly reflect the efforts of medical experts and legal advisors on behalf of those who generally seek compensation. Terms such as ‘‘exaggeration’’, ‘‘simulation’’, and ‘‘lying’’ are seldom applicable, even though a small number of people intentionally or unintentionally exaggerate in order to receive higher compensation. Legal proceedings A follow-up of 146 patients with previous soft tissue injuries of the neck associated with motor vehicle accidents was done by Hohl [103], who found that legal circumstances did not influence the proportion who were symptom-free after five years. Of those who received their compensation within six months, a higher proportion became symptom-free than among those whose legal proceedings lasted longer. This could, however, reflect the fact that cases with less severe symptoms and more rapid recoveries could be settled faster. Norris and Watt [181]

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found that legal dispute was associated with more persistent symptoms after whiplash injury, and also that a larger proportion of more severe cases ended up in court. Swartzman et al. [261] compared 41 patients who were in the process of seeking compensation via legal action for whiplash injury with 21 patients whose court hearings had already come to an end. Their study showed that the legal proceedings did not influence pain-related work capacity or psychological stress, but that it did influence the degree of pain experienced. Pain was felt to be more severe, to be distributed throughout more of the body, and to have a more pronounced influence on daily activities than in the case of patients who already had their compensation claims settled. In a cross-sectional study neck trauma patients reported more pain than patients without trauma, but not because of overriding litigation issues [201]. There is a myth, attributed to Miller [172] and accepted by many physicians and lawyers, that many people become ‘‘cured by judicial decision’’ as soon as the compensation process is over. Symptoms and functional impairment are said to disappear and the person can return to work. Mendelson [170], however, has assembled many international studies that show that this is not the case. Even if court proceedings can negatively influence symptoms and functional impairment, the situation when the case is finally settled—often after several years—is clinically and socially stabilised, and usually does not undergo any dramatic change. Conclusions • Epidemiological data concerning whiplash injuries are limited. The reported incidence of whiplash injuries in Sweden varies between studies, ranging from 1.0 to 3.2/ 1000 per year. In the rest of the western world, studies have shown an incidence of between 0.8 and 4.2/1000. • There is an almost complete lack of research into the costs of whiplash injuries. Whiplash injuries account for approximately 1/3 of all insurance claims in Sweden after motor vehicle accidents, with a medical disability rate of 10% or more. • Various studies of how possible insurance compensation may influence the course of whiplash injuries have produced diverging results. Generally, however, there is no evidence indicating any significant difference in the results between those who have applied for such compensation and those who have not.

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3 Pathology

It is largely unknown why certain individuals exposed to whiplash trauma develop pronounced, long-term symptoms. Many explanations have been presented over the years, and the explanation models range from organic injuries of particular structures to psychological and psychosocial explanations. Some authors take account of ethnic and cultural differences as well as differences between medical insurance systems, and regard these factors as having a major influence and as largely explaining the considerable difference in the incidence of whiplash injuries from country to country. Today, most clinicians and researchers in the field seem to agree that many factors can lead to the development of long-term problems after whiplash injury. Psychological and psychiatric symptoms can occur in association with a trauma such as whiplash trauma, and the importance of this for the course after the injury is described in Sect. 5, Psychological and psychiatric aspects (see also Sects. 4 and 7). Pathoanatomic explanations of the symptomatology have often been based on older experimental animal studies, cadaver studies, post-mortem observations, and findings at surgery. However, one should be careful when extrapolating the results of experimental animal and human cadaver studies to the clinical situation. Many factors complicate the evaluation and application of such findings. Not only are there differences between patients in terms of pre-trauma anatomical and physiological condition, but the magnitude and direction of the trauma as well as the exact position of the cervical spine at the moment of trauma are significant for the degree of impact on the various structures of the cervical spine. There is also uncertainty when extrapolating pathological findings at surgery to the initial pathology after whiplash trauma, since only a minority of patients with whiplashassociated disorders undergoes surgery, and that is usually a long time after the trauma. Tissue injuries recorded in post-mortem investigations of people who died as a result of high-energy trauma should

also be evaluated in a critical light when it comes to extrapolating the findings to the situation after indirect cervical spine injury—i.e., whiplash injury—as the injury mechanism is not comparable.

Anatomy The cervical spine consists of seven vertebrae; the two upper vertebrae, the atlas and axis, have special anatomical characteristics (Fig. 3). The vertebrae in the cervical spine are stabilised by several systems of ligaments. In the cervical spine there are eight pairs of spinal nerve roots, C1– C8 (Figs. 4, 5). The anatomical relationships between the nerve roots and the vertebrae and the discs differ between the cervical spine and the lumbar spine. The nerve roots in the cervical spine exit the vertebral column cranial to the pedicle of the vertebra corresponding in number to the nerve root in question. From the first thoracic level and caudally along the whole thoracic and lumbar spine, the nerve roots exit the vertebral column caudal to the pedicle of the vertebrae corresponding in number to the nerve root in question. Movements of the cervical spine include flexion, extension, lateral bending, and rotation. These movements should be tested when examining patients with pain conditions in the cervical spine region. Flexion is tested by investigating how far the patient can, for example, bend the head forward. Usually, patients can bring the chin very close to or into contact with the sternum. Normal rotation is usually close to 90 degrees and lateral bending close to 45 degrees. It is, however, important to remember that all movements of the cervical spine gradually decrease with increasing age [149]. Approximately 50% of the flexion and extension of the cervical spine takes place in the joint between the occiput and C1, and approximately 50% of the rotation occurs at the C1–C2 level.

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Fig. 5 Schematic drawing (transverse section) of the cervical vertebra with adjacent nerve structures

Fig. 3 Schematic lateral view of the cervical spine

Biomechanics Many experimental studies of the motion pattern of the cervical spine associated with simulated whiplash trauma have been performed using various biomechanical test setups (see, for example,110, 193, 194, 197–199]. These studies have shown, for example, that acceleration injury to the cervical spine includes hypertranslation of the head,

which can result in injurious hyperflexion or hyperextension of the craniovertebral region [198]. Panjabi et al. [193) have shown that both the upper and lower cervical spine can be influenced by extension trauma during rear-impact injury; flexion injury is less likely to occur. Other studies have shown that simulated pronounced whiplash trauma can lead to structural injuries of the anterior longitudinal ligament [109] and facet joint injuries [197]. Grauer et al. [80] have also shown that during whiplash trauma the neck assumes an S-shaped curvature, with hyperextension in the lower part of the cervical spine and function in the upper part of the cervical spine.

Pathoanatomy Intervertebral discs

Fig. 4 Schematic view of the cervical spine seen from behind. The laminae have been removed in the drawing in order to visualise the nerve roots and spinal cord

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Cervical spondylosis occurs commonly in the population, including in the age group usually exposed to whiplash trauma. MRI examination of the cervical spine can reveal pronounced degenerative changes, even in healthy individuals without any neck problems [21]. Prospective studies of patients with whiplash-associated disorders, compared with age-matched controls, are lacking, which means that it is difficult to evaluate whether the radiological changes diagnosed in patients with whiplash are part of the normal development of spondylosis or are a result of the cervical spine trauma. Watkinson et al. [283] reported, in a study using plain x-ray examination, an increased occurrence of degenerative changes in patients with residual symptoms ten years after whiplash trauma. Injuries of the annulus fibrosus and the attachment of the disc to the endplate have been reported from animal experimental studies [143, 286] and after hyperextension trauma in cadavers [42]. Disc herniation and also injuries of the anterior part of the annulus were reported in a small MRI study of nine patients with whiplash [52]. A prospective


MRI study of patients presenting WAD grades II and III, without a control group, showed that patients with residual symptoms after trauma displayed a higher degree of pathological changes in the disc than did the symptom- free group [203]. In contrast to these studies, a prospective MRI study of 100 patients found that in no case did whiplash trauma cause disc injury [223]. A recently published experimental study of cadaver cervical spine specimens shows that whiplash trauma can influence discs, as forces are exerted in whiplash conditions that exceed the levels of mechanical loading that exist during physiological movement in the cervical spine [194). In summary, experimental studies have shown that there are prerequisites for disc injuries in association with whiplash trauma; however, there is a lack of scientific documentation that verifies the existence of such disc injury in humans. The incidence of disc involvement in whiplash injuries is unknown, as is the importance of any such influence for the development of long-term symptoms.

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detectable instability. The ligamentum flavum is a very elastic structure that requires pronounced trauma in order to rupture. It is very seldom that a whiplash trauma develops the force needed for such a rupture (ruptures of the ligamentum flavum can be diagnosed using MRI). The clinical significance of injuries of the interspinal ligament can be discussed, since these structures only constitute a thin fascia separating the neck musculature on the right side from that of the left [217]. Injuries of the alar ligaments and the possibility of diagnosing such ligament injuries have been discussed recently; this is described in the section examining the use of radiological methods in diagnosing whiplash injuries (Sect. 10). In conclusion, it is very rare that ligament injuries can be detected in the acute phase after whiplash trauma; it is also rare for such injuries to display radiologically detectable instability later in their course. It is not known whether segmental dysfunction develops and contributes to the symptomatology in patients with long-term problems.

Facet joints Ligaments Injuries of the anterior longitudinal ligament have been described in experimental studies in animals and human cadaver specimens [109, 156, 293]. Ivancic et al. [109] recently presented an experimental study in which whiplash trauma was simulated in an experimental model of the cervical spine. The elongation of the anterior longitudinal ligament was recorded during physiological loading at four different acceleration speeds. The results show that the elongation of the ligament was dependent on the strength of the acceleration, and that it was most pronounced in the lower parts of the cervical spine. Inspection of the specimens after the experiments showed ruptures of the anterior longitudinal ligament at four of the 30 investigated levels. Injuries of the posterior longitudinal ligament have been observed in older animal experimental studies [286] and in cadaver studies [42]. An experimental study of indirect trauma to the neck found an increased elongation (strain) of the interspinal ligaments and ligamentum flavum as compared to conditions during physiological movement, but no significant effects on the posterior longitudinal ligament [193). No clinical reports exist of injuries of the posterior longitudinal ligament or the ligamentum flavum. Prospective studies using MRI have not found any ligament injuries [22, 203, 223]. Perhaps the experimental results of clinical studies cannot be verified using MRI because the experimental trauma models involve a type of trauma that seldom or never occurs in patients with whiplash, or because the described ligament elongations, if they do occur in whiplash patients, lead to no radiologically

The facet joints have long been regarded as affected by whiplash trauma, and thus have been considered as one source of persistent complaints. This opinion has previously mainly been based on older experimental studies [42, 143, 286]. One study often cited as a reference in this regard is a post-mortem study of individuals who died after high-energy trauma associated with motor vehicle accidents (Jońsson et al 116]. It is not possible to draw any conclusions from that study regarding the pathology in whiplash trauma, since the individuals examined are not comparable with patients with whiplash injuries. However, the study has one important finding that also applies to patients with whiplash injury, namely, that soft tissue injuries around the facet joints, such as facet capsule injury, are difficult to diagnose using plain x-ray and CT. On the other hand, articular process fractures and the dislocation/ subluxation of facet joints are easily detected, especially using CT. With MRI, an increased amount of fluid in a facet joint can be revealed but the cause of such increased fluid is difficult to determine. Fletcher et al. [69] also pointed out the difficulties of using plain radiological methods to verify minor musculoskeletal injuries in the cervical spine after cervical spine trauma. MRI examinations of patients with acute whiplash injury have not found any posttraumatic changes in the facet joints [22, 203, 223]. Recent experimental studies have indicated that whiplash trauma can lead to compression of facet joints [50, 197, 294] and stretching of the facet joint capsule [197]. Based on these experimental studies, a hypothesis has

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been presented that the facet joints, together with the surrounding soft tissues (which contain many nociceptive nerve endings), could be injured in connection with whiplash trauma and thus be a source of pain [50, 155, 294]. There are only a few clinical studies of facet joint pathology in whiplash injury [9, 152, 153]. These investigations have examined patients with persistent complaints after whiplash trauma, in which either the innervation of the facet joints was blocked or the neck pain was treated with intra-articular cortisone injections and percutaneous radiofrequency neurotomy. The authors determined that approximately half of the patients under study had facet joint-related neck pain. Treatment with percutaneous radiofrequency neurotomy had an effect on the neck pain while cortisone injections did not. In conclusion, recently published experimental studies indicate that whiplash trauma can place such a load on the facet joints as to supply the prerequisites for injuries of the various joint structures. However, there is a lack of scientific evidence confirming that whiplash trauma actually does lead to facet joint injury in humans. There is also limited documentation of the possible role of the facet joints as a source of pain in patients with long-term neck complaints.

