Paper Reviews

By Stephen May

Whiplash associated disorders (WAD) – a review

Introduction

Whiplash associated disorder (WAD) is the term applied to a collection of signs and symptoms that are said to result from a road traffic accident (RTA). The predominant symptoms are neck pain and headache, and the signs restricted neck movement. The pathophysiology of whiplash will be briefly considered. This review will primarily consider the epidemiology of whiplash and its management. There is however heated debate within the medical community even about the existence of this disorder, and the main arguments in this debate will be briefly considered.

What is whiplash?

Whiplash is a familiar term to patients and clinicians. It generally denotes neck symptomatology that has commenced during or shortly after a motor accident. Strictly the causal event for a true ‘whiplash’ injury is said to be a rear-end collision at a modest speed into a stationary vehicle, in which the victim is facing forwards (Bogduk 1986). In practice anyone involved in a car accident that develops symptoms is likely to be considered to have ‘whiplash’. Neck pain that develops after a diving incident or other high velocity impact to the neck is also sometimes included in the term. The Scientific Monograph authored by the Quebec Task Force (QTF), which is one of the fullest literature reviews of recent years, gives the following definition (Spitzer et al 1995).“Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during diving or other mishaps. The impact may result in bony or soft-tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations (Whiplash-Associated Disorders)”.

Pathophysiology

The kinematics of whiplash is discussed by Bogduk (1986). As the car and seat are propelled forward the body and shoulders are moved likewise; the head resists forward displacement, and is thrown into extension. Once the inertia of the head is overcome, the leverage provided by the neck allows the head to be propelled into acceleration, and it is catapulted into flexion. Head acceleration can be as high as 12G in the extension phase and 16G in the flexion stage.

The possible pathological events during this occurrence are numerous, and include damage to a range of soft tissues, the intervertebral disc, zygapophyseal joints, the odontoid process, the temporomandibular joint, and other structures, even including the brain (Bogduk 1986). The pathophysiology of whiplash is discussed in detail elsewhere (Barnsley et al 1994a, Bogduk 1986).

Following whiplash injury disc herniations (Petersson et al 1997, Jonsson et al 1994, Davis et al 1991), ligament damage and fractured end-plate (Davis et al 1991), cervical muscle dysfunction (Nederhand et al 2000), faulty vestibular functioning (Chester 1991), and vertebral artery occlusion (Giacobetti et al 1997) have all been reported with detailed investigations. Damage to the intervertebral disc and zygapophyseal joint in the cervical and lumbar spines has been reported in autopsy studies from road accident victims (Taylor & Twomey 1993, Twomey et al 1989).  

However despite these accounts of specific pathology other investigators using sophisticated diagnostic imaging have been unable to detect any soft tissue injuries in acute patients who nonetheless developed symptoms (Barton et al 1993, Ronnen et al 1996). Ronnen et al (1996) list six other papers that also had largely negative findings with MRI.

In over 300 patients with chronic neck pain following various neck traumas, using provocation and abolition of pain with intra-articular injections as the criteria, 53% had a symptomatic disc and 26% a symptomatic zygapophyseal joint (Aprill & Bogduk 1992). In a group of 56 patients symptom response in both structures was observed in 41%, to individual structures in about 20% each, with neither joint implicated in 17% (Bogduk & Aprill 1993).

One research group has demonstrated that one of the commonest sources of chronic neck pain or headache following whiplash is the cervical zygapophyseal joints. Several studies of consecutive patients with chronic symptoms referred to tertiary care have been undertaken. Very strict criteria were used, with double intra-articular injections to make the diagnosis. Repeat injections are necessary because there is roughly a 40% placebo response to a single injection. Between 27% and 54% of these groups were identified with this pathology (Barnsley et al 1995, Lord et al 1994, 1996). Symptomatic segmental levels were predominantly C2/3 and C5/6.

Is whiplash a real syndrome?

