Chapter | 8 |

Whiplash associated disordersMichele Sterling

CHAPTER CONTENTS

Introduction 112

The whiplash condition 113

Classification of whiplash injury 113

Physical and psychological characteristicsof the whiplash condition 113

Motor and sensori-motor controldysfunction 114

Augmented pain processing mechanismsin whiplash 114

Psychological factors in whiplashassociated disorders 116

The prediction of outcome followingwhiplash injury 117

Implications for assessment of whiplash 117

Implications for management ofwhiplash associated disorders 118

Conclusions 119

INTRODUCTION

Whiplash associated disorders are common, disabling, andcostly conditions that occur as a consequence of a motorvehicle crash (MVC). Recent data indicate that rapidimprovement in levels of pain and disability occur in thefirst three months post injury with little if any change afterthis period and that the majority of injured people will notfully recover (Kamper et al 2008). The associated costsecondary to whiplash injury, including medical care,

disability, lost work productivity, as well as personal costsis substantial (Crouch et al 2006, MAIC 2004).

Whiplash is a recalcitrant condition for some indivi-duals. Management options for both the acute andchronic stages of whiplash are not straightforward andwhilst offering some improvements in pain and disabilityare far from being a panacea. Trials of treatment for acutewhiplash have not demonstrated efficacy in terms ofdecreasing the incidence of those who develop persistentsymptoms (Provinciali et al 1996, Borchgrevink et al1998, Rosenfeld et al 2000, 2003). Whilst these trials haveprovided evidence to show that maintenance of activity issuperior to rest and prescription of a collar for most whip-lash injured people (Scholten-Peeters et al 2002), signifi-cant numbers of patients still transition to chronicity.Further, trials of treatment for the chronic stage of thecondition, including various exercise forms have offeredonly modest effects with only 10–20% of patients havinga completely successful outcome, that is minimal or nodisability at the 12-month follow-up (Jull et al 2007,Stewart et al 2007).

Recent research findings show that whiplash is a remark-ably complex and heterogeneous condition and this hetero-geneity may explain the modest effects of treatmentstrategies investigated to date. Most trials have previouslyinvestigated relatively non-specific approaches to treatmentwithout targeting interventions toward specific physical orpsychological characteristics of the condition. Howeverrecent investigations have begun to provide insight intothe characteristics of the whiplash condition – both physicaland psychological – that allows speculation on the potentialunderlying mechanisms.

This chapter will outline the whiplash condition andclassification before discussing the burgeoning knowledge

112© 2011 Elsevier Ltd.

DOI: 10.1016/B978-0-7020-3528-9.00008-X

of physical and psychological manifestations of the condi-tion and the implications for clinical practice.

THE WHIPLASH CONDITION

A motor vehicle crash can lead to bony or soft-tissue dam-age, which in turn may result in a variety of clinical man-ifestations called whiplash-associated disorders (WAD).The primary symptom is neck pain, although headache,arm pain, paraesthesia, dizziness and cognitive difficultiesare also frequently reported (Spitzer et al 1995).

It is conceivable that virtually any cervical spine struc-ture may sustain injury following whiplash. Bioengineer-ing studies where cadavers were subjected to simulatedrear end crashes have demonstrated perturbations in seg-mental movement including inter-segmental hyperexten-sion, S-curve formation and differential acceleration ofthe upper cervical spine (Cusick et al 2001). This togetherwith evidence from autopsy (Taylor & Taylor 1996) andanimal studies (Winkelstein et al 2000) indicates thatlesions may occur to cervical structures including bonyelements, intervertebral discs and zygapophyseal joints,ligaments, muscles and nerve tissues. Unfortunately,in vivo identification of structural pathology has proveddifficult probably due to the insensitivity of current radio-logical diagnostic imaging (Davis et al 1991, Uhrenholtet al 2002), although recent studies begin to provide hopethat this situation may change in the future for at leastsome structures (Krakenes & Kaale 2006). It is also gener-ally accepted that in some persons with chronic whiplash,the zygapophyseal joint is a symptomatic structure,demonstrated by placebo controlled nerve blocks to thesejoints (Lord et al 1996).

Whilst it could be argued to be beneficial if specificstructural lesion(s) could be identified in whiplash injuredpersons, it has more recently been promoted that theidentification of the patho-anatomical source of symptomsprovides little basis for appropriate management of muscu-loskeletal pain disorders and emphasis should instead beplaced on treatment approaches directed toward mechan-isms and processes underlying the painful condition(Jensen & Baron 2003). With respect to WAD, there isevidence that a variety of physical and psychologicalimpairments characterize the condition.

CLASSIFICATION OF WHIPLASHINJURY

Classification systems have been proposed in order toassist in the early assessment, prognosis and managementof whiplash. The most commonly used classification sys-tem is the Quebec Task Force (QTF) system (Spitzer et al1995). It broadly defines the condition into four groups

as WAD I (neck complaint, without musculoskeletalsigns); WAD II (with musculoskeletal signs); WAD III(with neurological deficits) and WAD IV (with a fractureor dislocation). While this system provides some neces-sary information related to condition classification, amajor systematic flaw exists as the majority of whiplashinjured people are grouped within one classification(WAD II), which falsely assumes homogeneity of the mostcommon complaints within this group (Sterling 2004).The QTF Classification system has received some criticismin the past for the lack of scientific validation (Hartlinget al 2001), failure to accommodate the heterogeneity ofthe WAD presentation (Sterling 2004) and its lack ofprognostic capacity (Kivioja et al 2008).

To date, neither the QTF classification system for WADnor trials investigating various management approachesfor this condition have considered both the physical(biological) and psychological factors that are emergingas playing a role in the pain and disability of whiplash.It is becoming apparent that whiplash is a heterogeneouscondition and more complex than previously assumed.Furthermore, it is emerging that whiplash is in some waysdifferent from neck pain conditions of a non-traumaticnature. In particular chronic whiplash shows marked sen-sory features indicative of central nervous system hyper-excitability that have now consistently been shown notto be a feature of chronic non-traumatic neck pain (Chienet al 2010, Elliott et al 2008, Scott et al 2005).