Central nervous system Animal experimental studies have demonstrated injuries/ dysfunction in various parts of the central and peripheral nervous systems after cervical spine trauma [58, 115, 260, 272]. As emphasised earlier in this review of the pathology in whiplash injuries, there is uncertainty when it comes to extrapolating animal experimental results to the conditions present in motor vehicle accidents that produce whiplash trauma in humans. Older EEG studies of humans reported EEG changes [75, 267]; however, a later study could find no such changes [112]. Nowadays, EEG is not regarded as meaningful in the evaluation of patients with whiplash injury. Several studies have shown that impaired voluntary eye movements may occur in the acute phase as well as among patients with persistent complaints after whiplash trauma [77, 93, 98, 100, 207]. The causes of these changes could be multiple, but in some patients the results were interpreted as indicating brain stem dysfunction. Mosimann et al. [174] interpreted their results as representing frontal or prefrontal changes and not as brain stem injury. A recent prospective study of 40 patients with whiplash (WAD grades II and III) described two patients with pronounced deviations in voluntary eye movements and brain stem audiometry. The findings in these patients were determined to be caused by impairment in the brain and in the brain

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stem [284]. Decreased vibration and temperature sensitivity in the skin innervated by the trigeminal nerve has been reported in patients with long-term complaints after whiplash trauma [128]. A prospective study with a longterm follow-up showed that certain patients displayed pronounced changes even soon after the trauma, changes that persisted at long-term follow-up [249). There may be several explanations for these results, and one possibility that the authors discussed was central dysfunction among patients with the most pronounced changes. Studies using positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in patients with long-term complaints after whiplash injury have found parieto-occipital hypoperfusion [188–191]. However, Bicik et al. [16] found no correlation between abnormal PET or SPECT findings and either cognitive symptoms or metabolic changes, and concluded that such examinations were of no diagnostic value for the individual patient. A study was recently presented in which the concentration of nerve injury markers was analysed in the cerebrospinal fluid in acute cervical spine injuries [83]. Three of 17 patients with whiplash (WAD grade III) displayed an increased concentration of neurofilament protein (NFL), which indicates that an axonal injury may exist. Dissection in vertebral and carotid arteries is uncommon, but even so is among the most common causes of stroke among young people [10]. This condition has mainly been recognised in the last decade, when non-invasive diagnostic methods such as MRI and CT angiography have become commonly available. The incidence of cervical vascular dissection after whiplash trauma is not known. It is known, however, that minor, indirect neck trauma, for example, neck manipulation treatment, is a common cause of vertebral artery dissection [10, 63, 182]. The symptoms of vertebral artery dissection are neck pain and signs of ischemia in the posterior cranial fossa. Neurological symptoms and signs may be absent [146]. There is no clear-cut scientific documentation showing that whiplash trauma can lead to injuries to the nervous system, but some recent studies indicate that dysfunction/ injuries can exist in a small proportion of patients who have sustained pronounced whiplash trauma. Additional research is required to verify this and to clarify what structures may be involved as well as the incidence and typical symptoms, and their importance for the development of long-term complaints.

Muscles Older animal experimental studies found evidence of muscle injuries [156, 286], while later experimental studies could not verify such findings [260]. Ultrasound


examination of patients with whiplash has identified muscle injuries, while MRI examination has shown no signs of muscle rupture [22, 203, 223]. MRI studies support the clinical experience that pronounced muscle injuries after whiplash injury are uncommon, and that such injuries do not significantly contribute to persistent symptoms. Conclusions • It is uncommon that ligament injuries can be detected in the acute phase after whiplash trauma, and it is

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uncommon for radiologically verified instability to present later in the course. • Experimental studies have shown that whiplash trauma can lead to a degree of loading of the discs and facet joints that could result in injuries to these structures. However, there is a lack of scientific documentation verifying such injuries in patients with whiplash injury. • Certain studies indicate that nervous system dysfunction can exist in a minority of patients with whiplash injury.

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4 Pain mechanisms

A review of the literature reveals that pain defined as acute can vary in duration, but a pain state defined as long-term generally persists for six months or more. The duration of an acute pain state depends to some extent on the degree of tissue injury, but other mechanisms, such as peripheral and central sensitisation as well as psychological mechanisms, have been discussed [49, 130]. Acute stiffness in the musculature is a prominent symptom, probably resulting from contraction of and tension in the musculature, or from minor bleeding. It is reasonable to assume that direct muscle injuries usually heal within a few weeks. Mechanisms other than mechanical factors are likely of importance in acute pain. A prospective study of early whiplash injuries found an increase in the concentration of pro- as well as anti-inflammatory cytokines from mononuclear cells in the blood [126]. However, such changes were not different from those seen in patients with acute ankle strains. Recently, altered cerebral blood flow has been found in patients with chronic neck pain but not in whiplash patients [84, 258]. These observations may indicate that, to some extent, different pain mechanisms might be involved in patients with chronic neck pain of non-traumatic origin compared to whiplash-related neck pain. Since it is difficult, in acute and long-term pain conditions, to explain the pain from the standpoint of traditional classification (i.e., as nociceptive or neurogenic), it is important to understand the pathophysiological mechanisms that affect pain intensity, distribution of pain, and the emotional experience. Notably, it is difficult to find mention in the literature of pathophysiological mechanisms for the development of long-term pain specific to whiplash injury, but changes in the pain transmission do occur soon after a whiplash injury [7, 244]. The discussion below is thus not specific to whiplash injuries, but is generally applicable to long-term musculoskeletal pain conditions.

How does the nervous system react to acute tissue injury? Peripheral pain mechanisms Pain intensity is dependent on the degree of tissue injury, and on the intensity of the inflammatory response that occurs via the cascade of reactions associated with acute injury. Pain intensity and distribution are not only dependent on inflammation, impaired blood circulation, and muscle contraction; the experience of increased pain is also affected by the considerable plasticity of the peripheral nervous system, and its ability to transmit pain, which may alter the impulse in the central nervous system (CNS) both acutely and in the long term [49, 130]. Most tissues are innervated by A delta fibres (type III in muscle tissue) and the thinner C fibres (type IV). Some of the A delta fibres in muscle tissue, the ‘ergo receptors’, are activated during strong muscle contraction; this signals physiological muscle activity and, with longer-term stimulation, can either cause the release of endorphins or give rise to pain. Some C fibres, the polymodal receptors, can be activated by various painful stimuli, such as heat, pressure, and chemical substances released during inflammation. These polymodal receptors have such a high threshold that the literature refers to them as ‘‘silent fibres’’ [232]. These fibres are one factor explaining why pain can occur and be experienced as more intense in inflamed than in non-inflamed tissue. In some structures, for example the knee joint, animal experiments have shown that up to 75% of the C fibres consist of ‘silent fibres’ under normal conditions [232]. A number of substances that are released, either in association with tissue injury or other peripheral nervous system activation, can increase the sensitivity of the pain nerve system as a whole. Among these substances, prostaglandins, which are produced in classic inflammation, play a role; as well, there are several other substances, such as bradykinin,

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potassium ions, serotonin, and a large group of cytokines which all make pain nerves more sensitive to stimulation [11, 41, 102, 296]. Nerves may be stimulated directly or these substances can release other pain-producing (algogenic) substances. When nociceptive nerve fibres are stimulated, i.e., an individual feels pain, the nerve itself produces small proteins called peptides. These peptides are produced in the cell nucleus and transported out to the tissue (e.g., muscle, skin, or in a joint), via axonal transport systems (see Fig. 6). Two important peptides that can increase sensitivity in the nerve are substance P (SP) and calcitonin gene-related peptide (CGRP) [147]. SP increases blood flow in the area both directly and through the release of histamine from mast cells, but it also causes swelling. CGRP causes a marked increase in blood flow by dilating the thinnest arteries. The release of SP and CGRP leads to an inflammatory-like reaction, but without the presence of prostaglandins, so regular anti-inflammatory drugs have little or no effect. Another group of substances that sensitises pain nerves, making them more sensitive to stimuli, are the cytokines. Of these, it is primarily TNF-alpha, the interleukins (especially IL-1 and IL-6), and the nerve growth factors (NGF) that are released during inflammation. The substances are released from immune cells, fibroblasts, vascular endothelial cells, and nerve cells, which all sensitise C fibres, leading to increased pain. In addition, the production of bradykinin, prostaglandin, SP, CGRP, and noradrenaline is activated, and this may also have a sensitising effect on pain nerves. If pain nerves are injured or compressed, they can become more sensitive to cytokines. Under musculoskeletal pain conditions, an increased concentration of cytokines in the blood has been demonstrated

Fig. 6 Schematic drawing of peripheral and central sensitisation that can occur in association with tissue injury

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[78, 126]. Studies on animals and humans have found that changes occur within the nervous system as a result of the stimuli to which it is subjected; in other words, the nervous system—peripheral as well as central—displays considerable plasticity [43, 95, 291]. Since acute pain gives rise to physiological reactions, it is an important warning signal that should not be ignored. If the muscle response persists for a long time, the acute pain will probably be sustained longer than necessary through the mechanisms mentioned above. One study showed that patients with whiplash injury who reported high pain intensity and disability, i.e., inability to maintain normal activity directly after the injury, displayed signs of decreased pain thresholds for local pressure as a result of peripheral sensitisation [246]. It is not known how intensive or prolonged a nociceptive influx must be in an acute pain state to result in long-term pain and sensitisation. The mechanical causes underlying the occurrence of long-term pain after whiplash trauma are probably less important than the physiological changes in the nervous system are. All acute pain states are accompanied, not only by physiological pain, but also by autonomic nervous system and emotional reactions (see Sect. 6).