The medical literature is divided between those who believe in the validity of WAD, and those who claim it to be a myth. It has been argued that “whiplash syndrome”, as opposed to brief and insignificant neck pain, is no more than a cultural construct within a biopsychosocial model of pain (Ferrari & Russell 1997, 1999). It is suggested that WAD exists only in cultures in which pain following RTA is expected, bred in an environment in which anxiety and fears are nurtured by health professionals, lawyers, and patients alike. These authors “believe that the “whiplash syndrome” is an example of illness actually induced by society, in general, and by physicians in particular.”  (Ferrari & Russell 1997, p618)

  • The following points are mentioned in support of their viewpoint:
  • studies that demonstrate no injury with sophisticated imaging studies, as mentioned above
  • the failure to cause injury in animals except with exceptional force
  • the lack of neck pain in those who crash cars for fun, or let themselves be involved in ‘crashes’ for the sake of experiment
  • the variability of symptoms in different cultures, which appears to reflect legal and medico-legal determinants, rather than the rate of accidents.

They seek to show that reporting ‘injuries’ in part reflects compensation systems, and that the prevalence of chronic symptoms varies in different countries. Where individuals do not witness WAD-type illness behaviour, the argument is that they don’t get whiplash. In this regard the study from Lithuania (Schrader et al 1996) is much quoted. “Where there is little knowledge or expectation of the potential of a whiplash injury to lead to chronic symptoms, and where involvement of insurance companies, litigation and even the therapeutic community is rare….(there is) no increased prevalence of chronic neck pain after a rear-end collision, when compared with the background risk of chronic neck pain in uninjured control subjects.”  (Ferrari & Russell 1999, p2).

The study from Lithuania (Schrader et al 1996) found symptoms in 35% in a retrospective investigation of police records of those involved in rear-end collisions one to three years previously; this compared to 33% in a non-injured control population. This study has been criticised as only 31 of the 202 (15%) who had been involved in an accident reported neck pain immediately afterwards. Thus if the intention was to study the natural history of neck pain following on from trauma a sample size of 3000 would have been necessary to detect a difference between the subjects and controls – in fact there were 404 in total (Freeman et al 1999). The authors state that in fact they wished to investigate chronic symptoms in an unselected cohort (Schrader et al 1996b).  

In a critical review based on a methodological approach that looks at the soundness of whiplash syndrome as an entity, its overall validity was found to be low (Stovner 1996).  Face validity was excellent, that is, it is a condition recognised by clinicians and patients, and descriptive validity was good with a multitude of descriptive studies. However construct validity and predictive validity was generally poor. “There is a virtual lack of proof of a causal relationship to the injury mechanism after which the syndrome has been named because strength of association has not been measured and temporality can not be ascertained with the methods that have been applied.”  (Stovner 1996, p2743)

Freeman et al (1999) produced a review that challenges those authors who refute the existence of the whiplash syndrome. They note that the QTF study concluded that WAD is usually self-limiting, and patients can be assured of a favourable prognosis. This stands in contrast to the four studies on prognosis that the QTF accepted, which show that on average about 40% of patients were still symptomatic two years after the accident (Spitzer et al 1995). As a result of their literature review Freeman et al (1999) determined that there is no epidemiological or scientific basis for the following ideas:

  • whiplash injuries do not lead to chronic pain
  • chronic pain from whiplash is psychogenic
  • the risk of chronic neck pain among acutely injured whiplash victims is the same as the prevalence of chronic neck pain in the general population.

Signs and symptoms

Neck pain is the most commonly reported symptom following a RTA, other symptoms that have been described are as in table 1 (Bogduk 1986, Hohl 1974, Pearce 1989, Hildingsson & Toolanen 1990, Norris & Watt 1983, Watkinson et al 1991, Maimaris et al 1988, Barnsley et al 1994a, Brison et al 2000, Radanov & Dvorak 1996, Radanov et al 1992, 1996, Mayou et al 1993, Wallis et al 1996).