PHYSICAL AND PSYCHOLOGICALCHARACTERISTICS OF THE WHIPLASHCONDITION

Historically much past research and certainly the clinicalassessment of spinal pain conditions, including whiplashhas aimed to identify the patho-anatomical source(s) of thepatient’s reported symptoms. This approach has had limitedsuccess as a patho-anatomical diagnosis is not possible in thevastmajority of patientswith commonmusculoskeletal painconditions nor does such a diagnosis necessarily shed lighton the most optimal intervention for a specific conditionor patient. As a consequence, the focus has shifted in recentyears more towards attempting to identify the underlyingmechanisms or processes of the patient’s pain syndrome(Max 2000). The purpose of this more specific diagnosisand classification of musculoskeletal pain syndromes is tohelp tailor interventions toward identifiable underlying pro-cesses to try to improve treatment success, particularly insome of the more recalcitrant conditions. Of all neck andupper quadrant conditions, there is arguably the mostdata for motor, sensory and psychological characteristicsavailable for whiplash. One reason for this may be due tothe easily defined onset of injury (MVC) versus amore insid-ious onset that often occurs with other conditions.

Chapter | 8 | Whiplash associated disorders

113

Motor and sensori-motor controldysfunction

One of the most common clinical characteristics ofpatients with WAD is that of movement loss or decreasedcervical range of movement (Heikkila & Wenngren 1998,Dall’Alba et al 2001). Most prospective studies haveshown that all whiplash injured subjects have a loss ofcervical active range of movement from soon after injury(Radanov et al 1995, Kasch et al 2001b, Sterling et al2004). Kasch et al (2001b) reported that restoration ofmovement loss occurred in all individuals by three monthspost-injury, irrespective of recovery or non-recovery.However if whiplash subjects are classified more precisely,it can be seen that those with persistent moderate/severelevels of pain and disability (measured with NDI) continueto display active movement loss several years post injury(Sterling et al 2006). In contrast, participants who hadrecovered or reported lesser (but still significant) painand disability showed restoration of movement loss within2–3 months of injury (Sterling et al 2003b), similar to thatseen by Kasch et al (2001b). This demonstrates the impor-tance of differentiating individuals with whiplash based onpain and disability levels.

Altered patterns of muscle recruitment in both the cervi-cal spine and shoulder girdle regions have been clearlyshown to be features of chronic WAD (Nederhand et al2002, Jull et al 2004). Longitudinal data demonstrate thatthese changes are apparent from very soon after injury(Nederhand et al 2002, Sterling et al 2003b) with greaterdeficits in those reporting higher levels of pain and dis-ability (Sterling et al 2003b). Sterling et al (2003b,2006) observed that the disturbed motor patterns per-sisted, not only in those with ongoing chronic symptoms,but also in those with milder pain and disability andthose who reported full recovery with this phenomenaoccurring at significant time periods post-injury – up to2 years. These persisting deficits in muscle control mayleave recovered individuals more vulnerable to future epi-sodes of neck pain but this proposal needs to be substan-tiated with further investigation (Sterling et al 2006).Altered patterns of muscle recruitment are not unique towhiplash and identical changes have also been observedin neck pain of insidious onset (idiopathic neck pain)(Nederhand et al 2002, Jull et al 2004, Woodhouse &Vasseljen 2008). These findings suggest that the driver ofsuch motor changes may be more due to the nociceptiveinput rather than the injury mechanism itself.

Recent investigation, using MRI, has shown markedmorphological changes to cervical spine muscles in peo-ple with chronic whiplash. Elliott et al (2006, 2010)demonstrated the presence of fatty infiltrate in both deepand superficial cervical extensor and flexor muscles inWAD patients compared to an asymptomatic controlgroup. Although the fatty infiltrate was generally higherin all muscles investigated for the patient group, it was

highest in the deeper muscles, the rectus capitis minor/major and multifidi (Elliott et al 2006). In contrast tomuscle recruitment changes, preliminary data indicatethat similar morphological changes are not apparent inindividuals with chronic idiopathic neck pain (Elliottet al 2008). The relevance of these findings in terms ofpain, disability or functional recovery and the cause ofthe muscle changes are not yet known but the findingsillustrate the profound disturbances in motor functionpresent in people with chronic WAD.

Dysfunction of sensori-motor control is also a featureof both acute and chronic WAD. Greater joint re-position-ing errors have been found in patients with chronicWAD and also in those within weeks of their injury, andwith moderate/severe pain and disability (Sterling et al2003b, Treleaven et al 2003). Loss of balance and dis-turbed neck influenced eye movement control are presentin chronic WAD (Treleaven et al 2005a,b) but theirpresence in the acute stage of the injury are yet to bedetermined. It is important to note that sensori-motor dis-turbances seem to be greater in patients who also reportdizziness in association with their neck pain (Treleavenet al 2005a,b).

Most of the documented motor deficits (movementloss, altered muscle recruitment patterns) seem to be pres-ent in whiplash injured individuals irrespective ofreported pain and disability levels and rate or level ofrecovery (Sterling et al 2003b). Additionally, apart fromcervical movement loss, motor deficits do not appear tohave predictive capacity (Sterling et al 2005). Further,treatment directed at rehabilitating motor dysfunctionand improving general movement shows only modesteffects on reported pain and disability levels (Jull et al2007, Stewart et al 2007). Together these findings suggestthat motor deficits, although present, may not play a keyrole in the development and maintenance of chronic orpersistent symptoms following whiplash injury. However,this is not to say that management approaches directed atimproving motor dysfunction should not be provided topatients with whiplash. Rather the identification of motordeficits alone may not equip the clinician with usefulinformation to either gauge prognosis or potentialresponsiveness to physical interventions.

Augmented pain processingmechanisms in whiplash

There is now considerable and consistent evidence of sen-sory disturbances in WAD which indicate the presence ofaugmented central pain processing mechanisms. Changesinclude both sensory hypersensitivity (or decreased painthresholds) to numerous stimuli such as pressure, ther-mal, electrical stimulation and light touch in both acuteand chronic WAD (Curatolo et al 2001, Sterling et al2003a, Raak & Wallin 2006). Sensory hypersensitivity is

Part | 2 | Cervical–thoracic spine

114

found not only over the cervical spine (area of injury) butalso at remote uninjured areas such as the upper andlower limbs (Koelbaek-Johansen et al 1999, Sterling et al2003a). The absence of tissue damage at the site of testingsuggests that central sensitization of nociceptive pathwaysis the cause of the pain hypersensitivity. Recently the pres-ence of widespread hypoaesthesia (that is, elevateddetection thresholds) occurring concurrently with hyper-sensitivity has also been found in WAD and suggestsdisturbances in central inhibitory processes as well (Chienet al 2008a,b).