Central pain mechanisms Long-term pain differs considerably from acute pain from a mechanism-based perspective. Acute pain is characterised mainly by nociceptive pain, while long-term pain associated with whiplash can be classified as neuropathic, idiopathic (of unknown cause), nociceptive, or a combination of these. In all these pain states, it is important to


bear in mind that there is a continuum from the acute phase to conditions that develop after several years, with all the psychological factors that affect the pain experience in such situations. A common denominator of many patient groups experiencing long-term pain is that one cannot, using current methods, demonstrate any injury or inflammation in peripheral tissue by clinical examination or laboratory testing. In recent years, research into pain mechanisms has focused on the CNS [291]. Animal experiments and human studies have shown that if pain occurs in peripheral tissue, for example, muscle, joint, or intervertebral discs, short- as well as long-term central changes will occur [231]. Such changes are referred to as central sensitisation and central hyperexitability. This has been found in patients with, for example, long-term low back pain [76]. The peripheral sensitisation described above leads in various ways to the altered perception of pain in the CNS by affecting protein synthesis; this in turn results in the alteration of receptors and transmitter substances. This can lead to increased sensitivity to pain stimulation, hyperalgesia, pain in association with non-painful stimulation, allodynia, and the perception of touch as unpleasant (dysesthesia). A receptor of primary importance in central sensitisation is the N-methyl-D asparat (NMDA) receptor. By activating the NMDA receptors, a pain impulse from the periphery can increase in amplitude and duration (in the wind-up mechanism) and release cykoloxygenase-2 (COX-2); this increases sensitivity to pain stimuli, not only locally at the site of pain, but in the whole spinal cord [38, 56]. The CNS consists of approximately 75% supporting or glia cells. These cells were previously regarded merely as supporting cells, without any nervous activity of their own. However, recent studies have shown that these cells centrally release SP and CGRP [108]. This, together with NMDA receptor activation, COX-2 production, an increase in the number of pain receptors, and decreased pain inhibition, will cause pain to increase. It can also cause pain to spread outside the area of injury, increase the intensity of pain impulses, and cause non-painful stimuli to be felt as painful. In patients with long-term neck pain, it has been shown that, for example, an injection of hypertonic saline is experienced as more painful, both in terms of intensity and distribution, than in healthy controls. The patients also demonstrated increased sensitivity to pain in other parts of the body, quite distinct from the originally painful area [145]. This can be noted in patients with whiplash, and also in patients with other long-term pain states, such as pain in neck muscles after mechanical loading or temporomandibular joint pain [48, 246]. ‘‘Long-term potentiation’’ is the term used to refer to the plastic changes that occur over time in an unresolved pain state. The NMDA receptor and its

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importance for the occurrence of long-term pain is known, and studies have been performed to determine how this receptor is modulated. An important factor is the endogenic pain inhibition activated by pain in ‘‘pain healthy’’ individuals. This inhibition is decreased in patients with longterm pain. The mechanisms underlying the decreased inhibition are regarded as multifactorial, but are probably not related to the onset of the pain [131, 274]. One reason may be the decreased production of inhibiting substances, such as gamma-amino-butyric acid (GABA) and endorphins. Sensory as well as emotional aspects of pain are transmitted to the brain stem and the brain via several ascending tract systems. Today, there is considerable knowledge of how pain and pain inhibition interact via a network of nerve tracts and that can alter the pain impulse through emotional influence, motivation, and previous experience. The placebo effect decreases pain by the release of endogenous uploads, endorphins in several areas involved in the ‘‘pain network’’ of the brain, for example, the anterior singular cortex (ACC), thalamus, and periaqueductal grey substance (PAG) [202]. All long-term pain due to injury of the nervous system, muscles, or skeleton, as well as pain of unknown cause, is most likely able to modify the pain experience itself, via central mechanisms not specifically related to the initial injury mechanism [7, 48]. In a recent study it has also become evident that genetic factors may predispose for the development of long-standing pain in humans [262]

Other mechanisms of importance for experience and intensity of pain sensation During long-term muscular tension, sensitisation of the nervous system as well as increased muscle spindle activity can be noted. This increased activity can give rise to reflex responses, which in turn result in muscle pain and ischemia, which has been proposed as an additional possible mechanism for pain after whiplash trauma [264]. Conclusions • Several physiological changes occur in both the peripheral and the central nervous systems in acute and long-term pain associated with whiplash injury. • Peripheral sensitisation is characterised by the release of pain-producing substances, such as prostaglandins, bradykinins, cytokines, and substance P. • Central sensitisation is characterised by the activation of the NMDA receptor, decreased production of endogenous opioids, production of pain-producing substances in the spinal cord and in the brain, and activation of a neuronal network that increases the pain impulse. This

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leads to an experience of increased pain in terms of intensity and distribution. • There is no scientific evidence indicating that these physiological changes and/or psychological reactions are

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specific to pain in whiplash injury. Similar changes have been shown to exist in several other pain states, both acute and long-term.


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5 Psychological and psychiatric aspects

Both the QTF classification system [242] and the Swedish National Board of Health and Welfare’s 1997 version of the ICD-10 system for classifying diseases and health problems [282] define whiplash injury without considering related psychiatric symptoms, despite the fact that several studies report their presence [163, 209]. This is remarkable, since one of the most common symptoms associated with whiplash injury is pain. The multidimensional nature of pain leads to both psychological (affective and cognitive dimensions) and physiological (sensory dimensions) reactions. According to Eisenberger et al. [64], both emotional and physical pain are processed in the brain in similar ways. This corresponds well with how pain is defined by the International Association for the Study of Pain (IASP), namely: ‘‘Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Pain is always subjective and can occur in the absence of tissue injury.’’ Psychological and psychiatric symptoms possibly associated with whiplash trauma can, based on clinical course, symptom profile, causation, and degree of complication, be classified as follows: • Psychological and/or psychiatric symptoms as a result of traffic accident • Psychological and/or psychiatric symptoms in reaction to acute pain • Complications and/or the co-existence of psychiatric and somatic conditions with trauma-related syndromes, such as acute stress disorder (ASD) and/or post-traumatic stress disorder (PTSD). The psychological and/or psychiatric symptoms that may occur in association with whiplash trauma should be diagnosed separately according to available diagnostic systems (ICD-10 or DSM-IV). We have chosen to use the ICD-10 classification system, except for the diagnosis of acute stress disorder, which is described only in the DSM-

IV system (DSM-IV-TR 2000). However, it is important to emphasise that irrespective of which diagnostic system is used, none of the described psychological or psychiatric symptoms exists only among patients with whiplash injury.

Psychological and/or psychiatric symptoms as a result of traffic accident After a traffic accident experienced as traumatic, individuals can experience a stress-related reaction/condition that persists for 2–3 days (acute stress reaction) and/or 2 days– 4 weeks (acute stress disorder) (see Table 1). Stressrelated symptoms can emerge within 1–3 months or more of the traumatic event and can persist for 3 months (acute posttraumatic disorder) or longer (chronic post-traumatic disorder) (Table 2). Psychological and/or psychiatric reactions after traffic accidents The psychological and/or psychiatric reaction to a traumatic event depends on the type, intensity, and duration of the trauma as well as on the interpretation of the trauma by the individual. Moreover, the personality of the individual and the ability of the individual to cope with the trauma also play a significant role. Traumatic events may imply a perceived threat of impairment or loss of several basic needs of the individual. The DSM-IV psychiatric diagnostic manual (DSM-IV-TR 2000) defines a traumatic event (Table 3) in terms of both its objective qualities and certain qualities of the stress response it elicits. According to ICD-10, reaction to pronounced stress is classified in diagnosis category F43 and is described as follows: ‘‘This category [F43] is different from others since it includes disturbances that are characterised not only

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Table 1 Diagnostic criteria for Acute Stress Disorder (ASD) according to DSM-IV (Mini-D IV 2000)

Table 2 Diagnostic criteria for Post-Traumatic Stress Disorder (PTSD) according to DSM-IV (Mini-D IV 2000)

A The person has been exposed to a traumatic event in which both of the following were present:

A The person has been exposed to a traumatic event in which both of the following were present:

1) The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others

The person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others

2) The person’s response involved intense fear, helplessness, or horror. B Either while experiencing or after experiencing the distressing event, the individual has three (or more) of the following dissociative symptoms: 1) a subjective sense of numbing, detachment, or absence of emotional responsiveness 2) A reduction in awareness of his or her surroundings (e.g., ‘‘being in a daze’’) 3) Derealisation 4) Depersonalisation 5) Dissociative amnesia (i.e., inability to recall an important aspect of the trauma). C The traumatic event is persistently re-experienced in at least one of the following ways: recurrent images, thoughts, dreams, illusions, flashback episodes, or a sense of reliving the experience; or distress on exposure to reminders of the traumatic event. D Marked avoidance of stimuli that arouse recollections of the trauma (e.g., thoughts, feelings, conversations, activities, places, people). E Marked symptoms of anxiety or increased arousal (e.g., difficulty sleeping, irritability, poor concentration, hypervigilance, exaggerated startle response, motor restlessness). F The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or impairs the individual’s ability to pursue some necessary task, such as obtaining necessary assistance or mobilising personal resources by telling family members about the traumatic experience. G The disturbance lasts for a minimum of 2 days and a maximum of 4 weeks and occurs within 4 weeks of the traumatic event. H The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition, is not better accounted for by Brief Psychotic Disorder, and is not merely an exacerbation of a pre-existing Axis I or Axis II disorder.

The person’s response involved intense fear, helplessness, or horror. Note: in children, this may be expressed instead by disorganised or agitated behaviour. B The traumatic event is persistently re-experienced in one (or more) of the following ways: Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions.Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed. Recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognisable content. Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated). Note: in young children, traumaspecific re-enactment may occur. Intense psychological distress at exposure to internal or external cues that symbolise or resemble an aspect of the traumatic event Physiological reactivity on exposure to internal or external cues that symbolise or resemble an aspect of the traumatic event. C Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following: Efforts to avoid thoughts, feelings, or conversations associated with the trauma Efforts to avoid activities, places, or people that arouse recollections of the trauma Inability to recall an important aspect of the trauma Markedly diminished interest or participation in significant activities Feeling of detachment or estrangement from others Restricted range of affect (e.g., unable to have loving feelings) Sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span). D Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following: Difficulty falling or staying asleep Irritability or outbursts of anger Difficulty concentrating

by symptom and course, but also by causative factor: an exceptionally traumatic event that gives rise to, for example, acute stress reactions.’’ Acute stress reactions (F43.0 according to ICD-10) The necessary diagnostic criteria are that the person must have been exposed to a traumatic event, and the symptoms should occur in association with the event (within hours). Moreover, there should be symptoms indicating tension as well as mixed symptoms initially comprising confusion, decreased ability to perceive stimuli, and disorientation. This phase can either be followed by further withdrawal

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Hypervigilance Exaggerated startle response. E Duration of the disturbance (symptoms in criteria B, C, and D) is more than 1 month. F The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Specify if: Acute: if duration of symptoms is less than 3 months Chronic: if duration of symptoms is 3 months or more Specify if: With delayed onset: if onset of symptoms is at least 6 months after the stressor


Table 3 Definitions according to DSM-IV (Mini-D IV 2000) Traumatic incident The person has been exposed to a traumatic event in which both of the following were present: the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others the person’s response involved intense fear, helplessness, or horror. Note: in children, this may be expressed instead by disorganised or agitated behaviour. Dissociation

Disturbance of the commonly integrated functions of consciousness, memory, identity, or perception of one’s surroundings. The disturbance can occur gradually or acutely, and can be transient or persistent.

from the person’s surroundings and situation or by agitation and overactivity. Symptoms usually disappear within 2–3 days (often within hours) Short.term depressive reaction (F43.2 according to ICD10) This transient depressive condition is characterised by a duration not exceeding one month Mixed anxiety and depressive reaction (F43.22 according to ICD-10) Symptoms of both anxiety and depression are pronounced, but are not serious enough to justify diagnoses such as mixed anxiety and depressive conditions (F41.2) or other mixed anxiety conditions (F41.3).

