WHIPLASH INJURIES - Rheumatology

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THE term whiplash describes the mechanism of acute
flexion/hyperextension of the neck, a frequent feature
of motor accidents. There is a spectrum of injury, ranging
from minor tearing of muscle fibres to (rarely) vertebral
fracture and spinal cord compression. Amongst
the public whiplash injury has long been associated
with chronic symptoms and financial compensation.
The problem for a variety of clinicians, including rheumatologists,
lies in identifying, the influence on the
clinical picture of three important factors—genuine
injury, psychological factors and compensation 'neurosis'.
Success to date in this regard has been hampered
largely by inadequate trial data and a modern medicolegal
epidemic continues unchecked.
Between 18 and 60 per cent of motor accidents
(including front, side and rear impacts) give rise to
whiplash injury [1,2]. Common symptoms are neck
pain, headache and upper limb paraesthesiae while
dysphagia and visual or auditory symptoms occur infrequently.
A number of noteworthy features in the
history suggest more severe injury including high speed
of impact, major damage to the vehicle, head injury
and immediate onset [3] or intense initial neck pain [4].
Increasing age and radiographic evidence of cervical
spondylosis are associated with the persistence of
symptoms [4, 5] and along with the features of more
severe injury may be useful in determining prognosis.
Diffuse muscle tenderness and limitation of movement
are the commonest clinical signs; neurological signs are
rare, with root signs more frequent in those with cervical
spondylosis. A review of cervical spine radiology in
whiplash injury demonstrated prevertebral soft tissue
swelling or angular deformity between vertebral
bodies in 42 of 73 patients [5]. This high incidence of
acute X-ray abnormalities has not been confirmed by
others [6] while neither abnormality, surprisingly, was
EDITORIALS 579
WHIPLASH INJURIES
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BC, Theofilopoulos AN. Mycoplasma arthritidis
mitogen. Vbeta engaged in mice, rats, and humans,
and requirement of HLA-DRalpha for presentation.
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Clinical consequences of altering cytokine production
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29. Burch RM, Mahan LC. Oligonucleotides antisense to
the interleukin 1 receptor mRNA block the effects
of interleukin 1 in cultured murine and human fibroblasts
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associated with the persistence of symptoms. The presence
of neurological signs and cervical fracture or
instability are indications for further investigation,
particularly magnetic resonance imaging (MRI). This
can demonstrate a range of injuries to bone, ligament
or disc and indicate the degree, if any, of root or cord
impingement [7].
Management of simple whiplash injury consists of
rest and analgesics for 1 to 2 weeks. A collar may usefully
be worn during this period but should be gradually
discontinued thereafter. Moulded collars holding the
neck in slight flexion appear better than the standard
soft collar [8]. A number of trials suggest that outpatient
physiotherapy is no more effective in relieving
pain and improving movement than merely advice on
home mobilization by a physiotherapist [8, 9]. Proper
communication between doctor and patient is important.
A common mistake in primary care is to assure
patients of healing within a couple of months as this
only creates anxiety and loss of confidence when it does
not occur. While mobilizing it should be stressed that
neck discomfort related to reasonable activities is not
retarding healing or creating a risk of permanent
damage.
Over 70% of patients settle in 2 to 3 months. Neurological
symptoms and signs occasionally first develop
some weeks after injury and are easily missed [3]. Judicious
further physiotherapy may be useful for continuing
symptoms, although clinical trials are lacking.
The major problem in whiplash injury is the assessment
and management of those patients who remain
symptomatic more than 6 months after injury. This
may be a significant percentage of the total (26% in one
large retrospective series) [10] although others dispute
such a high figure [11]. The term 'Late Whiplash Syndrome'
(LWS) is useful to define this group who, in
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580 BRITISH JOURNAL OF RHEUMATOLOGY VOL. XXXI NO. 9
addition to continuing symptoms of neck injury, frequently
develop anxiety, insomnia and depressive
symptoms. Many seem to cope poorly with what often
appears to have been minor injury and are slow to
regain their previous level of functioning, both socially
and at work. Do some of these patients have injuries
which are unrecognized and unresolved or are those
with LWS either psychologically frail or conscious
malingerers?
The lack of adequate long term prospective studies,
particularly of those not involved in litigation, makes it
difficult to draw firm conclusions about LWS. There is
no recognized symptom, clinical sign or radiographic
feature which is characteristic of true unresolved
injury. Attempts to identify pathological abnormalities
using magnetic resonance imaging in LWS have yielded
conflicting results [7, 12, 13]. Although the numbers in
these studies are small one paper suggested avulsion of
intervertebral disc from underlying end plate as a possible
cause of LWS [7]. This finding was previously
reported by MacNab [3] in seven patients whose persisting
symptoms settled following surgical repair of
the disc lesion.