Hypersensitivity has been shown not only to be presentin testing involving a cognitive response from the partici-pant. Facilitated flexor withdrawal reflexes in the lowerlimbs of participants with chronic WAD have beendemonstrated following electrical stimulation of the suralnerve (Banic et al 2004, Sterling et al 2008). In this test,reflex activity of the biceps femoris was measured and evi-dence of spinal cord hyper-excitability (central sensitiza-tion) was provided without relying on the subject’s selfreported response to the stimuli, as is required with painthreshold testing. It has also been shown that the height-ened reflex responses are not associated with psychologi-cal factors such as catastrophization and distress (Sterlinget al 2008).

In contrast to the apparently uniform presence of motordysfunction, sensory disturbances seem to differentiatewhiplash from less severe neck pain conditions and whip-lash sub-groupings with higher or lower levels of self-reported pain and disability. Individuals with chronicWAD manifest a more complex presentation involvinglowered pain thresholds to pressure, heat and cold stimuli

in areas remote to the cervical spine which are not presentin those with idiopathic (non-traumatic) neck pain (Scottet al 2005, Elliott et al 2008, Chien et al 2010). Similarlywidespread hypoaesthesia to vibration, thermal and elec-trical stimulation, whilst present in WAD is not a featureof idiopathic neck pain (Chien et al 2010). However thepresence of central hyper-excitability is not unique towhiplash with other painful musculoskeletal conditionssuch as fibromyalgia, tension-type headache and migrainealso manifesting such signs (Yunus 2007). With respect tothe cervical spine and upper quadrant, widespread sen-sory hypersensitivity is a feature of cervical radiculopathywith this condition and whiplash reporting similar painand disability levels (Chien et al 2008b) (Figs 8.1 &8.2). This suggests that chronic whiplash and chronic cer-vical radiculopathy share similar underlying mechanismsbut differ from idiopathic neck pain illustrating the diver-sity of processes involved in various neck pain conditions.

The reason as to why some whiplash injured peopledevelop a hypersensitive state is not clear but appears tobe related to levels of pain and disability (Sterling et al2003a). Numerous cervical spine structures are implicatedas possible sources of nociception following whiplashinjury. It is possible that injuries to deep cervical struc-tures do not rapidly heal and thus become a nociceptive‘driver’ of central nervous system hyper-excitability. Whilstthis proposal may meet opposition from those whobelieve injured soft tissues are healed within severalweeks, it is gaining support as a possible contributor tothe development of chronic musculoskeletal pain includ-ing whiplash (Curatolo et al 2006, Vierck 2006). Thereis also evidence from cadaver studies that certain lesions

600

500

400

300

200

100

0C5/6 Upper limb Lower limb

kPa

Control Idiopathic Radiculopathy WAD

**

**

**

**

Fig 8.1 Pressure pain thresholds (PPTs) (mean and standard deviation) at C5/6, upper and lower limbs of patients with idiopathic(non-traumatic) neck pain, whiplash associated disorders (WAD) and cervical radiculopathy compared to asymptomatic controls.The three neck pain groups showed decreased PPTs at the neck (C5/6) and upper limbs. The WAD and radiculopathy groups alsoshowed widespread decreased PPTs in the lower limb (*p < 0.05).

Chapter | 8 | Whiplash associated disorders

115

can persist unresolved in MVC survivors who die of unre-lated causes some years later (Taylor & Finch 1993). Addi-tionally, the sensory hypersensitivity seen in whiplash isoften also associated with other disturbances such asimpaired sympathetic vasoconstriction (Sterling 2006)and stress related factors (Sterling & Kenardy 2006). Theco-occurrence of these factors suggests that a complexinterplay between various mechanisms may lead to thisalmost systemic response in some following whiplashinjury. Research is now focusing on investigating suchcomplex models which may in the future shed light onthis intriguing issue (McLean et al 2005, Passatore &Roatta 2006, Sterling & Kenardy 2006).

Psychological factors in whiplashassociated disorders

There is no doubt that chronic whiplash is associated withpsychological distress including affective disturbances,anxiety, depression and behavioural abnormalities suchas fear of movement (Williamson et al 2008). Psychologi-cal distress is also present in the acute post-injury stagewith most people showing some distress regardless ofsymptom levels (Sterling et al 2003c). Data from somestudies indicate that the ongoing psychological distress isassociated with non-resolving pain and disability. A largecross-sectional study showed an association between anx-iety, depression and pain and disability in people whoseaccidents occurred over two years previously, but not inthose with acute injury, suggesting that symptom persis-tence is the trigger for psychological distress (Wenzelet al 2002). Longitudinal data indicate that initially ele-vated levels of distress decrease in those who recover,closely paralleling decreasing levels of pain and disability(Sterling et al 2003c).

Unique psychological factors may be involved in theetiology and development of chronic whiplash (Sterlinget al 2003c) when compared to other painful musculo-skeletal conditions. For example, the role of fear of move-ment beliefs seems to be a less important factor inwhiplash (Sterling et al 2005) than in low back pain(Vlaeyen et al 1995). The role of coping styles or strategiesin whiplash is unclear. Some data indicate that a palliativereaction (e.g. seeking palliative relief of symptoms such asdistraction, smoking or drinking) was associated with lon-ger symptom duration (Buitenhuis et al 2003, Carroll et al2006). In contrast Kivioja et al (2005) found no evidencethat different coping styles in the early stage of injuryinfluenced the outcome at one year post-accident. The dif-ferent cohort inception times of these studies may accountfor the differences in findings indicating that coping stra-tegies may vary depending on the stage of the conditionand this requires further investigation.

One factor that is likely unique to WAD (when com-pared to other common musculoskeletal conditions),due to the mode of onset being a traumatic event, is thatof post-traumatic stress. Symptoms of post-traumaticstress have been shown to be present in a proportionof people following a whiplash injury due to a MVC(Drottning et al 1995, Sterling et al 2003c, Kongstedet al 2008) and these symptoms have shown prognosticcapacity for poor functional recovery at six months andtwo years post-MVC (Sterling et al 2005, Buitenhuis et al2006, Sterling et al 2006). These studies mostly utilizedthe Impact of Events Scale (IES) (Horowitz et al 1979),an instrument that measures distress associated with aspecific event (in the case of whiplash a MVC). It shouldbe noted that a diagnosis of post-traumatic stress disordercannot be made from IES scores. However recent data uti-lizing a more robust tool, The Post-traumatic Stress Diag-nostic Scale (Foa et al 1997) demonstrated that 22% of a

Control Idiopathic Radiculopathy WAD

**

**

**

*20181614121086420

Cervical Upper limb

Fig 8.2 Cold pain thresholds (mean andstandard deviation) measured over thecervical spine and upper limb of patientswith idiopathic (non-traumatic) neck pain,whiplash associated disorders (WAD) andcervical radiculopathy compared toasymptomatic controls. The WAD andradiculopathy groups showed coldhyperalgesia over the cervical spinecompared to the idiopathic neck pain groupand controls. Only the WAD group showedcold hyperalgesia in the upper limb (*p <0.05).

