Incidence of whiplash-associated disorder

The incidence of reported cases of whiplash has risen dramatically in many Western countries. Since about 1982 (when statistics were first gathered), the incidence has risen in one carefully monitored region of the United Kingdom from 7.7% of all emergency accident cases in 1982 to 57% in 1995, a level that has been sustained through to 2000. This pattern has been reported in other regions of the world. Multiple factors are proposed to account for this increased reporting, such as changes in car design, increased traffic density, psychosocial aspects, and increased litigation. Seatbelt use is probably only a minor causative factor.


The incidence of whiplash seems to have increased dramatically in many parts of the world in the 1980s and 1990s. What accounts for this jump?


WHIPLASH DEFINED

“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—WAD).”[20]

Although classified as a minor or slight injuries, whiplash-associated disorders can be associated with significant morbidity, and they are expensive. It is estimated that, in the United Kingdom, whiplash-associated disorders cost the nation approximately £3.1 billion per annum ($6.8 billion) if one includes the National Health Service costs, Social Security costs, damage to property, and lost productivity. It is estimated that whiplash injuries cost Europe €10 billion per annum ($13.4 billion).[1] We have previously shown that the incidence was increasing on an annual basis.[2]

In a previous study, we looked at the annual incidence of patients with whiplash-associated disorders as a result of a traffic accident attending the accident and emergency department in three hospitals. Since then, we have continued to monitor the figures at Hope Hospital in a prospective way (see the Figure).

In the United Kingdom, the wearing of seatbelts for drivers and front-seat passengers became compulsory in February 1983. In the 12 months prior to the introduction of legislation we saw 929 patients in our accident and emergency department who had been injured in road traffic accidents. Of these 72 (7.7%) had a whiplash-associated disorder (WAD). In the following year, we saw 940 patients, of whom 193 had a WAD (20.5%). A number of other authors also reported a significant increase in whiplash-associated disorders following the introduction of compulsory use of seatbelts, although seatbelts protected car occupants from other injuries.

Since then the number of patients injured in traffic accidents continued to increase until 1997, and then it leveled off. The number of patients with a whiplash-associated disorder also continued to increase until 1997; again since then the numbers have leveled off. Compared with the 1982–1983 pre-legislation figures, the increase is more than twentyfold, and compared with the 1983–1984 figures, the incidence after the introduction of seatbelts, by which time any effect of seatbelts would have stabilized, the incidence has continued to increase another sevenfold.

Using these data—as well as national statistics and our previous comparison of police records and hospital records—we have assessed that the annual incidence of new cases of whiplash-associated disorder in the United Kingdom is approximately 250 000.[3-5]

An extensive search of the literature did not reveal similar studies in other countries. In 1992 it was estimated that the annual incidence in the United States was 1 million,[6] although it has been suggested that this incidence has increased since then. In Australia, the annual incidence is estimated as 3.8 per 1000 population.[7] Richter reported an increase of whiplash injuries in drivers in Hanover, Germany who were injured in motor vehicle collisions from less than 10% in 1985 to more than 30% in 1997.[8] Versteegen also reported a sharp increase in whiplash injuries from 1989 to 1995 in the Netherlands concerned with a more or less stable pattern of seatbelt use.[9]

The incidence of acute whiplash-associated disorders is not known in many other countries, but the incidence of chronic disorder has been shown to be much lower in Lithuania than in the United Kingdom or the United States.[10] The reasons for this are possibly explained by the possible causes of whiplash and their chronicity. The increase in incidence is probably due to a number of factors:

  • Traffic density. The increase in traffic density with an increase in low-impact accidents may be a factor. We have previously shown that the severity of a whiplash injury is unrelated to the severity of impact.[11]

  • Current car design. The current design of cars, with a rigid central section and a crumple front and back zone and resilient seats, may be a contributor to whiplash. The occupants appear to be better protected against severe injuries, but the rigidity of the chassis imparts more torque to the seat back and probably partially accounts for the increase not only in whiplash-associated disorders but also in low-back pain in car occupants. It is probably for this reason that Volvo and other car manufacturers have looked at the design of their seats and have introduced modified seat backs in an attempt to minimize the incidence of whiplash injuries. Although headrests may reduce the occurrence of whiplash, when it does occur, they do not appear to protect against the severity of symptoms; nor does their use or positioning in the vertical or horizontal position appear to affect the recovery from a whiplash-associated disorder.[11] This would suggest that there is something other than the mechanics of the injury that propagates chronicity.