Psychiatric syndromes after traffic accidents Several studies indicate an increased occurrence of PTSD among people who have experienced a car accident. Some studies show that the combination of serious traffic accident and the occurrence of ASD, depression, or anxiety can accelerate the development of PTSD [72, 140, 273]. Several studies have independently arrived at fairly similar results regarding the existence of PTSD (10–30%) within 1 year of a car accident [20, 26, 66, 97, 163); a similar prevalence has also been described for whiplash injuries [165, 166]. ASD and PTSD both involved significant changes in several neurobiological systems involved in coping and adaptation mechanisms, for example, the catecholamine, serotonin, dopamine, and endogenous opioid systems, the limbic systems, thyroid hormone, the sympato-adrenomedullary (SAS) system, and the cortisone/hypothalamicpituitary-adrenergical (HPA) axis [59, 167].

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Acute stress disorder (ASD: 308.3 according to DSM-IV) For a diagnosis of ASD, the individual must have been exposed to a traumatic event according to DSM-IV, and the onset of symptoms must occur within between 2 days and 4 weeks of the event and persist for between 2 days and 4 weeks. The diagnosis of ASD is based on 4 groups of symptoms: dissociative symptoms (Table 3), recurrent relapse of the traumatic event, avoidance of stimuli associated with trauma, and symptoms indicating psychological tension. Existence of at least three dissociative symptoms (Table 1) during or after the traumatic event and recurrent intensive relapse of the traumatic event are necessary for the ASD diagnosis. For the exact diagnostic criteria of ASD, see Table 1. Post-traumatic stress disorder (PTSD: 309.81 according to DSM-IV and F43.1 according to ICD-10) The remaining condition that may follow ASD and that may occur after an individual has been exposed to a traumatic event, if the symptoms (according to Table 2) occur within 1–3 months, is called acute PTSD. The diagnostic criteria, which are similar in both ICD-10 and DSM-IV, are that the individual has been exposed to a traumatic event, experiences recurrent intense relapse of the traumatic event (e.g., memory images, nightmares, and flashbacks of the experience), avoids stimuli associated with trauma (e.g., avoids particular thoughts and places and displays memory deficit, indifference, estrangement, and restricted affective behaviour), and experiences persistent symptoms of increased arousal (e.g., irritability, sleeping problems, vigilance, concentration difficulties, and exaggerated startled response). For the exact diagnostic criteria of PTSD, see Table 2. According to Sterling and colleagues [247] higher initial post-traumatic stress symptom scores measured by Impact of Events Scale remained significant predictors of poor outcome at long-term follow-up (2–3 years postaccident).

Psychological and/or psychiatric symptoms as a reaction to acute pain Psychological symptoms in association with acute pain The experience of acute pain negatively influences attentiveness and memory. This in turn is associated with altered activity in the ACC (anterior cingulate cortex) area (Fig. 6) [202]. The ventral and dorsal aspects of the ACC area represent integration or affective [55] and cognitive pain components, respectively [31], according to MRT studies.

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The results of several neuropsychological studies of patients with whiplash injury have shown cognitive dysfunction in terms of impairment of memory, concentration, and attention. In a meta-analysis, Kessels et al. [125] examine the results of 22 studies of patients with whiplash injury, in which the patients were examined 1 week and 6 months after the injury. Decreased performance was recorded in several tests conducted one week after the injury [57, 211, 214]. In one of these three studies, a control group comprising healthy individuals was included, and examination after 6 months revealed a difference between the experimental and control groups (p \ 0.04) regarding attentiveness [214]. The test results are discussed in relation to data in the literature regarding ‘‘the effect of cerebral dysfunction, simulation, painrelated factors, importance of coping strategies and PTSD’’ [125]. Two studies analyse the connection between neuropsychological functions and SPECT (Single Photon Emission Computed Tomography) in order to identify cerebral perfusion disturbances associated with whiplash injury characterised by long-term problems [151, 216]. The results are inconclusive, and additional study is required to allow conclusive interpretation of these phenomena. Similar neuropsychological dysfunctions associated with whiplash injury (e.g., impairment of memory, concentration, and attentiveness) have also been reported as associated with other conditions, for example, PTSD [271], depression [1, 205], sleep impairment [62], and anxiety [295], and associated with the use of certain pharmacological agents [175]. Since such conditions can occur concurrently with a whiplash injury, it is important to conduct differential diagnosis.


Increased prevalence of depression among patients with pain is a well-known clinical phenomenon [4] that still lacks both full scientific explanation and treatment guidelines. According to recent neurobiological theory, depression and pain follow the same descending nerve tracts in the CNS. The central pain-modulating system can both decrease and increase nociceptive signals. Both serotonin and noradrenalin can decrease peripheral nociceptive signals. In association with depression, the level of both these neurotransmitters decreases, which can lead to a lack of inhibitory effect. An increased frequency of depressive symptoms has been described among patients with whiplash injury [220, 285]. According to Holm and colleagues [107] patients with WAD who report early depressive symptoms and more severe neck injury symptoms are at risk of developing widespread pain after motor vehicle collision.

Complications and/or co-existence of psychiatric and somatic conditions with trauma-related disorders such as ASD and PTSD The clinical picture of psychiatric symptoms associated with acute whiplash injury can comprise several components, namely, reaction to the traumatic event, reaction to pain, and reaction to somatic conditions/whiplash injuries. Such symptoms are also fairly commonly found alongside trauma-related disorders (ASD and PTSD), other psychiatric conditions (e.g., depression, anxiety, drug abuse, and psychosomatic symptoms) [3], and somatic symptoms [168]. If the background to the psychiatric symptom picture associated with the whiplash injury is suspected to be complex, referral for psychiatric consultation is recommended.

Psychiatric symptoms/disorders associated with acute pain Sleep impairment symptoms, such as tiredness, irritability, and tension are common in patients with whiplash injuries [233]. Sleep impairment also often occurs in association with PTSD [91], depression, anxiety [111], and acute and long-term pain [222]. Since these conditions can occur concurrently with whiplash injury, it is important that possible sleep impairment be diagnosed and adequately treated so as not to exacerbate the extent of the whiplash injury problems. Anxiety accompanied by symptoms of uneasiness, memory and concentration problems, intense fear or uneasiness when driving, and avoidance of driving is common in patients with whiplash injury [216]. According to Mayou and Bryant [165], up to 19% of patients with whiplash injury develop traffic phobia within one year of the traffic accident.

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Research into psychological and psychiatric aspects More research into the psychological and psychiatric symptoms associated with whiplash injury is needed. Welldesigned studies would be useful to better identify and clarify prognostic psychosocial factors as well as the occurrence and course of psychological and psychiatric symptoms. Conclusions • It is likely that any previous mental ill-health and the patient’s current mental state are both relevant to the development and course of symptoms associated with whiplash injury. It is therefore important to gather information about previous conditions and examine the patient’s current mental health so as to exclude or diagnose the possible occurrence of psychiatric symptoms or disorders.


• To minimise the risk of long-term problems in people with acute whiplash injury, concurrently occurring ASD and/or PTSD should be diagnosed and treated. Psychiatric consultation is recommended in difficult and/or complicated cases. • It is important to diagnose and adequately treat possible sleep impairment, depression, or anxiety in people

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with whiplash injury. In cases involving complications and/ or the co-existence of psychiatric and somatic conditions with trauma-related disorders such as ASD and PTSD, psychiatric consultation is recommended.

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6 Symptoms and signs in the early phase

The diagnosis of whiplash injury, like the diagnosis of any other condition, is made on the basis of medical history and clinical examination. There are no ‘‘specific’’, ‘‘typical’’, or ‘‘characteristic’’ symptoms or signs indicating that a person has a whiplash injury; diagnosis is instead based on how symptoms and signs develop temporally in relation to a whiplash trauma.

Neck symptoms Neck symptoms in terms of pain and stiffness are the most important and common symptoms associated with whiplash injuries (Table 4). Pain can radiate from the neck to the posterior parts of the head and down to the shoulder regions. The pain may also spread to the temporal regions and towards the forehead, and is often increased by neck motion. In patients with relatively minor problems, pain may occur only at the endpoints of the range of motion, but in those with severe problems, neck motion may be considerably restricted because of pain but also due to stiffness. Neck pain often occurs soon after a whiplash trauma, while stiffness can occur later [242]. A Swedish study found that pain occurred within 5 hours among 82% of whiplash trauma patients [99]. Within a few days of a whiplash trauma, neck pain occurs in almost all patients with a whiplash injury. However, in some cases the patient may suffer from a general shock reaction, while in others competing injuries may have occurred. In such situations, neck symptoms may not be noted until later. Neck symptoms in the acute phase of a whiplash injury may exist without objective findings during clinical examination (WAD grade I). Tenderness at palpation over muscle attachments and over muscles in the cervical spine and in the shoulder regions is common (WAD grade II). Tenderness over the spinous processes in the cervical spine

and between these structures can also occur. Neck pain is often accompanied by stiffness and restricted range of neck motion, which should be examined in terms of flexion/ extension, lateral bending, and rotation. Approximately 50–60% of patients who present to emergency rooms have WAD grade II [89, 250], and one study found that 16% suffered from neurological deficit [181]. In some other studies, WAD grade III has been found to affect 2–6% of patients [89, 186, 250]. Nederhand et al. [178] have shown that in the acute phase of a whiplash injury, a reorganisation of muscle activation in painful neck and shoulder muscles occurs in order to decrease the use of these muscles. This altered motor function seems to be consistent with what are called the pain adaptation model [81] and fear avoidance models [71]. It is not known how such regulatory mechanisms may affect the development of long-term neck symptoms after a whiplash injury. Neck pain, like headache, is common in the population. One Swedish study found that 23% of the women and 15% of the men in the study, aged 20–74 years, had, in the previous 12 months, experienced persistent or regularly recurrent neck pain lasting at least 3 months [12]. Another Swedish study reported that 22% of the women and 16% of the men studied had long-term neck pain, i.e., pain that had persisted for more than 6 months [82]. Recurrent tension headache is sometimes accompanied by stiffness and neck and shoulder pain. Among most people with recurrent or long-term neck symptoms, it is not possible to demonstrate a single underlying cause of the pain, even after a careful work-up. It is thus reasonable to assume that the underlying mechanisms in many cases are multifactorial. Given this knowledge, it is important to bear in mind that neck pain may have been caused by something other than the whiplash trauma. The most important factor indicating that particular neck symptoms may be the result of a whiplash trauma is that the symptoms first occur, or become worse,

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Table 4 Occurence of symptoms in whiplash injury Symptom

Total number

Prevalence (%)

Studies (1–5)

Neck pain

334

94

1–4

Neck stiffness

195

96

1, 3

Interscapular pain

107

35

5

Headache

334

44

1–4

Numbness/paraesthesia

232

22

1, 3, 4

Vertigo

232

15

1, 3, 4

Eye symptoms Hearing symptoms

232 232

12 13

1, 3, 4 1, 3, 4

Sleeping problems

78

35

3

Memory problems

78

15

3

107

30

5

Signs of stress

The table refers to symptoms that occur within one week of traffic accidents involving whiplash trauma. The data are drawn from the following studies: (1) Hildingsson and Toolanen [99] (n = 93); (2) Norris and Watt [181] (n = 61); (3)Radanov et al. [209] (n = 78); (4)Maimaris et al. [159] (n = 102); and (5) Drottning et al.[60](n = 107). Adapted from Sterner and Gerdle[251]

immediately or very soon after—i.e., within a few days of—an accident involving whiplash trauma.