Part | 2 | Cervical–thoracic spine

116

prospective sample of 155 whiplash injured people had aprobable diagnosis of PTSD at three months post-MVCwith this figure dropping slightly to 17% by 12 monthspost-injury (Sterling et al 2009). These findings indicatethe need for further psychological evaluation of thesepatients (Forbes et al 2007) and clinicians should beaware of this factor in their assessment of whiplashinjured people.

THE PREDICTION OF OUTCOMEFOLLOWING WHIPLASH INJURY

The capacity to predict those at risk of poor recovery fol-lowing whiplash injury is important because it may allowthe institution of appropriate early interventions targetedat modifiable risk factors. This could potentially reducethe transition to chronicity in those individuals deemedat risk. Numerous factors have been investigated for theirprognostic capability including: sociodemographic status;crash related variables; compensation and/or litigation,psychosocial and physical factors (Radanov et al 1995,Cassidy et al 2000, Kasch et al 2001a). However, recentsystematic reviews of prospective cohort studies on whip-lash found that only greater initial pain intensity andgreater initial disability were the most consistent predic-tors of delayed functional recovery (Carroll et al 2008,Kamper et al 2008, Walton 2010). Other factors reportedby individual systematic reviews include post-injury psy-chological factors such as coping strategies (Carroll et al2008), less than post-secondary education, female gender,history of previous neck pain (Walton 2010) andsymptoms of post-traumatic stress and poor self-efficacy(Williamson et al 2008). Whilst some of these factorssuch as pain intensity, psychological distress may be mod-ifiable many of the others (age, education) are not.Furthermore when potentially modifiable factors of initialpain and disability levels are considered alone, whilst hav-ing high specificity had relatively low sensitivity to predictthose with ongoing moderate to severe symptoms at sixmonths post-accident (Sterling et al 2005). Furthermoremeasurement of pain and disability levels alone isunlikely to assist in the direction of secondary and tertiarymanagement stages of this condition. Nonetheless it willbe important for clinicians to obtain a measure ofreported pain and disability (e.g. Neck Disability Index)in the assessment of the whiplash injured.

Additional prognostic factors have emerged but requirereplication and validation in further studies before theyare included in systematic reviews. These include physicalfactors of decreased range of neck movement, cold hyper-algesia or cold intolerance and impaired sympatheticvasoconstriction (Kasch et al 2005, Sterling et al 2005,2006). The psychological domain of post-traumatic stresssymptoms is emerging as a dominant factor in poor

outcome following whiplash injury (Buitenhuis et al2006, Sterling et al 2006) with the latter study demon-strating a superior predictive capacity of this variablewhen compared to other psychological domains. Addi-tional psychological factors such as high catastrophising,low self efficacy and palliative coping strategies have alsobeen identified, in some studies, as potentially influen-cing recovery (Buitenhuis et al 2003, Hendricks et al2005).

The role of the controversial issue of compensationrelated factors is inconclusive with some studies showingit has predictive capacity (Carroll et al 2008) and othersreporting no predictive capacity of this factor (Scholten-Peeters et al 2003). A recent systematic meta-review out-lined the limitations of research of the influence of injurycompensation on health outcomes including the lowquality of primary research papers in this area, the hetero-geneous nature of compensation schemes studies andthe lack of use of validated health outcome measures(Spearing & Connelly 2010). These authors could findonly one systematic review that could be considered bothinternally and externally valid and based on this, theirfindings were: ‘that there is evidence of no associationbetween fault-based injury compensation and poor healthoutcomes among people with whiplash’ (Spearing &Connelly 2010).

IMPLICATIONS FOR ASSESSMENTOF WHIPLASH

It is clear that the whiplash condition involves complex-ities between physiological and psychological factors.Whilst the presence of high initial levels of pain and/ordisability are consistent predictors of poor outcome(Scholten-Peeters et al 2003), the additional presence ofsensory hypersensitivity (particularly cold hyperalgesia)and also post-traumatic stress symptoms have beenshown to substantially improve predictive capacity(Sterling et al 2005). These factors have also been shownto be associated with non-responsiveness to physicalinterventions (Jull et al 2007). The long-term functionalstatus following whiplash may be established within afew months of injury with little further improvement afterthis time (Kamper et al 2008). This reiterates the impor-tant role clinicians play in the early post-injury stage andeven towards the prevention of chronicity.

The patient assessment will need to include an ade-quate history such as previous history of neck pain andheadache as well as the possible mechanism of injury.The patient should be screened for the presence of any‘red flag’ condition (WAD IV – fracture or dislocation).Whilst accident related features have not been shownto be consistent prognostic indicators of outcome(Scholten-Peeters et al 2003), they have shown some

Chapter | 8 | Whiplash associated disorders

117

predictive capacity in certain studies (Sturzenegger et al1995). Since pain and disability levels have been repeat-edly shown to be a consistent indicator of prolongedrecovery (Hendricks et al 2005), it is essential that a vali-dated questionnaire, such as the NDI, is used in the initialassessment. Certain physical factors, such as loss of neckmovement, cold hyperalgesia, are predictive of poorrecovery and must also be carefully assessed for. Withrespect to whiplash injury the psychological factor ofpost-traumatic stress appears to be involved in the transi-tion from the acute to chronic stages of the condition andclinicians may want to include a measure of post-trau-matic stress symptoms (e.g. Impact of Events Scale) intheir assessment of the whiplash injured patient.