Table 1. Presenting signs and symptoms from whiplash

Common symptoms (> 70%, multiple studies)

  • Neck pain
  • Neck stiffness/ limited range of movement

Moderately common symptoms (20 -70%, multiple studies)

  • Headache
  • Shoulder pain
  • Low back pain

Uncommon symptoms (<20%)

  • Arm pain
  • Scapulae pain
  • Numbness / paraesthesia in arm
  • Visual symptoms
  • Auditory symptoms
  • Muscular tenderness
  • Dizziness
  •  Nausea

 Occasional reports

  • Dysphagia
  • Weakness
  • Horner’s syndrome
  • Tinnitus
  • Concussion
  • Insomnia
  • Short-term memory disturbance
  • Cognitive impairment
  • Psychological disturbance, such as
    • Anxiety
    • Irritability
    • Depression
Classification of WAD

As the identification of specific pathology is highly problematical classification is usually based on symptomatology. Most commonly this is related to duration of symptoms, which are described as either acute or chronic. The QTF classification attempts to portray some level of the severity of symptoms resulting from a whiplash injury, table 2 (Spitzer et al 1995).

Table 2. QTF classification of WAD

Grade

Clinical presentation

0

No neck pain

No mechanical signs

1

Neck pain, stiffness or tenderness only

No mechanical signs

2

Neck pain AND

Mechanical signs

3

Neck pain

Mechanical signs AND

Neurological signs

4

Neck pain AND

Fracture or dislocation**

Mechanical signs = reduced movement, tenderness.

Neurological signs = sensory, motor, or reflex deficit.

** This group is obviously not for normal conservative management.

This classification scheme has been found to have prognostic value, in that higher grades have been associated with poorer outcomes at 6, 12, 18, and 24 months (Hartling et al 2001).

Epidemiology

Numerous studies have investigated the natural history of the effects of motor vehicle accidents. Difficulties exist in collecting such data in a way that has generalisability. In order to determine the prevalence of neck pain resulting from such accidents a study would need to find the prevalence of symptoms in a given sample of all accidents at a given place and time period. Few studies approximate to this model. Galasko et al (1993) looked at the incidence of neck sprain in those attending three Accident and Emergency departments (A & E) because of RTA on four different occasions between 1982 and 1991 (see table). Their data shows two distinct features – namely a dramatic increase in the proportion of those involved in RTAs developing neck sprain (not clearly defined) over the decade, as they term it, ‘a modern epidemic’. Secondly it is still less than half of those involved in accidents and who attend A & E departments who develop neck sprain.

Table 3. Incidence of neck sprain after RTA over 10 years

(Galasko et al 1993)

Year

Period

Number of patients

injured in RTA

Incidence of

neck sprain (%)

1982-1983

1 year

  929

  8%

1983-1984

(after seat belt legislation)

1 year

  940

20%

1988

1 year

4319

31%

1990

6 months

2661

42%

1990-1991

1 year

6149

46%

Other sources also suggest that neck symptomatology is not universal following a road accident. A retrospective case note review from two separate years of a random sample of those attending an A & E department following an RTA was conducted. This was to investigate the role of legislation that had made the wearing of seat belts compulsory between the two dates (Thomas 1990). After legislation 52% were recorded as having no injuries, there was a reduction of all injuries but an increase in WAD, and out of 85 sampled only 13 (15%) had whiplash.  Freeman et al (1999) quote various government statistics from the USA – these report that there were five and a half million Americans involved in RTA in 1995, and that 53% of these include whiplash injuries. The information above would suggest that about half of those involved in car accidents, or even less, develop symptoms in the neck.

Most studies actually sample a group who attend health-care with neck pain said to be related to a recent vehicle accident. This may not include all those with neck pain, especially in the earlier studies. Data from other musculoskeletal problems, such as back or shoulder problems, relate that 50% or less of those with such symptoms seek health-care. It is unknown if the traumatic aspect of motor vehicle accidents makes this independence less likely. Any tendency of individuals to self-manage such neck pain may have been partially de-motivated in more recent years by the encouragement of the legal profession to seek compensation for their ‘injury’. Ultimately we cannot be sure that these studies represent all those with WAD, only those who have sought care. This group may be those with more severe symptoms, or those with greater anxiety concerning their symptoms; they may thus represent a biased sample more likely to be symptomatic at follow-up. If this were the case then a more pessimistic prognostic outlook would be presented than actually occurs in all those involved in accidents. In support of this perspective one report describes a few patients refusing participation in a study because they regarded the incident as trivial (Mayou & Bryant 1996).