Other symptoms and signs in the acute phase Neurological symptoms can occur together with neck symptoms (WAD grade II) in the acute phase (Table 4). The patient may report pain, paraesthesia, sensory deficit, and weakness in an arm or hand. These symptoms often include referred pain from muscles and joint structures in the neck, shoulders, and thoracic spine, pain that can also radiate out into an arm and hand without dermatomal distribution. Sensory deficit that does not follow dermatome borders can occur in association with nociceptive pain (Sect. 4). Other symptoms reported in the acute phase, together with neck problems, include pain in the thoracic spine, sleep impairment, memory and concentration problems, eye symptoms, vertigo, and hearing impairment (Table 4).

Concurrent occurrence of objective signs, i.e., suspected post-traumatic cervical rhizopathy (WAD grade III), is probably very uncommon in association with whiplash injury. It is characteristic for symptoms to occur immediately or very soon after—i.e., within 1 or 2 days of—an accident involving whiplash injury. The clinical picture associated with the most common cervical nerve root disorder is summarised in Table 5. The symptoms seen in rhizopathy are usually dominated by sensory symptoms in terms of pain and paraesthesia, distributed in the dermatome supplied by the injured nerve root. Sensory deficit, such as decreased sensibility, is most easily demonstrated in the most peripheral parts of the dermatome. Motor symptoms in terms of objectively demonstrable paresis are often missing, even in cases of severe nerve root injury; this is because single muscles are usually innervated by neighbouring nerve roots as well. In the case of visible peripheral paresis with possible muscle atrophy, EMG changes can be detected at the earliest within several weeks of the injury. Symptoms and signs indicating spinal cord injury (myelopathy) are seldom directly associated with a whiplash trauma, and are most common in elderly people. Such injuries may stem from the existence of posterior osteophytes or a disc herniation, which, in association with the whiplash trauma, can cause spinal cord affection. A narrow spinal canal, i.e., a small sagittal diameter, can further increase this risk. The symptoms vary in degree of severity, from minor sensory deficit below the injury level to symptoms of more or less complete transverse lesion. Clinical examination may indicate varying degrees of sensory and motor deficit below the injury level, possibly including sphincter impairment, a positive Babinski sign, increased reflexes, walking and balance impairment, and poor Romberg test results. Objective findings of cervical rhizopathy and suspected myelopathy require special management (Sect. 9). Conclusions • Neck symptoms in terms of pain and stiffness, with or without objective clinical signs such as restricted range of motion and tenderness at palpation (WAD grades I-II), are most common.

Table 5 Symptoms and signs in cervical nerve root disorders Affected nerve root

Sensory symptoms/ decreased sensibility

Motor symptoms (paresis, possible atrophy)

Reflexes (decreased and/or missing)

CV

Lateral upper arm

Deltoid, and supra- and infraspinatus muscles

Biceps brachioradialis

C VI

Thumb, radial hand and forearm

Biceps and brachioradialis muscles

Biceps brachioradialis

C VII

Three middle fingers, proximal to this in hand and forearm

Triceps muscle

Triceps

C VIII

Little finger, ulnar hand and forearm

Intrinsic muscles of the hand

No reflex impairment

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• Symptoms usually occur within one to several days of the whiplash trauma; headache is common, as is pain in the shoulders and the cervical spine. • Neurological symptoms occur among approximately 20% of patients, but only 3–4% display objective neurological signs (WAD grade III).

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• Symptoms such as sleep impairment or memory and concentration problems as well as signs of stress are reported among approximately 25% of the cases.

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7 Prognostic factors for long-term symptoms

The prognosis for a whiplash injury is usually favourable, and follow-up studies have shown that up to 95% of patients recover within a few months [221, 256]. Approximately 70% of the injured recover within a few days up to 2–3 weeks.; approximately 20% of the injured have remaining symptoms, but these do not impair their working ability, while approximately 5–10% experience limitations in their work and leisure activities [212, 242, 250]. If symptoms persist more than 2 months after a whiplash injury, there is a considerable risk of long-term problems [159]. In cases where symptoms persist for 6 months, the prognosis is usually unfavourable, even though improvement has been demonstrated up to 4 years after a whiplash injury [73, 186]. It is important to be able to predict the prognosis of a person with acute symptoms induced by a whiplash trauma; to this end, the individual roles of several factors in the development of long-term problems have been analysed (see Table 6).

run a relatively high risk of suffering long-term symptoms [44, 179, 220]. Holm et al. [106] recently showed that neck pain intensity in WAD seems to be influenced by factors other than those directly related to the injury event itself, i.e. factors such as low income, prior neck pain, etc.).

WAD grade WAD grades I–III are also significant: the higher the WAD grade, the worse the prognosis for recovery, up to 2 years after the injury [89, 250]. The occurrence of neurological symptoms and positive neurological signs is also related to the WAD grade (Sect. 6). Accordingly, patients with neurological symptoms have an increased risk of developing long-term symptoms [90, 256].

Psychological factors Acute neck pain Norris and Watt [181] reported that the intensity of neck pain and the occurrence of other neurological symptoms in the first three days after a car accident negatively influenced the prognosis, in terms of the likelihood of persistent symptoms after 6 months. A review of 12 prospective studies of relatively high quality indicated that high initial pain intensity is an important predictor of an unfavourable prognosis [234].A prospective study found the same [94]. Impaired active range of motion in the cervical spine in the acute phase of a whiplash injury has also been shown to be an important prognostic factor for long-term complaints one year after the injury [89, 123, 246]. Other studies have shown that patients with whiplash injury and a combination of severe acute pain, neck stiffness, fear of movement, restricted activity level, and a perception of impaired health

Drottning et al. [60] found that high scores on the impact event scale (IES), which measures the degree of post-traumatic stress reaction as determined a few hours after a traffic accident, correlated significantly with persistent pain 4 weeks later. Also, a high level of stress, unrelated to an accident involving whiplash injury, has been shown to exert a negative impact on the course of a whiplash injury [237]. In a prospective study [85] the role emotional scores of the Short Form-36 health questionnaire showed a consistent significant positive association with better outcomes. Higher levels of somatisation and sleep difficulties have been shown to be risk factors related to poor recover [94] and in the presence of depressive symptomatology, individuals using high levels of passive coping recovered 75% more slowly than those who coped less passively [37].This finding is consistent with observations that apprehension and uneasiness, anxiety, sleep deprivation, depressed mood, and other

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Table 6 Prognostic factors in the acute phase of a whiplash injury for the development of long-term symptoms

Other prognostic factors

Strong support for increased risk

Initial pain intensity (the greater the pain, the greater the risk) WAD grade (the higher the grade, the greater the risk)

Some support for increased risk

Biopsychosocial factors (large number of current stress factors, fear of movement; low level of activity; work-related difficulties; limited education; poor selfconfidence; anxiety about the future; previous whiplash injury, neck complaints or headache)

A number of other factors are, according to several studies, related to unfavourable prognosis and an increased risk of long-term neck problems (Table 6). Significant factors in this regard include previous whiplash injury, previous neck symptoms or headache, previous psychological problems, occurrence of acute eye symptoms, multiple symptoms, female gender and older age, work disability limited selfconfidence and limited education [13, 14, 28,39, 53, 88, 90, 118, 127, 142, 173, 185, 187, 195,209, 212, 248–250, 257]. The importance of various vehicle- and impact-related factors has also been studied [61, 94, 113, 114, 132, 133, 141, 260] Studies of the roles of all these prognostic factors in the development of long-term symptoms in whiplash patients have produced inconsistent results, since several of the factors considered in the above, as well as in other studies and reviews, have not been found to be related to unfavourable prognosis.

Multiple symptoms Psychiatric symptoms (sleep deprivation; anxiety; uneasiness; depressed mood; ASD; PTSD) Female gender Advanced age Vehicle- and impact-related factors Medical insurance-related factors Factors related to the primary medical management

stress reactions can potentiate pain in all types of acute pain conditions (Sect. 5).The possible importance of other psychological factors in the development of long-term problems after a whiplash injury has attracted considerable attention in recent years. Normally, we experience multiple symptoms every day, but we usually ignore them. In a stress reaction, there is a risk that normally occurring bodily symptoms will be amplified and perceived as threatening [54], and a whiplash injury can easily supply the source of such a stress reaction [27] Media attention and a widespread impression that whiplash injury is serious and debilitating are factors that may also contribute to aggravating normal symptoms, raising the risk of long-term problems [68]. In countries such as Lithuania and Greece, symptoms after whiplash injury are almost always short term, and very rarely become long term. In these countries there is no financial compensation for whiplash injury, and the health care systems are used to only a very limited extent for whiplash injuries [185, 196]. Another potential stress factor that might influence the development of long-term symptoms is the involvement of legal counsel and the initiation of legal action soon after a whiplash injury. Several studies devoted to these issues have produced conflicting results [44, 61, 85, 124, 161, 261]. These results, however, are not transferable to all countries. In some countries legal counsel usually only becomes involved after symptoms have persisted for six months or longer The scientific analysis of suitable timeframes for settling medical insurance claims after whiplash injuries would seem to be a pressing matter.

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Importance of the initial medical examination and treatment in the development of long-term symptoms The treatment of a whiplash injury is part of one’s first postinjury visit to a doctor and is incorporated into the initial examination (Sect. 9). The circumstances and experience of this first medical consultation probably also influence the prognosis in an acute whiplash injury. If the patient feels that she or he has been carefully examined, trusts the doctor, and believes that the doctor is taking his or her complaints seriously, the probability of a favourable outcome is likely to increase. It is also important that the patient obtain, from the outset, consistent information regarding the fact that the condition is not usually serious and that the prognosis is usually favourable. The patient should also be informed that an early return to normal activities is the best way to improve the chances of recovery and prevent long-term problems. The patient should also be offered adequate treatment, for example, for pain and sleep impairment. Furthermore, the patient should be informed of how to contact the doctor by telephone, and of how to sign up for a return visit within about a week of the initial examination in case of persistent or worsened symptoms. Such simple measures may seem trivial, but their importance cannot be overstated [160]. Several investigators [40, 29, 30, 61, 94) have focused on the complex relationship between physical, psychological, and other factors in the development of longterm problems after a whiplash injury. Now is the time to develop strategies according to this knowledge and show if this has a significant effect on outcome. Further research in this field is urgently needed to clarify the role of these


factors and to identify measures that can reduce the proportion of patients with long-term symptoms

Summary The prognosis is favourable, and 90–95% of whiplash injury patients become symptom-free or experience only minor problems. However, 5–10% of these patients develop or have persistent long-term problems involving impairment of, for example, working ability. It is thus important, even in the first few weeks after an injury, to identify those patients belonging to the latter category. This group is often characterised by high initial pain intensity and high WAD grade. Females seem to have a higher risk of developing long-term problems than men do. The risk of long-term problems may further increase if a patient also has a fear of movement, post-traumatic stress, a low level of general activity, work-related problems, limited education, and previous neck problems [94, 179, 180, 250]. Uneasiness, anxiety, sleep impairment, depressed mood, and other stress reactions must always be considered, since they could aggravate pain in all types of acute pain conditions. Even in this early phase, one should already be paying special attention to the existence of prognostic negative factors. Patients who have a high prevalence of such factors, and thereby are at risk of developing long-term problems, should as early as possible be given an

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individually designed activity program. How such a program should be designed depends on local conditions and the availability of various experts. Patients with whiplash injury thus do not constitute a homogeneous group; they do not all have the same type of injury and the same underlying causes of persistent or longterm problems that can be treated according to a single, across-the-board programme. Treatment should therefore be individualised, and the aim of all treatment should be to implement measures to promote a return to normal activity as soon as possible. Improved management of patients with acute whiplash injury requires that all treating personnel and clinical examiners possess sound knowledge of whiplash as a whole, and of the role of prognostic factors in the development of long-term symptoms. Conclusions • The prognosis for a whiplash injury is usually favourable and 90-95% of patients recover or have only minor remaining symptoms. • Risk factors for long-term symptoms are often present early on, and high initial pain intensity and high WAD grade are warning signs. The possible occurrence of fear of movement and other psychiatric symptoms should be identified early in the course. • Patients with whiplash injuries constitute a heterogeneous group in terms of severity, clinical symptoms and objective findings. Treatment, therefore, should be individualised.