Recent calls have been made to direct clinical examina-tion toward the recognition and identification of mechan-isms involved in the patient’s pain syndrome (Max 2000,Treede et al 2002). At present sensory examination such asthat required to detect the variety of sensory disturbancesoutlined above is rarely performed and if it is performed,is usually limited to rudimentary assessment of musclepower, deep tendon reflexes and light touch sensation.More detailed assessment of sensory changes in neck painpatients is necessary. The first stage of this assessmentwould be thorough recording of the patient’s symptomsincluding the nature of pain. Although the usefulness ofsymptom classification as a way of clarifying painmechanisms is debatable, it is a necessary part of thepatient’s assessment (Jensen & Baron, 2003). In recenttimes questionnaires have been developed that aim tospecifically identify neuropathic like pain (Bennett et al2007). Using the S-LANSS questionnaire (Bennett et al2005), it has been shown that 20% of an acute whiplashcohort likely have a predominantly neuropathic pain con-dition with certain items being particularly associatedwith higher levels of pain and disability (Sterling & Pedler2009). These were ‘electric shock’ type pain that comes inbursts, burning pain in the neck and hyperalgesia to man-ual pressure. Inclusion of this questionnaire with particu-lar attention to these items may be a useful addition tothe clinical assessment of acute WAD.

Quantitative sensory testing can also be used. Thiscould include the measurement of mechanical painthresholds with pressure algometry (Fig. 8.3) and determi-nation of the presence of allodynia with light tactile stim-ulation. Cold hyperalgesia is emerging as an importantfactor in both the prediction of outcome (Sterling et al2005) and for gauging treatment responsiveness (Jullet al 2007). It is more difficult to measure clinically butoptions may include the use of thermorollers set at prede-termined temperatures (Sterling 2008) or the time takento reach pain threshold following the application of ice(Cathcart & Pritchard 2006). However, it has been shownthat there is little relationship between S-LANSS items andcold pain threshold indicating that physical measuresof sensory hyper-sensitivity will also need to be included

in the assessment of acute whiplash (Sterling & Pedler2009).

However it should be noted that whilst such sensoryassessments can provide useful information, at presentthere is no consensus about the most appropriate methodto use and what to compare findings with (Jensen &Baron 2003). The development of the most appropriatesensory examination of whiplash injured patients is atan early stage and moves toward further development intoclinically valid and useful measures is of vital importance.

Physiotherapists routinely assess cervical range ofmovement and this will remain a mainstay of assessmentof whiplash due to the prognostic capacity of this mea-sure. Assessment will also need to include muscle recruit-ment patterns of the cervical and shoulder girdle regions.Further, the assessment of sensori-motor control is rela-tively simple to undertake in the clinical situation and willbe particularly important in whiplash injured patientswho report dizziness associated with their neck pain.Readers are referred to Jull et al (2008) for a detailedaccount of how to undertake these assessments.

IMPLICATIONS FOR MANAGEMENTOF WHIPLASH ASSOCIATEDDISORDERS

Clinical guidelines for the management of acute andchronic WAD promote education, assurance to thepatient, the maintenance of activity levels, general andspecific exercises, simple analgesics and encouragementof coping strategies (Scholten-Peeters et al 2002, MAA2007, TRACsa 2008). Some recent clinical guidelines have

Fig 8.3 Measurement of pressure pain thresholds (PPT)(Somedic AB, Sweden) over the median nerve trunk. Decreasedpressure pain thresholds in areas remote to the cervical spinemay reflect augmented central pain processing mechanisms.

Part | 2 | Cervical–thoracic spine

118

become more cognizant of the complex presentation ofsome individuals with whiplash and have attempted toinclude recommendations for the identification of factorssuch as sensory disturbance and psychological distress(MAA 2007).

Whilst the resumption of activity is almost universallyrecommended, the case for the avoidance of pain provoca-tion may be an important aim of any physical interventionfor patients demonstrating features of sensory hypersensitiv-ity. The application of non-judicious physical mechanicallystimulating treatments may serve to maintain and prolongthis hypersensitivity and have a deleterious effect on thepatient’s long-term outcome (Sterling & Kenardy 2008). Itis not suggested that these patients avoid activity, as themaintenance of activity levels opposed to rest and use of acollar has been shown to be important in the managementof acute whiplash (Rosenfeld et al 2003). Certainly studiesinvestigating fibromyalgia syndrome, a condition also pro-posed to have disturbed central pain processing mechan-isms, have shown that sensory hypersensitivity increasesfollowing some forms of exercise including isometric andsub-maximal aerobic exercise (Vierck 2006).

Possible treatment modalities for central hyperexcitabil-ity in pain of musculoskeletal origin are largely unex-plored. Pharmacological management approaches havebeen suggested (Curatolo et al 2006) but effectiveness ofthis form of treatment is yet to be investigated in WAD.Furthermore the side-effects of some drug therapyapproaches are daunting (Vierck 2006). A predominantlymedication-based approach to management, particularlyin the acute stage may not be feasible. An importantunanswered question is whether specific physiotherapyinterventions have the capacity to modulate central hyper-excitability in WAD.

Theoretically physical interventions such as TENSand acupuncture may be useful in modulating sensoryhypersensitivity and these have not been specifically

investigated in WAD. Few studies have investigated theeffects of psychologically based interventions in this con-dition. However Blanchard et al (2003) found that psy-chological intervention directed toward post-traumaticstress disorder in chronic whiplash, whilst influencingpost-traumatic stress symptoms, did not have an effect ofpain levels in this group.

This is not to suggest that exercise and movementapproaches are not indicated for those with a more ‘com-plicated’ whiplash presentation. A combined specific exer-cise and manual therapy approach has demonstratedefficacy in the management cervicogenic headache (idio-pathic neck pain) (Jull et al 2002) and this treatmentapproach has shown to decrease pain and disability inpatients with chronic whiplash without the presence ofmechanical and cold hyperalgesia (Jull et al 2007). Itmay be that such an approach has a greater role in thesesubgroups of neck pain. However it is apparent that it willbe important to identify those patients with the presenceof sensory hypersensitivity (and psychological distress,particularly post-traumatic stress) such that additionalmanagement can be provided.

CONCLUSIONS

Whiplash is a complex, heterogeneous intriguing conditioninvolving both physical (motor and sensory) disturbancesand psychological distress. It is also one of the mostfrustrating conditions for clinicians to manage. It wouldappear that the quest to better understand WAD has onlyjust begun and the results from recent research efforts havepaved the way for further directions for research. As newknowledge emerges, the clinical assessment of the condi-tion will become more informed and this will translate toimproved outcome for injured people.

REFERENCES

Banic, B., Petersen-Felix, S.,Andersen, O., Radanov, B.,Villiger, P., Arendt-Nielsen, L., et al.,2004. Evidence for spinal cordhypersensitivity in chronic pain afterwhiplash injury and in fibromyalgia.Pain 107, 7–15.

Bennett, M., Smith, B., Torrance, N.,Potter, J., 2005. The S-LANSS scorefor identifying pain of predominantlyneuropathic origin: validation for usein clinical and postal research. J. Pain6, 149–158.