Given the limitations of these studies their quality is improved if certain factors are incorporated in the design (Barnsley et al 1994, Freeman et al 1998). To study the natural history of a disease an unselected, inception cohort needs to be assembled at the outset of the study. The cohort needs to be of a reasonable size. Studies are unlikely to be representative if they only include patients who are studied simply because they are accessible to follow-up. Hospital based, rather than private practise, studies suffer least from possible sample bias, especially if drawn from the population attending the A & E department. However it cannot be known if others involved in car accidents never attended hospital.  The reports of consecutive patients are likely to be most inclusive, and high rates of follow-up are important to ensure valid statistics.

A population-based study from Canada followed nearly 3,000 individuals who had sustained a car crash and were receiving compensation (Harder et al 1998). About 20% recovered in a week and about 75% recovered in about 3 months; the median recovery time was 30 days, and 3% had not recovered at one year. However those without a police accident report were excluded from analysis, and recovery was measured by the last date of compensation. This is an indirect measuring tool for symptoms, likely to underestimate persistent complaints, and so this report is not listed.

Table 4. The prognosis of whiplash disorders

Reference

Country

Initial number of patients in sample

Setting

Follow-up

Follow-up time (mean)

Symptoms present at follow-up / control group

Hohl 1974

USA

534 no degenerative changes

Private orthopaedic office.

146

(27%)

5 years

43%

Deans et al 1987

Northern Ireland

175

A & E

137

(78%)

1-2 years

62%/7%

Pearce 1989

England

Unknown

Unknown

100

1/12

3/12

6/12

1 year

38%

29%

18%

15%

Hildingsson & Toolanen 1990

Sweden

93 consecutive patients

Hospital

93

(100%)

2 years

44% S+

14% s

Norris & Watts 1983

England

61 consecutive patients

 A & E

61

(100%)

2 years

QTF 1 44%

QTF 2 81%

QTF 3 90%

Gargan & Bannister 1990

England

61 consecutive patients

A & E

43

(70%)

10 years

40% S+

48% s

Watkinson et al 1991

England

61 consecutive patients

A & E

35

(57%)

11 years

35% S+

51% s

Squires et al 1996

England

61 consecutive patients

A & E

40

(66%)

15 years

42% S+

27% s

Gargan et al 1997

England

50 consecutive patients

A & E

50 (100%)

3/12

2 years

33% S+, 38% s.

35% S+, 29% s.

Maimaris et al 1988

England

120 consecutive patients

A & E

102

(85%)

2 years

34%

Radanov et al 1991

Switzerland

104 consecutive patients

Referred by GPs

78

(75%)

6/12

27%

Pennie & Agambar 1991

England

152

2 A & E

144 (95%)

5/12

14%

Parmar & Raymakers 1993

England

204

144 traced

Medicolegal reports of consultant

100 (69%)

8/12

I year

2 years

3 years

50%

44%

22%

18%

Robinson & Cassar-Pullicino 1993

England

121

46 traced

Medicolegal reports of consultant

21 (46%)

8/12

13 years

81%

86%

Radanov et al 1993

Switzerland

164 referred consecutive patients

Referred by GPs

117 (71%)

Baseline

3/12

6/12

57% H

35% H

27% H

Radanov et al 1994

Switzerland

164 referred consecutive patients

Referred by GPs

117 (71%)

3/12

6/12

I year

44%

31%

24%

Schrader et al 1996

Lithuania

 

Police records, rear end, 1-3 years before.