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8 Balance impairment, vertigo, and hearing symptoms

As humans walk on two legs and in an upright posture, when walking we are in a state of dynamic equilibrium that entails constant adjustment to prevent falling. Our sensory organs constantly monitor the position and movement of the body in relation to our surroundings and the gravitational field of the earth. The senses involved are vision, the vestibular sense (involving the vestibular organ of the inner ear), and proprioception (the ‘‘joint/muscle sense’’). Information from the sensory organs and functions involved is integrated at all levels of the central nervous system, and is used for reflexive, feedback control of the positional muscles of the body and to orient the body in relation to its surroundings. The functional connections between the various sensory systems are very complex and are also affected by cognitive mechanisms (‘‘will’’) and by limbic system activity (‘‘feelings’’). Vision provides information about our movements in relation to our surroundings, and about movements of our surroundings in relation to us. Vision enables us to detect obstacles beforehand, and to plan our movements accordingly (‘‘feedforward control’’). The vestibular system of the inner ear actually comprises two different types of sensory organs: the semicircular canals and the otolith organs. The semi circular canals detect rotational movements of the head (angular acceleration). The information from the semicircular canals is primarily important for reflex control of the eyes in counter phase, during the rapid movements that occur when we walk and run. This so-called vestibulo–ocular reflex stabilises the eyes in space and contributes to maintaining sharp vision during movement. The otolith organs detect linear acceleration (the force that affects us when, for example, we brake a car) and the position of the head in relation to the gravitational field of the earth acting on the body. The information from the otolith organs primarily controls the positional muscles of the body and enables us, for example, to keep our balance on a boat deck during rough seas.

Information in the proprioceptive system is derived from receptors in joints and muscles. The most studied part of this system is the muscle spindle system, the receptors of which run parallel to the muscle fibres in the skeletal muscles. Of all the muscles of the body, it is the deep neck muscles that have the highest concentration of muscle spindles [281]. Animal experiments have shown that information from the deep neck muscles converges with information from the vestibular organs at all levels of the central nervous system [169]. Since the vestibular organs are localised in the head, which in turn is positioned on a neck with ample movement ability, there must be a reference signal that exactly indicates the position of the head in relation to the trunk in order to make the elicited balance reflexes adequate. Most likely, it is the muscle spindles in the deep neck muscles that provide this reference signal. Conditions or injuries that affect the muscle spindles in the neck muscles might give rise to impaired neck proprioception, which in turn might give rise to vertigo when incorrect proprioceptive information converges with information from other sensory organs. As is often the case with whiplash-related symptoms, the mechanisms underlying any vertigo that occurs, mainly in association with long-term problems, are only partially, or not at all, understood. Vertigo in association with neck problems is usually called cervicogenic vertigo (in analogy to cervicogenic headache). The condition is characterised by a feeling of instability, which hypothetically occurs as a result of impaired neck proprioception [292]. Both consensus and diagnostic tests are lacking in this regard. Several studies have shown that patients with long-term, non-traumatic neck pain have impaired postural function [121, 122, 298], and that successful treatment of neck problems can lead to decreased pain and vertigo [122, 200]. Since diagnostic tests for cervicogenic vertigo are lacking, there is currently no justification for routinely performing vestibular

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tests on patients with whiplash injury. Vestibular and other neurophysiological tests should be performed as part of research projects.

Acute vertigo following whiplash trauma The most common type of vertigo, of all categories, is benign paroxysmal positional vertigo (BPPV), or simply benign positional vertigo [87]. During acceleration or deceleration of the head, as occurs in whiplash or in direct head trauma, the otoliths can become loose and end up in one of the semicircular canals [278]. When the head position is being changed, these loose otoliths induce fluid movements in the semicircular canals, which causes a sensation similar to that of riding a carousel, and a pronounced but usually rapidly resolving vertigo occurs. Posttraumatic positional vertigo always occurs within a few days of a trauma. This vertigo disease is diagnosed using the Dix–Hallpike test, in which the patient is placed in the position that provokes the vertigo and transient nystagmus and vertigo occur (Fig. 7). After diagnosis, the patient can easily and effectively be cured by a manoeuvre that aims to reposition the loose otoliths to where they belong. This treatment, Epley’s manoeuvre (Fig. 8), is not harmful, is easy to

Fig. 7 The Dix–Hallpike test for benign paroxysmal positional vertigo. The patient begins by sitting upright on an examining table. The head is turned approximately 45 degrees towards the ear to be examined. In a rapid movement, the patient is brought to a supine position with the head, still held at a 45-degree angle, extended slightly backwards. If the test is positive, the patient experiences vertigo after one or a few seconds, and one can often observe vertical–torsional nystagmus. The patient should remain in the provoking position, and within a minute the vertigo and nystagmus disappear. When the patient sits up from the supine position, a transient vertigo often also occurs. If the Dix–Hallpike test is repeated 2–3 times, the vertigo reaction becomes exhausted and disappears

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perform, and has repeatedly been shown to provide excellent results [290]. In rare cases, a whiplash injury can give rise to acute, pronounced rotational vertigo due to one-sided inner ear injury [278]. The injury mechanism might be a pressure wave impacting on the inner ear [235, 236]. The injury appears in association with the trauma, and the vertigo is much more pronounced than the diffuse vertigo of the positional type associated with long-term whiplash-related symptoms.

Audiological impairment If a patient complains of newly appearing, pronounced hearing impairment or tinnitus during the acute phase after a whiplash trauma, a hearing test should be performed. In rare cases, a whiplash trauma might give rise to injury of

Fig. 8 Epley’s manoeuvre for treating benign paroxysmal positional vertigo. The first part of Epley’s manoeuvre comprises the Dix–Hallpike test. Let the patient remain in the vertigo provoking position for approximately 3 minutes after the vertigo has disappeared. Then turn the patient’s head 90 degrees to the opposite side, keeping the patient’s neck extended all the time. Let the patient remain in this position for 3 minutes. Then let the patient move to lie on that side and continue rotating the head until the patient’s nose points obliquely towards the floor. Let the patient remain in this position for about 3 minutes. Bend the patient’s chin towards the chest and help the patient to sit up. For the first 24 hours after the manoeuvre the patient should avoid extending the head backwards, should sleep with some extra pillows under the head, and should avoid lying on the vertigo-provoking side. The patient should be followed up within 1–2 weeks


the inner ear, by means of sudden pressure alterations that affect various inner ear structures [235, 236]. These injuries occur at the time of the injury and produce symptoms immediately. It has not been possible to demonstrate any specific types of injuries associated with the audiological symptoms (tinnitus and subjective hearing impairment) sometimes observed in late whiplash-related disorders [70, 266]. However, it is well known that a relationship exists between neck and jaw problems and the subjective feeling of audiological symptoms, though the injury mechanisms are not known [34]. Depression is also an important aetiological factor in long-term tinnitus [297].

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Conclusions • If a patient complains of vertigo that has occurred acutely after a whiplash injury (or head injury), one should primarily suspect benign positional vertigo and tests for this condition should be performed. • Dizziness characterized as unsteadiness is not an uncommon late whiplash-related symptom. The background to the dizziness is usually unclear, and there are no diagnostic tests that can demonstrate a connection between the dizziness and the whiplash trauma. • If pronounced hearing impairment or tinnitus occurs during the acute phase after a whiplash trauma, a hearing test should be performed.

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9 Early management, work-up and examination methods

This section aims to provide sufficient information to allow the application of scientific knowledge and experience (as described in other sections) in supporting personal interaction between patient and doctor in the diagnosis of whiplash injury. The number of people with whiplash-related injuries has increased considerably, in many countries, as reviewed by the Whiplash Commission in Sweden [35]. The principles of managing whiplash-related injuries seem to vary depending on local tradition and the health care that is available and many patients have experienced deficient primary health care management [289]. Our experience is that these deficiencies are mainly related to ‘‘the art of medicine’’ and to the practical medical specialist competence In particular, three areas of ‘‘the art of medicine’’ offer considerable potential for improving the initial management of whiplash injuries, improvements that might limit negative consequences associated with such injuries. These areas are as follows: (1) doctor handling of patient perceptions of the condition and its symptoms, (2) practical clinical techniques used in examining the degree and amount of tissue injury, and (3) the doctor’s ability to gain the patient’s confidence, so that the doctor can gradually increase his or her knowledge of the patient’s overall circumstances [6, 15, 23, 51, 117, 148, 157, 229, 255]. However, despite these cornerstones in medical practice, some controversy exists regarding optimal initial clinical care following whiplash trauma [45]. Several studies of varying quality have examined early intervention in whiplash injuries. Most physical therapies, such as massage, heat treatment, stretching, manual treatment, TENS, acupuncture, cold spray, laser treatment, infrared light, and electrotherapy, have no or only marginal effects [17, 177, 242]. Evidence-based and updated reviews of treatment strategies conducted by the Cochrane Group concluded that active strategies, without the wearing of a

cervical collar, are the most effective at preventing the development of long-term problems, though some patients may need more individualized strategies [277].Active involvement and intervention in patients also reduces costs [225] What is meant by ‘‘active strategies’’? Five studies, Borchgrevink et al. [22], So¨derlund and Lindberg [240], Crawford et al. [46], Rosenfeld et al. [224] and Vassiliou et al.[275], concur, emphasising the importance of suitable information, regular, daily movement of the head and shoulder to the pain limit, relaxation, exercise, and walking. Some patients likely need more advice and follow-up from both the doctor and physiotherapist, and it is important that these two collaborate Bunketorp et al. [29] reported that supervised training was significantly more favourable than home training, with a more rapid improvement in self-efficacy. In 1995, the Quebec Task Force [242] recommended a protocol for use at the initial medical consultation; however, the protocol has proven to be too wide-ranging for routine health care use, and has seen little practical application.

General principles regarding the management of patients with acute whiplash injury Meeting the patient It is important for both diagnosis and management that the doctor understand the patient’s experiences, fears, beliefs, and expectations regarding whiplash trauma and injury, and that the doctor allow the patient to describe his or her worries during the consultation. Active listening makes it possible to collect the necessary information, even in a short time [5], a fact underlined by the SBU report of 1999 [192]. A consistently patient-oriented consultation can, in our experience, be an important factor in avoiding longterm pain development [162, 253].