Bennett, M., Attal, N., Backonja, M.,Baron, R., Bouhassira, D.,Freynhagen, R., et al., 2007. Using

screening tools to identifyneuropathic pain. Pain127, 199–203.

Blanchard, E., Hickling, E., Devineni, T.,Veazey, C., Galovski, T., Mundy, E.,et al., 2003. A controlled evaluationof cognitive behaviour therapy forposttraumatic stress in motor vehicleaccident survivors. Behav. Res. Ther.41, 79–96.

Borchgrevink, G., Kaasa, A.,McDonagh, D., Stiles, T.,Haraldseth, O., Lereim, I., 1998.Acute treatment of whiplash necksprain injuries. A randomized trial oftreatment during the first 14 days

after a car accident. Spine 23, 25–31*LHM: Herston Medical, BiologicalSciences *LHC: RD768.S67.

Buitenhuis, J., Spanjer, J., Fidler, V., 2003.Recovery from acute whiplash – therole of coping styles. Spine28, 896–901.

Buitenhuis, J., DeJong, J., Jaspers, J.,Groothoff, J., 2006. Relationshipbetween posttraumatic stress disordersymptoms and the course ofwhiplash complaints. J. Psychosom.Res. 61, 681–689.

Carroll, L., Cassidy, D., Cote, P., 2006.The role of pain coping strategies in

Chapter | 8 | Whiplash associated disorders

119

prognosis after whiplash injury:passive coping predicts slowedrecovery. Pain 124, 18–26.

Carroll, L., Holm, L., Hogg-Johnson, S.,Cote, P., Cassidy, D., Haldeman, S.,et al., 2008. Course and PrognosticFactors for Neck Pain inWhiplash-Associated Disorders(WAD). Results of the Bone and JointDecade 2000–2010 Task Force onNeck Pain and Its AssociatedDisorders. Spine 33, 583–592.

Cassidy, J.D., Carroll, L.J., Cote, P.,Lemstra, M., Berglund, A., Nygren, A.,2000. Effect of eliminatingcompensation for pain and sufferingon the outcome of insurance claimsfor whiplash injury. N. Engl. J. Med.20, 1179–1213.

Cathcart, S., Pritchard, D., 2006.Reliability of pain thresholdmeasurement in young adults.J. Headache Pain 7, 21–26.

Chien, A., Eliav, E., Sterling, M., 2008a.Hypoaesthesia occurs in acutewhiplash irrespective of pain anddisability levels and the presence ofsensory hyper-sensitivity. Clin. J. Pain24, 759–766.

Chien, A., Eliav, E., Sterling, M., 2008b.Whiplash (Grade II) and cervicalradiculopathy share a similar sensorypresentation: An investigation usingquantitative sensory testing. Clin. J.Pain 24, 595–603.

Chien, A., Eliav, E., Sterling, M., 2010.Sensory hypoaesthesia is a feature ofchronic whiplash but not chronicidiopathic neck pain. Man. Ther.15, 48–53.

Crouch, R., Whitewick, R., Clancy, M.,Wright, P., Thomas, P., 2006.Whiplash associated disorder:incidence and natural history overthe first month for patientspresenting to a UK emergencydepartment. Emerg. Med. J.23, 114–118.

Curatolo, M., Petersen-Felix, S.,Arendt-Nielsen, L., Giani, C.,Zbinden, A., Radanov, B., 2001.Central hypersensitivity in chronicpain after whiplash injury. Clin. J.Pain 17, 306–315.

Curatolo, M., Arendt-Nielsen, L.,Petersen-Felix, S., 2006. Centralhypersensitivity in chronic pain:mechanisms and clinicalimplications. Phys. Med. Rehabil.Clin. N. Am. 17, 287–302.

Cusick, J., Pintar, F., Yoganandan, N.,2001. Whiplash syndrome: kinematicfactors influencing pain patterns.Spine 26, 1252–1258.

Dall’Alba, P., Sterling, M., Trealeven, J.,Edwards, S., Jull, G., 2001. Cervicalrange of motion discriminatesbetween asymptomatic and whiplashsubjects. Spine 26, 2090–2094.

Davis, S., Teresi, L., Bradley, W.,Ziemba, M., Bloze, A., 1991. Cervicalspine hyperextension injuries: MRfindings. Radiology 180, 245–251.

Drottning, M., Staff, P., Levin, L.,Malt, U., 1995. Acute emotionalresponse to common whiplashpredicts subsequent pain complaints:a prospective study of 107 subjectssustaining whiplash injury. Nord. J.Psychiatry. 49, 293–299.

Elliott, J., Jull, G., Noteboom, T.,Darnell, R., Galloway, G.,Gibbon, W., 2006. Fatty infiltrationin the cervical extensor muscles inpersistent whiplash associateddisorders: an MRI analysis. Spine31, E847–E851.

Elliott, J., Jull, G., Sterling, M.,Noteboom, T., Darnell, R.,Galloway, G., 2008. Fatty infiltrate inthe cervical extensor muscles is not afeature of chronic insidious onsetneck pain. Clin. Radiol. 63, 681–687.

Elliott, J., O’Leary, S., Sterling, M.,Hendrikz, J., Pedler, A., Jull, G., 2010.MRI findings of fatty infiltrate in thecervical flexors in chronic whiplash.Spine 35, 948–954.

Foa, E., Cashman, L., Jaycox, L., Perry, K.,1997. The validation of a self-reportmeasure of posttraumatic stressdisorder: the posttraumaticdiagnostic scale. Psychol. Assess.9, 445–451.

Forbes, D., Creamer, M., Phelps, A.,Bryant, R., McFarlane, A., Devilly, G.,et al., 2007. Australian guidelines forthe treatment of adults with acutestress disorder and posttraumaticstress disorder. Aust. N. Z. J.Psychiatry 41, 637–648.

Hartling, L., Brison, R., Ardern, C.,Pickett, W., 2001. Prognostic value ofthe Quebec classification of whiplashassociated disorders. Spine26, 36–41.

Heikkila, H., Wenngren, B., 1998.Cervicocephalic kinestheticsensibility, active range of cervicalmotion and oculomotor function in

patients with whiplash injury. Arch.Phys. Med. Rehabil. 79, 1089–1094.

Hendricks, E., Scholten-Peeters, G., vander Windt, D., Neeleman-van derSteen, C., Oostendorp, R.,Verhagen, A., 2005. Prognosticfactors for poor recovery in acutewhiplash patients. Pain114, 408–416.