In the last 3 years studies of brain stem and spinal
cord electrophysiology, two of which were controlled,
have shown significant changes in oculomotor [14] and
trigeminal sensory [15] nerve function and electronystagmographic
abnormalities [16] in LWS. This may be
due to the traction on spinal cord and associated neural
structures which occurs as the trunk accelerates forwards
at impact while the neck hyperextends. The
importance of the changes is unclear but deserves
further study.
As already mentioned psychological symptoms are
common in LWS. If these symptoms merely reflected a
frail or susceptible personality type, it should be possible
to predict the development of LWS from psychological
profiles. However a well executed study [4]
which performed such profiles in whiplash cases within
1 week of injury found that the presence of neurotic or
depressive traits at baseline was not predictive of outcome.
Perhaps the psychological impact of the accident
itself is a more important influence on the development
of LWS. As suggested by Pearce [11], LWS shares
many of the features of Post Traumatic Stress Disorder,
a condition which can occur in any individual
following a life-threatening event. Furthermore head
injury, either from direct trauma or due to violent
movement of the brain within the cranium at impact
may also produce psychological disturbance. Natural
frustration at the persistence of symptoms despite
repeated assurances and numerous treatments may
also play a role in illness behaviour in LWS.
Those primarily seeking compensation present with
unconvincing symptoms and inconsistent or inexplicable
clinical signs. Where this is strongly suspected it is
best to inform the patient that the complaints appear
unrelated to the accident. Previously severe symptoms
including muscle weakness, paraesthesiae and restricted
neck movement often improve dramatically. True
malingering is probably quite uncommon; this is sup-
ported by indirect evidence such as the tendency for
other injuries in whiplash cases to heal in the expected
time [3], the similar numbers with LWS pursuing and
not pursuing litigation [17,18] and the tendency for
symptoms to persist for long periods following compensation
[19].
The management of LWS is largely empirical. Strong
analgesics and hypnotics should be avoided and treatments
minimally or temporarily effective are best discontinued.
While maintaining a sympathetic approach
patients should be encouraged to take responsibility
for coping with their symptoms. Repeat cervical spine
radiographs in flexion and extension occasionally
reveals abnormal or restricted movement at one segment,
which is easily missed at presentation when
muscle spasm is often intense. This and the presence of
unremitting paraesthesiae are possible indications for
MRI.
Long-term prospective trials of cases not involved in
litigation are needed to answer some of the questions
posed by whiplash injuries. Those factors suggesting
more severe injury or persistence of symptoms should
guide predictions of outcome and be used to promote
early settlement of legal cases. The practice of awaiting
the levelling off of symptoms before proceeding with
the court case should be changed as this encourages
malingering and can, in certain cases, prolong
suffering.
MAURICE BARRY
Rheumatology Research Unit, Unit E6, Addenbrooke's
Hospital, Hills Road, Cambridge CB2 2QQ
REFERENCES
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10. Balla JI. Report to the Motor Accidents Board of Victoria
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ANNOUNCEMENTS AND CALENDAR FOR 1992-93
Core Course in Rheumatology. LONDON (Dr D. Isenberg).
Senior Registrar Travelling Fellowship. BIRMINGHAM (Prof. P. Bacon).
Update Management of RA preceded by Midlands Rheumatology Society Meeting. COVENTRY
(Dr J. Coppock).
Closing dates for Abstracts for the BSR Xth AGM.
Synovial Fluid. MANCHESTER (Dr A. Freemont).
BSR Core Course on 'Examination and Radiology of Joints'. (Dr M. Doherty).
BSR Xth AGM. HARROGATE.
Update Vascular Endothelium. HARROGATE (Dr D. Haskard).
Advanced Course in Rheumatology. GLASGOW (Prof. R. Sturrock).
Rehabilitation Course. DERBY (Dr C. F. Murray-Leslie).
Heberden Round. CAMBRIDGE (Dr B. Hazleman).
Core Course. LIVERPOOL (Dr R. N. Thompson)
SR Travelling Fellowship. LEEDS (Prof. V. Wright).
BSR Paediatric Rheumatology Course. NEWCASTLE UPON TYNE (Dr I. D. Griffiths)
CLOSING DATES FOR EDUCATION PRIZES FOR 1993
Michael Mason Prize 1993 - 12 November 1992.
BSR Non-Clinical Bursary 1993 - 16 September 1993.
SR Travelling Fellowship 1993 - 31 May 1993.
Further information about these events from Ms. H. Verraest, British Society for Rheumatology, 3 St Andrew's Place,
Regent's Park, London NVV1 4LE.
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