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Medical history Accident description The following should always be noted regarding the accident: date, speed and direction of the impact to the car, type and age of the car, whether the car had a towing hook, whether safety belts and/or neck supports were present and used, whether there was time for preparation or whether the patient was completely unprepared, and whether other people were injured or died. In cases of whiplash trauma occurring in situations other than car accidents, data that may be relevant to understanding how the neck was injured should be recorded. Symptoms Enquire whether the patient was unconscious, or alternatively, displayed any other signs of impaired consciousness, memory deficit, and amnesia. Examine the distribution of pain, stiffness, paraesthesia, weakness, and other neurological symptoms, such as vertigo, vision impairment, and hearing impairment. Check whether the patient is displaying signs of anxiety or catastrophic thoughts, and ask whether there are signs of sleep impairment. The patient should estimate ongoing pain levels using a numerical, visual analogue scale (VAS), in which 0 represents ‘‘no pain’’ and 10 represents the ‘‘worst possible pain’’. Patient´s medical history shall clearly describe whether pain, stiffness, and neurological and/or acute stress symptoms (Sect. 5) are present at the time of examination. Previous and current disease conditions Is the patient currently experiencing pain or has the patient previously experienced neck pain, headache, or other recurrent or long-term pain that has required treatment or absence from work? What medications are being taken, including any pain medication? Does the patient suffer from another debilitating disease, such as rheumatoid arthritis or Bechterew’s disease (ankylosing spondylitis)? Social conditions Does the patient work, and if so, what type of work does he or she do? Is the work physically demanding, in particular, of the neck and shoulders? Is the patient on sick leave? It is important for treatment management to have a clear understanding of the patient’s overall lifestyle, educational, and work circumstances; this is especially important if the patient’s condition does not improve or happens to deteriorate. Physical findings The extent of the physical examination should be related to the patient’s symptoms and other circumstances, and should not usually take more than a few minutes. During

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the examination, the doctor should describe and explain the findings to the patient; this will build the patient’s understanding of the condition, and make him or her feel part of the examination process improving the chances of the patient taking an active role in his or her treatment. Does the patient appear to be psychologically affected and/or disoriented? Does the patient move stiffly? Are there signs of local tenderness? If so, describe the localisation, extent, and degree of such tenderness. Is there tenderness over the spinous processes? Examine the range of motion in the neck and note any decreased motion of recent origin. If the patient reports pain in the face, for example, in the jaw, check oral gap function and palpate the temporomandibular joints. Routine neurological examination of motor function, reflexes, and sensory function should be performed regularly. The extent of this examination should be related to the patient’s symptoms and other circumstances.

Evaluation • •

• •

• • •

How does the patient’s description of his or her condition correspond to the clinical findings? Does the patient have a whiplash injury, symptoms due to other causes, or a combination of both? Indicate the WAD grade (see Fig. 2). Is the patient experiencing pain of high or low intensity? Does the patient display any psychological symptoms? If so, indicate them, and classify them as ASR, ASD, or PTSD. Are there any indications of a need for radiological examination? (see Sect. 10). Are there any indications of a need for acute evaluation by another specialist? The patient needs continuity of contact with the doctor and the clinic. To this end, ask whether the patient already has an established contact with a particular doctor. If not, make sure that such a contact is established. Consider whether it is necessary to refer the patient to another specialist or to a physiotherapist.

Rare conditions •

•

If a patient complains of vertigo that has occurred acutely after whiplash trauma (or head trauma), benign positional vertigo should be suspected as the primary differential diagnosis; this condition should thus be tested for, and if present, treated (Sect. 8). If pronounced hearing impairment or tinnitus is present in the acute phase after whiplash trauma, hearing examination is recommended.


•

•

In cases of cervical rhizopathy or myelopathy, immediate contact with an orthopaedic surgeon, neurosurgeon, or neurologist is recommended, depending on local practices and specialist availability. In cases of cervical rhizopathy or myelopathy, special attention should be paid to patients with advanced rheumatoid arthritis or Bechterew’s disease (ankylosing spondylitis). Where pronounced symptoms of acute stress disorder (ASD) or posttraumatic stress disorder (PTSD) are present, case management should be done in collaboration with a psychiatrist.

Management in relation to pain intensity Irrespective of WAD grade, the patient needs to receive detailed, specific information. This information should comprise accepted knowledge regarding whiplash injuries, namely, that this condition usually has a favourable prognosis. Individually adapted programmes that aim to normalise activity, involving, for example, regular, daily head and shoulder movement to the pain limit, relaxation exercises, and walking, are recommended. It is worth remembering that in WAD grade I cases, radiological examination is unnecessary; however, patients with WAD grades II and III should be examined radiologically. If radiological examination (Sect. 10) reveals no fracture, dislocation/subluxation, or other injury, the following measures are recommended, in relation to pain of different intensity levels, according to the VAS.

Pain intensity 4 of 10, i.e., low to moderate pain (irrespective of WAD grade) Provide concrete information about the favourable prognosis of the condition and emphasise that there are no restrictions on work or leisure activities.

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adding centrally acting substances if the previous strategy is insufficiently effective. The medication should be taken regularly, the aim being gradually to decrease the effective dosage. Recommend that the patient contact his or her doctor (general practitioner or equivalent) within approximately a week if no improvement is noted. Depending on work situation(heavy or light work) discuss the possibility of change of worktask or limited (part time) sickleave, or consider prescribing several days of sick leave. Send information, for example a copy of the medical case records, to the patient’s own doctor.

Pain intensity 7 of 10, i.e., severe pain (irrespective of WAD grade) Inform the patient, without causing anxiety, that the healing process may be prolonged. For pain medication, administer a peripherally acting substance, i.e., paracetamol and/or an NSAID, possibly in combination with a centrally acting substance. See the above recommendations for additional information and advice. Follow-up telephone contact is recommended. Consider prescribing sick leave, depending on the work demands of the individual patient.

Pain intensity 7 of 10, i.e., severe pain and WAD grade III Special attention should be paid to this group of patients because of the risk of long-term symptoms. Inform the patient that recovery will most likely take a long time. Provide information as outlined above. In such cases, the patient should completely refrain from work for one week until making a return visit to the doctor. Administer pain medication as described above. A follow-up visit to the doctor is recommended within one week, and if possible, telephone contact should be made after several days.

Pain intensity 5–6 of 10, i.e., moderately severe pain (irrespective of WAD grade)

Documentation

Inform the patient that it may take several weeks for symptoms to improve. Instruct the patient to perform repeated head movements. Recommend normal physical activities such as brisk walks and light jogging. It is recommended that patients wait a while, depending on the case, before resuming more intense training and sports. All leg and trunk training is positive, as is balance training. If pain medication is needed, use paracetamol in combination with an NSAID, if not contraindicated. Consider

We believe that clear requirements for systematic documentation can lead to concrete improvements in medical management and diagnosis. Proper documentation is also useful in developing knowledge of whiplash injury, and, in particular, in identifying prognostic factors for long-term problems. It is not only important to document psychiatric and somatic findings, but also patient expectations, beliefs, and fears. The medical records should state who has the ongoing responsibility for medical co-ordination.

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Return visit within 1–3 weeks A new evaluation should be made on the first return visit. In cases of persistent neurological symptoms, a new neurological examination should be performed. If pain relief has not been obtained, consider prescribing pharmacological substances such as gabapentin or amitryptylin, and contact a pain clinic if necessary. In cases of pronounced symptoms persisting for more than a few weeks, plain x-ray examination with flexion-extension views of the cervical spine (Sect. 10) should be considered; alternatively, contact an orthopaedic surgeon or specialist at a pain clinic. Treat sleep impairment, if present, for only a limited time. Catastrophic thoughts regarding pain, fear of movement, anxiety, uneasiness, and leisure or work restrictions should be noted, since such phenomena may increase the pain experience. How restricted is the patient in his or her daily life and at work? Provide information and advice as described above. Consider contacting a physiotherapist for motion and co-ordination training, relaxation exercises, instruction in self-training, and follow-up. Passive mobilisation or manipulation is not recommended, because of the risk of injury [86, 238, 252]. All ongoing treatment, pharmacological as well as physiotherapeutic, should be continuously evaluated. Some people may have to be cautioned to slow down somewhat, while others may have to be prompted to be more active. In any case, use of cervical collars has no place in the treatment.


treated in the same way as acute nociceptive pain is. Most medications that we can offer patients should thus be used for only a limited time. Muscle tension/pain is not the same as muscle inflammation. When it comes to neurogenic pain because of nerve injury, other pharmacological and nonpharmacological treatment modes may be indicated; in such cases, referral to a neurologist or pain specialist can be recommended.

If the patient does not recover A patient experiencing persistent high pain intensity and difficulties working after one month should have the option of obtaining a combined evaluation by the available health care professionals (i.e., general practitioners, physiotherapists, occupational therapists, psychologists, cognitive behavioural experts, and possibly social workers) at the primary care unit where the patient is being treated. If indicated, refer the patient to an orthopaedic department, neurosurgical department, pain clinic, or other multidisciplinary pain unit. Early multidisciplinary rehabilitation has been shown to have positive effects [206, 276]. All delays, as well as back-and-forth referrals between specialists, are negative, and it is important to improve the co-ordination of medical management. For certain patients with pronounced psychiatric or neurological impairment, specialist evaluation may be necessary. It is important that all patients know what doctor is responsible for co-ordinating the rehabilitation [65].

Patients at increased risk Irrespective of pain intensity and WAD grade, it is always recommended that patients who, even before the accident, had neck pain, or who were on sick leave, who has concentration problems, sleep impairment, post-traumatic stress symptoms or strong anxiety, catastrophic thoughts, fear, or working disability, should contact their own general practitioners or equivalent doctors. On the first return visit, a detailed medical history should be established, especially regarding current and previous psychological, emotional, and physical stress and regarding social circumstances, which may be of significance for how the patients handle current problems.

When the acute injury has healed When the acute phase is over, long-term medication with NSAIDs, codeine, or muscle-relaxant medications is not indicated in most cases. The pain condition in this phase is no longer inflammatory, nociceptive, or acutely neurogenic. It should be noted that acute neurogenic pain is

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Summary Primary management and adequate documentation are probably crucial for the prognosis and can most likely be improved. In connection with the examination, the doctor should explain the findings to the patient; this will increase patient understanding and participation. If the patient feels that he or she is being carefully examined, and from the beginning obtains clear information about the benign nature of the condition and its generally favourable clinical picture and course, the chances of a favourable prognosis is increased. The diagnostic procedure should include evaluation of the degree of tissue injury, its functional consequences, (work ability) and classify the injury according to the WAD grades. Measurement of pain intensity from 0 to 10 using should always be performed. Necessary specialist and radiological examinations should be initiated as soon as possible via well-established and rapid referral routes. Patients with whiplash injury shall receive adequate pain relief, information, advice, and follow-up that stress the


importance of regular, daily head and shoulder movement to the pain limit, relaxation exercises, and walking. Most people do not benefit from meeting a large number of different care providers, as is often the case today. Extensive evaluations and prolonged, often passive, treatment may instead make the patient worse and delay improvement, and enhance the feeling that something is seriously wrong with the neck. The hallmark of case management should be the implementation of actions that promote rapid return to normal activity. This requires good knowledge of whiplash injuries as a whole, as well as of the risk factors that predispose a patient to negative development after whiplash trauma. The main responsibility for patients with whiplash injury lies with general practitioners with expertise in general medicine. It is therefore important that general practitioners be offered concrete support for professional development in this field that will help prepare them to manage such patients. These doctors also have a particular responsibility for not delaying the rehabilitation process; the goals should be short waiting times and effective referral routes.