Horowitz, M., Wilner, N., Alvarez, W.,1979. Impact of Event Scale: ameasure of subjective stress.Psychosometric Medicine41, 209–218.

Jensen, T., Baron, R., 2003. Translationof symptoms and signs intomechanisms in neuropathic pain.Pain 102, 1–8.

Jull, G., Trott, P., Potter, H., Zito, G.,Niere, K., Emberson, J., et al., 2002. Arandomized controlled trial ofphysiotherapy management forcervicogenic headache. Spine27, 1835–1843.

Jull, G., Kristjansson, E., Dall’Alba, P.,2004. Impairment in the cervicalflexors: a comparison of whiplashand insidious onset neck painpatients. Man. Ther. 9, 89–94.

Jull, G., Sterling, M., Kenardy, J.,Beller, E., 2007. Does the presence ofsensory hypersensitivity influenceoutcomes of physical rehabilitationfor chronic whiplash? A preliminaryRCT. Pain 129, 28–34.

Jull, G., Sterling, M., Falla, D.,Treleaven, J., O’Leary, S., 2008.Whiplash, headache and neck pain:research based directions for physicaltherapies. Elsevier, Edinburgh.

Kamper, S., Rebbeck, T., Maher, C.,McAuley, J., Sterling, M., 2008.Course and prognostic factorsof whiplash: a systematic reviewand meta-analysis. Pain138, 617–629.

Kasch, H., Flemming, W., Jensen, T.,2001a. Handicap after acute whiplashinjury. Neurology 56, 1637–1643.

Kasch, H., Stengaard-Pedersen, K.,Arendt-Nielsen, L., Jensen, T., 2001b.Headache, neck pain and neckmobility after acute whiplash injury.Spine 26, 1246–1251.

Kasch, H., Qerama, E., Bach, F.,Jensen, T., 2005. Reduced coldpressor pain tolerance innon-recovered whiplash patients: a 1year prospective study. Eur. J. Pain9, 561–569.

Part | 2 | Cervical–thoracic spine

120

Kivioja, J., Jensen, I., Lindgren, U., 2005.Early coping strategies do notinfluence the prognosis afterwhiplash injuries. Injury36, 935–940.

Kivioja, J., Jensen, I., Lindgren, U., 2008.Neither the WAD-classification northe Quebec Task Force follow-upregimen seems to be important forthe outcome after a whiplash injury.A prospective study on 186consecutive patients. Eur. Spine J.17, 930–935.

Koelbaek-Johansen, M.,Graven-Nielsen, T., Schou-Olesen, A.,Arendt-Nielsen, L., 1999. Muscularhyperalgesia and referred pain inchronic whiplash syndrome. Pain83, 229–234.

Kongsted, A., Bendix, T., Qerama, E.,Kasch, H., Bach, F., Korsholm, L.,et al., 2008. Acute stress response andrecovery after whiplash injuries. Aone year prospective study. Eur. J.Pain 12, 455–463.

Krakenes, J., Kaale, B., 2006. Magneticresonance imaging assessment ofcranio-vertebral ligaments andmembranes after whiplash trauma.Spine 31, 2820–2826.

Lord, S., Barnsley, L., Wallis, B.,Bogduk, N., 1996. Chronic cervicalzygapophyseal joint pain afterwhiplash: a placebo-controlledprevalence study. . . includingcommentary by Derby R Jr. Spine21, 1737–1745.

MAA, 2007. Guidelines for themanagement of whiplash associateddisorders. Motor Accident Authority(NSW), Sydney.www.maa.nsw.gov.au.

MAIC, 2004. Annual Report 2004.Motor Accident InsuranceCommission, Brisbane.

Max, M., 2000. Is mechanism-based paintreatment attainable? Clinical trialissues. J. Pain 1, 2–9.

McLean, S., Clauw, D., Abelson, J.,Liberzon, I., 2005. The developmentof persistent pain and psychologicalmorbidity after motor vehiclecollision: integrating the potentialrole of stress response systems into abiopsychosocial model. Psychosom.Med. 67, 783–790.

Nederhand, M., Hermens, H.,Ijzerman, M., Turk, D., Zilvold, G.,2002. Cervical muscle dysfunction inchronic whiplash associated disorder

grade 2. The relevance of trauma.Spine 27, 1056–1061.

Passatore, M., Roatta, S., 2006. Influenceof sympathetic nervous system onsensorimotor function: whiplashassociated disorders (WAD) as amodel. Eur. J. Appl. Physiol.98, 423–449.

Provinciali, L., Baroni, M., Illuminati, L.,Ceravolo, M., 1996. Multimodaltreatment to prevent the latewhiplash syndrome. Scand. J.Rehabil. Med. 28, 105–111.

Raak, R., Wallin, M., 2006. Thermalthresholds and catastrophising inindividuals with chronic pain afterwhiplash injury. Biology ResearchNursing 8, 138–146.

Radanov, B., Sturzenegger, M., DiStefano, G., 1995. Long-termoutcome after whiplash injury. A2-year follow-up considering featuresof injury mechanism and somatic,radiologic, and psychologicalfindings. Medicine 74, 281–297.

Rosenfeld, M., Gunnarsson, R.,Borenstein, P., 2000. Earlyintervention in whiplash-associateddisorders. A comparison of twoprotocols. Spine 25, 1782–1787.

Rosenfeld, M., Seferiadis, A., Carllson, J.,Gunnarsson, R., 2003. Activeintervention in patients withwhiplash associated disordersimproves long-term prognosis: arandomised controlled clinical trial.Spine 28, 2491–2498.

Scholten-Peeters, G., Bekkering, G.,Verhagen, A., van der Windt, D.,Lanser, K., Hendriks, E., et al., 2002.Clinical practice guideline for thephysiotherapy of patients withwhiplash associated disorders. Spine27, 412–422.

Scholten-Peeters, G., Verhagen, A.,Bekkering, G., van der Windt, D.,Barnsley, L., Oostendorp, R., et al.,2003. Prognostic factors of WhiplashAssociated Disorders: a systematicreview of prospective cohort studies.Pain 104, 303–322.

Scott, D., Jull, G., Sterling, M., 2005.Sensory hypersensitivity is a featureof chronic whiplash associateddisorders but not chronic idiopathicneck pain. Clin. J. Pain 21, 175–181.

Spearing, N., Connelly, L., 2010. Iscompensation “bad for health”? Asytematic meta-review. Injury Jan 7[Epub ahead of print].