Response

202 /240 (84%). Control: (63%)

 

35%

33%

Mayou & Bryant

England

74 consecutive patients

A & E

57 (77%)

3/12

1 year

51%

37%

Brison et al 2000

Canada

446 consecutive patients, 380 eligible (rear end, > 18 years)

2 A & E

88% at 6/12

Onset

1/12

3/12

6/12

12/12

2 years

61% S+

51% S+

37% S+

35% S+

34% S+

36% S+

Hartling et al 2001

Canada

 

2 A & E

126 (75%)

2 years

QTF 0   9%

QTF 1 29%

QTF 2 47%

  • A & E = accident and emergency department in hospital.
  • QTF = Quebec Task Force classification at baseline.
  • S+ = major /intrusive symptoms, s = minor/nuisance symptoms.
  •  H = headache

It can be seen that there is considerable variety of outcome across different studies. It is unknown if this reflects the natural variety of a heterogeneous disorder or in some way is a reflection of the different study designs. Prevalence rates of 30-40% one to two years after a car accident are quite common. Three reviews have investigated prognosis, only including the methodologically better studies, with a set of minimum quality criteria. Freeman et al (1998) selected 11 studies – these contained a total of over a thousand patients, with an average of 32 months follow-up; an average of 33% of patients still had symptoms. Studies accepted by the QTF show 27% to 66% still symptomatic at 6 months or more (Spitzer et al 1995). Barnsley et al (1994) found 8 studies fitting their criteria, which together indicated that between 14% and 42% develop chronic symptoms, and that approximately 10% will have constant, severe pain indefinitely. They considered the outcome to be dichotomous with resolution for the majority in the first few months, but for the minority indefinite persistent symptoms.

Examination of the figures in the table above by length of follow-up and quality of study does not essentially alter outcomes, but is not entirely logical either. Studies with a follow-up greater than one year give an average rate of symptoms of 60%, whilst those under a year give an average of 40%. Good quality studies give a prevalence of 68%, poorer quality studies of 43%. 

Clearly there is considerable individual variation in the natural history of WAD; it does not follow a uniform or a predictable course. For some it would seem the incident is very trivial, no or minimal symptoms ensue, and no or minimal health care is sought. For those who attend A & E many will improve in the first few weeks, and become asymptomatic within a month or so. However a substantial minority of those who seek health care will have persistent symptoms two or three months later – further improvements occur in this group, but recovery appears to be less and less likely the longer symptoms persist. Those with long-term symptoms may comprise at least a third of all those who seek help.

Prognostic factors

Various studies have tried to identify factors that are associated with persistent symptoms (Hohl 1974, Deans et al 1987, Hildingsson & Toolanen 1990, Norris & Watts 1983, Watkinson et al 1991, Maimaris et al 1988, Gargan & Bannister 1990, Hartling et al 2001, Stovner 1996, Allen et al 1985, Olney & Marsden 1986, Mayou & Bryant 1996, Pennie & Agambar 1991, Gargan et al 1997, Radanov et al 1991, 1994, Harder et al 1998). A wide range of potential prognostic factors has been considered in different studies. Simply because a factor is associated with persistent pain it cannot be known that it is causative. For certain factors the evidence is contradictory, and thus certain items appear in more than one column in table 5.

The strongest and most consistent factor associated with a poor prognosis is severe initial symptomatology. This is especially so if associated with headache, arm pain, neurological signs or symptoms, and restricted range of movement (QTF WAD 3).

Table 5. Prognostic factors in whiplash disorders

Factors associated with good outcome

Factors associated with persistent pain

Factors found not to affect outcome

 

CLINICAL

 
 

Arm pain**

Initial symptoms

Mild symptoms

Moderate to severe initial symptoms**

Previous NP

 

Arm paraesthesia / numbness**

Arm pain

 

Higher QTF grade*

 
 

Limited ROM*

Limited ROM

 

Scapular pain

 

Later onset pain

Immediate pain*

Time of onset of pain

 

Neurological signs

 
 

Back ache*

 
 

Headache**

 
 

X-ray findings**

X-ray findings

 

Previous headache for subsequent headache

 
  THERAPY  
 

Collar > 12 weeks

 
 

Home traction

 
 

Resumption of therapy

 
 

Hospitalisation following accident

 
  ACCIDENT  
   

Extent of property damage to car

 

Wearing seat belt

Wearing seat belt

 

Rear/front impact**

Type of collision**

 

Passenger*

Position in car

   

Head rest

   

Severity of accident

  Truck or bus  
  INDIVIDUAL  

Younger age*

Older age**

Age

 

Having dependents

 
 

Women*

Sex**

 

Not having full time employment

 
 

Psychological response at 3 months

Baseline psychological variables**

  LITIGATION  

Settlement of compensation

Litigation

Settlement of compensation*

   

Litigation*

*/** = two/or more studies.