  • Cultural and sociopsychological aspects. Cultural and sociopsychological factors may explain why more patients report acute injuries in the United Kingdom and North America than in many other areas.[12] It has also been shown that the development of chronicity is related to sociopsychological factors. [13,14]

  • Increased litigation. There is no doubt that the increasing recourse to litigation could lead to an increased reporting of acute symptoms once it became known that part of the medicolegal assessment would depend on whether the individual had reported their initial symptoms. Prolonged litigation is also probably responsible for some cases of permanent disability.[15] Since 1997 the incidence has levelled off. Presumably this is because the factors causing the increase have continued to operate at the 1996–1997 level without an added increase.

Not only has the incidence of whiplash-associated disorders increased, but the impairment and disability as a consequence has also increased. Only a minority of patients are left with a permanent disability; most studies suggest a figure between 6% and 18%, although some authors suggest that only a minority of patients make a full recovery.[16]

An analysis of the data in the Swedish Road Traffic Injury Commission showed that there was an increase from 16% in 1989 to 28% in 1994 for patients left with a medical impairment of 10% or more.[17] The cause of chronicity is not known, but appears to be associated with psychological factors. For example, patients who developed nervousness as a result of their accident had a significantly greater risk of long-term chronicity.[18] Shrader and colleagues suggested that disabling or persisting symptoms did not occur as a result of the whiplash injury, but that the symptoms were due to the expectation of disability, a family history of neck pain, or the attribution of pre-existing symptoms to the trauma.[10] They based their study on a retrospective analysis of accident victims and sex-matched and age-matched controls. Crowe, who first described the term whiplash (see the box Whiplash defined), felt that many patients were more disabled by the diagnosis than by the injury itself.[19] Wallis and colleagues studied 137 patients with chronic neck pain following WAD using the SCL-90R psychological profile and the McGill Pain Questionnaire, and found a homogeneous pattern of responses among the chronic complainers that was characterized by high somatization, obsessive-compulsive behavior, and depression.[14] Linton, in reviewing 913 articles assessing psychological risk factors in neck and back pain, concluded that:

  • Psychosocial variables were clearly linked to the transition from acute to chronic pain.

  • Psychological factors were associated with reported onset of back and neck pain.

  • Psychosocial variables had more impact than biomedical or biomechanical factors on back pain disability.

  • Cognitive factors (attitudes, cognitive style, fear, avoidance beliefs) were related to the development of pain and disability.

  • Depression, anxiety, distress, and related emotions were related to pain and disability.

  • Psychosocial factors might be used as predictors of the risk for developing long-term pain and disability.[13]

Other risk factors for chronicity include the severity of the injury (patients with a WAD III injury being significantly worse than patients with a WAD I or WAD II injury), prolonged litigation, and prolonged inappropriate treatment[18] (see the Table for classification of WAD 0, I, II, III, and IV).

Little is known about the optimum management of whiplash injuries.[20] There are very few well-controlled studies, and most modalities of treatment are unproven. Although the health care professions would be expected to have no impact on changing the litigation environment for the health of their patients, some health care approaches do seem prudent. Prolonged physiotherapy, osteopathy, and other treatments are not only unproven but are likely to have the same adverse effects as prolonged litigation, leading to somatization and behavioral dysfunction. Collars and rest may be a serious impediment to recovery. Double-blind controlled studies are required to evaluate methods of physical and psychological treatment as well as therapeutic regimens. In the interim, it is suggested that reassurance, the encouragement of early return to activity, the avoidance of rest and collars, and the use of non-steroidal anti-inflammatory drugs and/or analgesics for symptomatic relief to allow early activity with early activation therapy may be useful, and may prevent the chronicity caused by unnecessary, prolonged, and ineffective therapy. It has been shown that where low-back pain lasts for more than 6 weeks it is increasingly likely to become chronic, but early active mobilization may be helpful in reducing such chronicity.[21] It is likely that the pain from a whiplash injury behaves in the same way.

Summary

Whiplash-associated disorders are a major cause of ill-health in some countries and a major drain on resources, and although we have some indications as to the cause of the increase of incidence and the possible causes of chronicity, we know virtually nothing about prevention or treatment. Research agencies, insurance companies, and research councils should be investing significantly into research of this condition if we are to reduce its cost and minimize the misery that it brings to so many victims of traffic accidents.