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Conclusions • Pain intensity, stiffness, and neurological symptoms and signs should be documented, along with possible stress, fear, and anxiety. The WAD grade should be determined. Treatment initiatives are dependent on pain intensity and WAD grade, bearing in mind the patient’s overall circumstances in cases of delayed recovery. • Information and advice offered the patient should be directed towards a rapid return to normal activity, since most people do recover. Patients’ own active, adaptive strategies, such as regular, daily head and shoulder movement to the pain limit, relaxation exercises, and walking should be encouraged. The cervical collar has no role in treatment. • Possible pharmacological and other treatments should be regular, time-limited, and followed up. • In cases of persistent pain after one month and difficulties performing work and daily activities, coordinated evaluation at the primary care unit or pain specialist clinic is recommended.

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10 Radiological and neurophysiological methods

Radiological methods The value of plain x-ray, CT and MRI With plain x-ray examination of the cervical spine, the skeletal structures are well visualised and can usually be adequately evaluated. The discs can be evaluated by the distance between the endplates of the vertebral bodies; the absence of deformity between the vertebral bodies suggests that the ligaments in the cervical spine are intact. Otherwise, the soft tissues and ligaments around the cervical spine are difficult to evaluate. X-ray examination in combination with flexion–extension views provides useful information if there is normal sagittal movement in the various cervical spine segments. It also allows one to determine whether there is decreased, or sometimes increased, movement in one or several segments. Flexion– extension mobility provocation is usually done with the patient in a sitting position; lateral x-rays are taken when the patient has been told to flex and extend the neck. With this examination, one can obviously detect increased motion (instability), though one cannot always exclude instability. This is especially the case if the patient is experiencing pain in the cervical spine and is thus moving cautiously while flexing and extending the neck. If so, it is a good idea to repeat the x-ray examination, including the flexion–extension views, a few weeks after the trauma, when the muscle contraction in the cervical spine has partly or completely disappeared. Computerised tomography (CT) has developed very rapidly over the past decade. The whole cervical spine can now be examined in millimetre-thin sections in just a few seconds and image reconstructions can be performed in all planes. The radiation dose nowadays is similar to that of a plain x-ray examination (approximately 1 mSv). CT provides better information concerning details of the skeleton than plain x-ray does. As with plain x-ray, it does not allow

direct evaluation of the ligaments; however, it does indicate the relative positions of the various skeletal structures, and thus indirectly provides information about the ligaments. Mobility provocation is rarely used in combination with CT, and is regarded as a special examination to be performed only in the case of special indications. Moreover, only a few radiologists can perform such examinations. Such provocation is usually not performed in the sagittal direction—it is much better to use plain x-ray in such cases. However, one can examine the cervical spine in the neutral position, and then compare the relationships between the vertebral bodies when the examination is repeated with the head rotated to the right and to the left, respectively. The cervical spine can also be examined with the head bent laterally. Interpreting CT combined with mobility provocation requires special knowledge of cervical spine biomechanics. Standard magnetic resonance imaging (MRI) allows evaluation of at least the anterior longitudinal ligament and the ligamentum flavum as well as of the discs. As well, the posterior longitudinal ligament and its continuation up towards the base of the skull—the tectorial membrane— can be evaluated. Evaluating the alar ligaments and the transverse ligament behind the dens requires additional series with thinner sections.

Radiological investigation in the acute phase In acute cases, the indications for radiological investigation and the choice of method are the same for patients with either direct or indirect trauma of the head/cervical spine. Plain x-ray examination is usually sufficient in the case of moderate symptoms. If, based on plain x-ray, one suspects a fracture, additional examination using CT should be done, as this gives a more detailed image of the skeletal

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structures, especially at the junction of the thoracic and cervical spine and in the upper parts of the cervical spine. In the case of more pronounced symptoms, or if the patient is experiencing symptoms indicating nerve root or spinal cord involvement, CT is recommended as the primary method of examination. This should be supplemented with MRI if any of the x-ray examinations has indicated that there might be an unstable cervical spine injury, and in the case of objective neurological findings. There is no justification for using MRI as the primary method of examination in the acute phase.

Guidelines for radiological investigation of whiplash injuries WAD Grade I Patients experiencing pain and stiffness in the cervical spine, but with normal clinical findings, do not need to be radiologically examined. This conclusion is based on two large prospective studies performed in the USA and Canada, referred to as NEXUS [101] and the Canadian C-spine rule [254], respectively. As well, it is important to avoid unnecessary ionising radiation, medicalisation, etc. However, patients at risk of increased fracture or cervical spine injury, as in the case of trauma, should be examined using plain x-ray or CT, as should patients with Bechterew’s disease (ankylosing spondylitis), rheumatoid arthritis, and patients aged 65 and over. WAD Grade II Patients experiencing pain and stiffness, with or without symptoms indicating nerve root or spinal cord involvement, as well as tenderness at palpation and/or decreased range of motion, should be examined using plain x-ray or CT. In the case of nerve root or spinal cord symptoms, MRI examination may also be justified. WAD Grade III Patients who also display objective neurological findings in addition to pain and stiffness should primarily be examined using CT; additional examination using MRI is often indicated as well.

Radiological investigation in the case of long-term symptoms In the case of cervical spine symptoms that persist long after a trauma, plain x-ray examination, with or without flexion–extension views, is usually sufficient. In this phase, CT provides about the same information as plain x-ray examination does. When only neck pain is present, MRI is usually not indicated. However, MRI should be considered

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in cases of nerve root or spinal cord involvement. In such cases, MRI examination may be indicated in order to exclude (common) degenerative conditions, such as disc herniation and spinal stenosis, as well as other conditions, such as tumours. When examining the ligaments in the upper part of the cervical spine (C0–C2) using MRI, it is necessary to supplement the standard investigation with a special series, which will double the duration of the investigation. Additional examination using plain x-ray or CT, with or without flexion–extension views, should also be performed. MRI examination and functional CT with special reference to the ligaments in the upper part of the cervical spine are complicated procedures and should only be performed in clinical research.

What is the current position of radiology in whiplash diagnosis? Kra˚kenes et al. have shown that it is possible, using conventional MRI equipment, to obtain higher image quality (which facilitates evaluating the ligaments in the upper part of the cervical spine) than is generally obtained in MRI examinations using a standard protocol [134–137, 119, 138]. These studies found more changes in the alar ligaments and in the transverse ligament behind the dens in patients 2–9 years (mean 6 years) after whiplash injury than in healthy control subjects. These studies made use of a head coil, normally not used when examining the cervical spine, since the cervical spine can only be examined down to approximately the C3 level using a head coil. Another question concerns the changes that Kra˚kenes et al. found in these ligaments. It has still not been demonstrated that such changes, more common in patients with whiplash injury than among healthy controls, are direct signs of old ligament injury or whether they result from long-term pain associated with stiffness, inactivity, or increased motion. Reliable MRI studies of the ligaments in the upper part of the cervical spine in whiplash-injured patients in the acute phase after the trauma are still lacking. Volle has considerable experience of MRI in combination with mobility provocation, which he performs in an open MRI camera, initially at 0.5 Tesla, but later at 1.0 Tesla [279, 280]. In investigations involving mobility provocation, images are taken during flexion and extension, as well as while laterally bending and rotating the head, however without control groups. The image quality obtained in such examinations is inferior to what Kra˚kenes has shown is possible. However, the emphasis of Volle’s functional investigations is not, according to the author, on image quality but rather on function. The diagnostic criteria Volle uses with functional MRI have not been


adequately documented in the referee-evaluated literature, so there are doubts as to the value of his investigations [2]. Wilmink and Patijn [288] studied the alar ligaments in whiplash patients and in control subjects using MRI methology similar to that described by Volle, but did not find support for alar ligament injuries as a cause for long-term problems after whiplash trauma. Problems and controversies when using MRI for evaluation of alar ligament morphology have been pointed out by several investigators [204, 227, 287]. On the other hand, Mikkonen et al. [171] found, with a blinded observer, differences between patients with long-term problems after whiplash trauma and control subjects regarding pathologic changes in the alar ligaments and movements at the C1-C3 segments and movements of the dens axis. Conclusions • In the acute phase, x-ray examination is not justified for patients under the age of 65 presenting WAD grade I, except in those with concurrent skeletal disease, such as Bechterew’s disease (ankylosing spondylitis) and rheumatoid arthritis. • In the case of WAD grade II, plain x-ray or CT examination is recommended. If there are symptoms indicating nerve root or spinal cord involvement, CT is recommended. • In the case of WAD grade III with objective neurological findings, CT should be the primary mode of examination, and additional examination using MRI is often indicated.

Neurophysiological examinations Several different neurophysiological tests have been used in an attempt to demonstrate certain possible injuries, particularly in the central nervous system. Only a few studies have been performed prospectively or in the early phase after whiplash trauma. Eye movement test Many studies have found that patients with late whiplashrelated symptoms display signs indicating impairment of voluntary eye movement [207, 284]. This has often been interpreted as indicating brain stem injury. Eye movement tests are very sensitive and are influenced, for example, by the degree of consciousness, voluntary concentration, and medication. Impairment of voluntary eye movement has been found in patients with, for example, fibromyalgia [36], tension headache [226], and in healthy controls when neck motion is restricted with a cervical collar [120]. The results of a study of patients with late whiplash-related

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symptoms and of patients who have become symptom-free after whiplash trauma do not indicate that the impaired eye movement is related to brain stem injuries, but rather to frontal or prefrontal cortical disturbances [174].

Neck torsion test In the neck torsion test, the ability of the eyes to follow moving objects is tested when the patient is sitting with the head rotated approximately 45 degrees to the side. This test has been reported to have high sensitivity and specificity in distinguishing patients with whiplash-related dizziness from healthy controls or from those with vertigo related to central or vestibular mechanisms [265, 269]. However, other research groups have been unable to reproduce these findings [144, 207].

Cervical kinaesthesia/joint position error Since it has been hypothesised that neck proprioception is impaired in association with whiplash-related symptoms, it would be of interest to be able to measure neck proprioceptive function. However, there is no way of directly measuring cervical proprioception. By asking a person, after actively rotating his or her head, to resume the original position and then measure the possible deviation (position error) from the original position, one can obtain an indirect measure of cervical position sense. This test has been used in several studies and has indicated that patients with neck problems, irrespective of cause, have impaired cervical position sense compared to that of healthy controls [218]. Successful treatment of neck symptoms would imply a decrease in pain, and such pain reduction also leads to improvement of the cervical position sense [92, 219]. Patients with whiplash-related symptoms have a more impaired cervical position sense than do patients with other neck symptoms, but the test cannot be used to distinguish individual patients [67, 93, 139, 154, 268]. One problem with the test is that it is indirect and is dependent on factors such as will, cognition, and vestibular function.

Posturography By measuring the force a person generates on a support surface in order to keep their balance while standing, one can estimate the postural ability of the person. Several studies have found that patients with various pain conditions in the neck have impaired postural ability compared with that of healthy controls [121, 122, 298]. Successful treatment of these neck problems, which results in

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decreased pain, leads to improved postural ability [122, 200]. Studies have also shown that patients with late whiplash-related symptoms have impaired postural function [129, 158, 228, 270]. However, pathological posturographic testing provides no information regarding the aetiology of the symptoms in individual patients.

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Conclusions • The tests mentioned above should not be used in routine health care since they are of no proven diagnostic value for whiplash injuries. • These tests should be used only in clinical research.


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