Baseline psychological variables do not predict future pain (Radanov et al 1991, 1994). One study that looked at psychological variables as defined by the General Health Questionnaire found that within a week scores were normal in 82% of the group. However in the group who developed persisting and intrusive symptoms at three months scores had become abnormally high in 81% of the patients (Gargan et al 1997). Outcome at two years was predicted both by these raised scores and restricted neck movement. These findings suggest that the disorder has both physical and psychological components, but the psychological response develops after the physical damage, and that these responses are established within three months of injury. Psychological features exhibited by these chronic pain patients would appear to be the consequences of somatic symptoms and not their cause (Wallis et al 1996, Radanov et al 1996).

A controversial factor is the role of litigation, but several studies discount the prognostic value of whether or not compensation is sought, and whether a settlement has been reached (Pennie & Agambar 1991, Mayou & Bryant 1996, Paramar & Raymakers 1993). As can be seen in table 5 the prognostic significance of litigation issues is not clear, with different reports finding contradictory conclusions.

Management of WAD

Maxwell (1996) investigated physiotherapy management of WAD by sending 72 questionnaires to 18 randomly chosen hospitals, from which there was a response rate of 68%. On initial examination physiotherapists most commonly used a Maitland approach (49%), and less commonly a Cyriax (20%) or McKenzie (18%) approach. A wide range of therapies was used, often in combination: mobilisation or mobilisation and exercise (100%), massage (45%), exercise only (40%), McKenzie only (40%), manipulation or manipulation and exercise (50%), mechanical or manual traction (90%), adverse neural tension techniques (50%), electrical modalities and posture advice (90%). Figures are estimated as results are only presented as a bar graph, and clearly show multiple interventions to be common. The proportion that used electrical modalities is not given, but the most commonly used are ultrasound, PEME, TENS, interferential, and short-wave diathermy. As in other areas of musculoskeletal medicine it would appear that physiotherapy management is something of a lottery with common usage of techniques and modalities for which there is little or no evidence.

A recent systematic review of conservative treatments for whiplash has been conducted (Peeters et al 2001). They found 11 studies that met their inclusion criteria, most of poor quality, which undermined their ability to draw conclusions. In 5 studies comparing rest and collar with activity, 4 favoured activity. They concluded that active treatments show a beneficial long-term effect, and that ‘rest makes rusty’. A review of physiotherapy management options for whiplash was made by Thacker (1998).

Logically the management of WAD should be considered in its acute or chronic stage. In the studies looking at interventions for acute WAD most patients were recruited within a few days of the accident, in one study (Provincilai et al 1996) recruitment was on average about a month since injury. Not all significant outcomes have been tabulated. As well as the results listed below, other statistically significant results supported the same outcome – these related to improved range of movement, areas of pain, neck stiffness, or patient assessment of change. In the table the intervention that is superior is underlined.

As far as acute whiplash is concerned the appropriate management is reasonably clearly delineated from the evidence (table 6). This should consist primarily of advice about normal activity, no or minimal sick leave, no use of collar, and a regular and progressive exercise programme starting with rotation and retraction. If with a general progressive exercise routine there is failure to improve then a McKenzie protocol should be instigated.

An active treatment approach is supported by numerous studies (Mealy et al 1986, McKinney et al 1989, McKinney 1989, Borchgrevink et al 1998, Soderlund et al 2000, Rosenfield et al 2000), and this is combined with a McKenzie protocol by Rosenfield et al (2000). Use of collars and rest lead to worse outcomes than active treatment (Mealy et al 1986, McKinney et al 1989, McKinney 1989, Borchgrevink et al 1998), or is no different to no collar (Gennis et al 1996). Mobilisation is better than collar and rest (Mealy et al 1986), but in the long term leads to worse outcomes than exercise and advice (McKinney 1989).