Spitzer, W., Skovron, M., Salmi, L.,Cassidy, J., Duranceau, J., Suissa, S.,et al., 1995. Scientific Monograph ofQuebec Task Force on Whiplashassociated Disorders: redefining“Whiplash” and its management.Spine 20, 1–73.

Sterling, M., 2004. A proposed newclassification system for whiplashassociate disorders – implications forassessment and management. Man.Ther. 9, 60–70.

Sterling, M., 2006. Sensoryhypersensitivity and psychologicaldistress following whiplash injury: Isthere a relationship?, Australian PainSociety Annual Scientific Meeting.Melbourne.

Sterling, M., 2008. Testing forsensory hypersensitivity orcentral hyperexcitability associatedwith cervical spine pain.J. Manipulative Physiol. Ther.31, 534–539.

Sterling, M., Kenardy, J., 2006. Therelationship between sensory andsympathetic nervous system changesand acute posttraumatic stressfollowing whiplash injury – aprospective study. J. Psychosom. Res.60, 387–393.

Sterling, M., Kenardy, J., 2008. Physicaland psychological aspects ofwhiplash: important considerationsfor primary care assessment. Man.Ther. 13, 93–102.

Sterling, M., Pedler, A., 2009. Aneuropathic pain component iscommon in acute whiplash andassociated with a more complexclinical presentation. Man. Ther.14, 173–179.

Sterling, M., Jull, G., Vicenzino, B.,Kenardy, J., 2003a. Sensoryhypersensitivity occurs soon afterwhiplash injury and is associatedwith poor recovery. Pain104, 509–517.

Sterling, M., Jull, G., Vizenzino, B.,Kenardy, J., Darnell, R., 2003b.Development of motor systemdysfunction following whiplashinjury. Pain 103, 65–73.

Sterling, M., Kenardy, J., Jull, G.,Vicenzino, B., 2003c. Thedevelopment of psychologicalchanges following whiplash injury.Pain 106, 481–489.

Sterling, M., Jull, G., Vicenzino, B.,Kenardy, J., 2004. Characterization of

Chapter | 8 | Whiplash associated disorders

121

acute whiplash associated disorders.Spine 29, 182–188.

Sterling, M., Jull, G., Vicenzino, B.,Kenardy, J., Darnell, R., 2005.Physical and psychological factorspredict outcome following whiplashinjury. Pain 114, 141–148.

Sterling, M., Jull, G., Kenardy, J., 2006.Physical and psychological predictorsof outcome following whiplashinjury maintain predictive capacity atlong term follow-up. Pain122, 102–108.

Sterling, M., Pettiford, C., Hodkinson, E.,Curatolo, M., 2008. Psychologicalfactors are related to some sensorypain thresholds but not nociceptiveflexion reflex threshold in chronicwhiplash. Clin. J. Pain 24, 124–130.

Sterling, M., Hendrikz, J., Kenardy, J.,2009. Developmental trajectories ofpain/disability and PTSD symptomsfollowing whiplash injury, AustralianSpine Society Annual Conference.Brisbane.

Stewart, M., Maher, C., Refshauge, K.,Herbert, R., Bogduk, N.,Nicholas, M., 2007. Randomisedcontrolled trial of exercise for chronicwhiplash associated disorders. Pain128, 59–68.

Sturzenegger, M., Radanov, B.,Stefano, G.D., 1995. The effect ofaccident mechanisms and initialfindings on the long-term course ofwhiplash injury. J. Neurol.242, 443–449.

Taylor, J., Finch, P., 1993. Acute injury ofthe neck: anatomical and

pathological basis of pain. Ann. Acad.Med. Singapore 22, 187–192.

Taylor, J., Taylor, M., 1996. Cervicalspinal injuries: an autopsy study of109 blunt injuries. Journal ofMusculoskeletal Pain 4, 61–79.

TRACsa, 2008. A clinical pathway forbest practice management of acuteand chronic whiplash-associateddisorders. South Australian Centre forTrauma and Injury Recovery,Adelaide.

Treede, R.D., Rolke, R., Andrews, K.,Magerl, W., 2002. Pain elicited byblunt pressure: neurobiological basisand clinical relevance. Pain98, 235–240.

Treleaven, J., Jull, G., Sterling, M., 2003.Dizziness and unsteadiness followingwhiplash injury – characteristicfeatures and relationship withcervical joint position error. J.Rehabil. 34, 1–8.

Treleaven, J., Jull, G., Low Choy, N.,2005a. Standing balance in persistentwhiplash: a comparison betweensubjects with and without dizziness.J. Rehabil. Med. 37, 224–229.

Treleaven, J., Jull, G., Low Choy, N.,2005b. Smooth pursuit neck torsiontest in whiplash associated disorders:relationship to self-report of neck painand disability, dizziness and anxiety.J. Rehabil. Med. 37, 219–223.

Uhrenholt, L., Grunnet-Nilsson, N.,Hartvigsen, J., 2002. Cervical spinelesions after road traffic accidents.A systematic review. Spine27, 1934–1941.

Vierck, C., 2006. Mechanisms underlyingdevelopment of spatially distributedchronic pain (fibromyalgia). Pain124, 242–263.

Vlaeyen, J., Kole-Snijders, A., Boeren, R.,1995. Fear of movement/re-injury inchronic low back pain patients andits relation to behaviouralperformance. Pain 62, 363–372.

Walton, D., 2010. Prognosis for chronicpain and disability followingwhiplash: A meta-analysis. J. Orthop.Sports Phys. Ther. (in press).

Wenzel, H., Haug, T., Mykletun, A.,Dahl, A., 2002. A population study ofanxiety and depression amongpersons who report whiplashtraumas. J. Psychosom. Res.53, 831–835.

Williamson, E., Williams, M., Gates, S.,Lamb, S., 2008. A systematic reviewof psychological factors and thedevelopment of late whiplashsyndrome. Pain 135, 20–30.

Winkelstein, B.A., Nightingale, R.W.,Richardson, W.J., Myers, B.S., 2000.The cervical facet capsule and its rolein whiplash injury. Spine25, 1238–1246.

Woodhouse, A., Vasseljen, O., 2008.Altered motor control patterns inwhiplash and chronic neck pain.BMC Musculoskelet. Disord. 9, 90.

Yunus, M., 2007. Fibromyalgia andoverlapping disorders: the unifyingconcept of central sensitivitysyndromes. Semin. Arthritis Rheum.36, 339–356.

Part | 2 | Cervical–thoracic spine

122