Competing interests

The salaries of Mrs Murray and Mr Stephenson are paid by research grants.

Table. Clinical classification of WAD

Type

Clinical presentation

0

No complaints about neck, no physical sign(s).

I

Neck complaints of pain, stiffness, or tenderness only, no physical sign(s).

II

Neck complaints and musculoskeletal signs, including decreased range of motion and point tenderness.

III

Neck complaints, and musculoskeletal signs (above), and neurological sign(s) (reflex, sensory, and motor deficits).

IV

Neck complaints and fracture or dislocation.


References

1. Radanov BP, Dvorak J. Spine update. Impaired cognitive functioning after whiplash injury of the cervical spine. Spine 1996;21:392-397. PubMed Abstract
2. Galasko CSB, Murray PA, Pitcher M, et al. Neck sprains after road traffic accidents: A modern epidemic. Injury 1993;24:155-157. PubMed Abstract
3. Hopkin JM, Murray PA, Pitcher M, et al. Police and hospital recording of non-fatal road traffic accident casualties: A study in Greater Manchester, United Kingdom. Transport Research Laboratory Project Report PR/SRC/1/93; Transport Research Laboratory, Crowthorne, UK: 1993a. 
4. Hopkin JM, Murray PA, Pitcher M, et al. Police and hospital recording of non-fatal road traffic accident casualties: A study in Greater Manchester, United Kingdom. Transport Research Laboratory Project Report 379. Transport Research Laboratory, Crowthorne, UK: 1993b.
5. Galasko CSB, Murray PA, Pitcher M. Whiplash associated disorders. Proceedings of the 15th International Technical Conference in Enhanced Safety of Vehicles. US Department of Transportation, National Highway Traffic Safety Administration, 1996:1504-1513. 
6. Evans RW. Some observations of whiplash injuries. Neurologic Clinics 1992;10:975-997. PubMed Abstract
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8. Richter M, Otte E, Pohlemann T, et al. Whiplash-type neck distortion in restrained car drivers; frequency, causes and long-term results. Eur Spine J 2000;9:109-117. PubMed Abstract
9. Versteegen GJ, Kingma J, Meijler WJ, et al. Neck sprain after motor vehicle accidents in drivers and passengers. Eur Spine J 2000;9:547-552. PubMed Abstract
10. Schrader H, Obelieniene D, Bovin G, et al. Natural evolution of late whiplash syndrome outside the medico-legal context. Lancet 1996;347:1207-1211. PubMed Abstract
11. Minton R, Murray P, Stephenson W, et al. Whiplash injury—Are current head restraints doing their job? Accident Analysis Prevention 2000;32:177-185. PubMed Abstract
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13. Linton, SJ. A review of psychological risk factors in back and neck pain. Spine 2000;25:1148-1156. PubMed Abstract
14. Wallis BJ, Lord SM, Barnsley L, et al. Pain and psychological symptoms of Australian patients with whiplash. Spine 1996;21:804-810. PubMed Abstract
15. Mersky H. Psychological consequences of whiplash. Spine State of Art Reviews 1993;7:471-480. 
16. Gargan MF, Bannister BC. Long-term prognosis of soft-tissue injuries of the neck. J Bone Joint Surg Br 1990;72-B:901-903. PubMed Abstract
17. Holm L, Cassidy JD, Sjogren Y, et al. Impairment and work disability due to whiplash injury following traffic collisions. An analysis of insurance material from the Swedish Road Traffic Injury Commission. Scand J Public Health 1999;27:116-123. PubMed Abstract
18. Galasko CSB, Murray PA, Pitcher M. Prevalence and long-term disability following whiplash associated disorder. J Musculoskeletal Pain 2000;8:15-27. 
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Charles S.B. Galasko, ChM, FRCS, P. Murray, RGN and W. Stephenson, BSc

Dr Galasko is professor of orthopedic surgery at the University of Manchester, England. Mrs Murray is a clinical research nurse at the University of Manchester. Mr Stephenson is a computer programmer and data analyst at the University of Manchester.

Charles S.B. Galasko, ChM, FRCS, P. Murray, RGN, W. Stephenson, BSc. Incidence of whiplash-associated disorder. BCMJ, Vol. 44, No. 5, June, 2002, Page(s) 237-240 - Clinical Articles.



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