Traction, TENS, and ultrasound are ineffective (Pennie & Agambar 1990, Provinciali et al 1996). For pulsed electro-magnetic therapy (PEMT) or pulsed short wave one study found significant improvements over placebo at 2 and 4 weeks, but no difference at 12 weeks (Foley-Nolan et al 1992); another study found this ineffective as part of treatment package (Provinciali et al 1996). One study, not placebo controlled, found ultra-reiz current to be effective immediately after treatment; with less difference, though still significant, at 6 weeks (Hendriks & Horgan 1996)

Table 6. Intervention studies – Acute/subacute WAD

Reference

Patient Nos.

(% follow-up)

Longest

follow-up

Group 1

Group 2

Group 3

Differences

Mealy et al 1986

61 (84%)

8 weeks

Mobilisation & exercise

Collar, rest 2 weeks

 

Pain:

1: -4, 2: -2.5 (P<0.01).

ROM:

1: +14, 2: +5 (P<0.05)

McKinney et al 1989

247 (69%)

2 months

1 off advice session on posture & movement

Multiple sessions physio

Rest 2 weeks

Pain:

1: -3.5,

2: -3.4,

3: -2.6 (1+2 v 3 P<0.01)

McKinney 1989

247

(68%)

2 years

1 off advice session on posture & movement

Multiple sessions physio

 

Pain:

1: 23%,

2: 44%,

3: 46%. (1 v 2+3 P=0.02)

Pennie, Agambar 1990

152 (89%)

5 months

Traction + exercise

Collar 2 weeks, exercise

 

Pain-free:

1: 81%,

2: 91% (NS)

Foley-Nolan et al 1992

40 (100%)

12 weeks

PEME collar

Placebo collar

 

Pain:

1: -5.2

2: -4 (NS)

Provinciali et al 1996

60

(NR)

6 months

Multi-disciplinary

TENS, US, PEMT

 

Pain:

1: -5.9,

2: -2.6 (P<0.001).

Hendriks & Horgan 1996

20 (70%)

6 weeks

Ultra-reiz

Current

+ as 2

Ice + exercises

 

Mean pain difference: 3.2 (P<.005)

Gennis et al 1996

250 (78%)

6 weeks

No collar

Collar

 

No pain/ better:

1: 79%

2: 86% (NS).

Petterson et al 1998

40 (97%)

6 months

Oral steroid

Placebo

 

Mean sick days:

1: 4.7,

2: 51.7 (P=0.0097).

Borchgrevink et al 1998

201 (89%)

6 months

Act-as-usual

Collar + sick leave 2 weeks

 

Neck pain & headache: 

1 v 2 P<.05 & P<.01

Rosenfield et al 2000

102 (86%)

6 months

1A: < 4 days. 1B: > 2 weeks. Rotation exercises, McKenzie protocol

2A: < 4 days. 2B: >2 weeks.

Advice leaflet

 

Pain:

1A: -30,

1B: -15,

2A: +1,

2B: -7

(1 v 2 P<0.001).

Soderlund et al 2000

66

(53)

6 months

Neck care advice + mobilising exercises

As 1 + isometric exercises

 

Pain (10):

1: -1.7,

2: -2.5 (NS),

Disability (70):

1: -6.4,

2:-10.6 (NS).

(1+2 over time P<.001)

NS = no statistical difference.

US = ultrasound.

PEMT = pulsed electromagnetic therapy. 

NR = not reported.

Underlined intervention = statistical significance in favour of that intervention.

For chronic WAD the literature is generally so sparse and of such poor quality that it is impossible to use evidence to construct an appropriate conservative management strategy (table 7). Most trials relate to injection interventions. An uncontrolled study using a multidisciplinary functional rehabilitation approach reported significant before/after changes in pain, disability, and psychological factors (Vendrig et al 2000). Schofferman & Wasserman (1994) reported significant before/after changes in pain and disability using injections, NSAIDs, and stabilisation exercises, but again without a control group. Harding (1998) describes ways to try to minimise chronicity following whiplash, and Shorland (1998) describes management for chronic symptoms. This is a self-management approach using cognitive-behavioural concepts and exercise and planned activity.

Feine and Lund (1997) reviewed the literature on physiotherapy management of chronic musculoskeletal pain in general. No modality was shown to have a long-term effect greater than placebo, but treatment (including placebo) was always better than no treatment, with the more therapies included in the package the better the outcomes. In other words, whatever you do (active treatment or placebo) will help at the time and the more you do the better the response will appear to be, but the benefit will not outlast the giving of therapy. Only two of 22 trials reported significant long-term benefit; the intervention was exercise.

As in acute patients a mechanical assessment should be conducted. An unreduced derangement may be present requiring a specific directional preference of movement. Multiple direction dysfunctions also occur in this group, as a result of reluctance to move in the earlier stages of recovery. Failure to respond is likely to be high; poorer prognosis is more probable the longer symptoms have been present, and if previous unsuccessful therapy has been received.

Table 7. Intervention studies – Chronic WAD

Reference

Patient nos.

(% follow-up)

Mean length

of symptoms

Group 1

Group 2

Differences

Byrn et al 1993

40 (100% at 8 months

5 years

Tenderpoints injected with sterile water

Tenderpoints injected with saline

Pain: 1: -1.6, 2: +1.1 (P<0.001)

Barnsley et al 1994b

42 with ZJP

(100% at

20 weeks)

39 months

Intra-articular injection corticosteroid

Intra-articular injection anaesthetic

Median time to return to 50% pain level: 1: 3 days, 2: 3.5 days (NS)

Fitz-Ritson 1995

30 (100%

at end of treatment – 8 weeks)

> 12 weeks

Chiropractic + stretching / strengthening exercise

Chiropractic + “phasic” rotation exercise

Neck disability index: 1: -7% (P>.05),

2: -48% (P>.001)

Lord et al 1996b

24 with ZJP (100% at 1 year)

34 months

PRFN

Placebo PRFN

Median time to return to 50% pain level: 1: 263 days, 2: 8 days (P= 0.04)

Z = zygapophyseal joint pain established by response to double intra-articular anaesthetic blocks.

NS = not significant.

RCT = randomised controlled trial - the strongest level of evidence.

PRFN = percutaneous radio-frequency neurotomy.

Rejected studies: Su & Su (1988), Vendrig et al (2000), Schofferman & Wasseman (1994) – no control group.

Underlined intervention = statistical significance in favour of that intervention.

Summary

Although the existence of whiplash as a clinical entity is still debated in the medical community, both patients and clinicians largely accept it. WAD is the occurrence of neck pain and headache arising as a direct result of a road traffic accident – other symptoms occur with less frequency. Such neck pain does not always result from car accidents, available studies suggest that about 50% or less of those involved in accidents go on to develop significant neck symptoms. Of those who do develop neck pain the natural history is extremely varied and unpredictable. Whilst the majority appear to resolve their symptoms within the first few months; the rate of resolution then slows considerably, and a significant minority of patients will be left with persistent symptoms.  Numerous factors have been found to be suggestive of a poor outcome, but for many of these the evidence is contradictory. The most consistent factor across multiple studies associated with poor outcome is to do with severity and spread of symptoms.

Management of acute whiplash is dependent upon exercise, advice, and patient-centred care. The available evidence makes clear the importance of a return to normal activity and movement as quickly as possible. Regular repeated movements are essential, starting with rotation and retraction, to recover full range of movement. Posture correction and interruption of static postures are also important. A graded return to full activity should be supplemented by a full mechanical assessment to determine the presence of derangement and the need for a particular directional preference. In the absence of this a more general approach is required.  For chronic whiplash patients the evidence is much less convincing, and the possibility of persistent and unrelenting symptoms must be considered. Again an exercise, patient-centred approach is essential. Multiple direction dysfunction is not an unusual finding in those with chronic symptoms.

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