MAY 2008

THE HONG KONG

MEDICAL ASSOCIATION

www.hkmacme.org

This month
n Spotlight
Whiplash Associated
Disorders — Myths &
Controversies – Part 3
n Cardiology
A 72-year-old lady
complained of recurrent
dizzy spells and shortness
of breath on exertion
n Dermatology
Multiple red papules on
scrotum
n CNS Medicine
A 14-year-old male with
complaints of tics
n Infectious Disease
An 8-year-old male who
had diarrhoea for a week
n Learning Centre
Stroke prevention and
treatment series
SPOTLIGHT
Whiplash Associated Disorders —
Myths & Controversies – Part 3
Dr. KONG Kam Fu, James
MBBS (HK), MSc (Bath) (Ex. & Sports Med.), FCSHK, FRCSEd, FRCSEd (Orth),
FHKCOS, FHKAM (Orth)
Specialist in Orthopaedics & Traumatology
Honorary Clinical Assistant Professor
Department of Orthopaedic Surgery, University of Hong Kong
‘Wisdom is what’s left after we’ve run out of
personal opinions.’ — Cullen Hightower
OUTLINE
This chapter we concentrate on:
1. Biomechanics of whiplash syndrome; and
2. Clinical examination.
BIOMECHANICS OF WHIPLASH
SYNDROME
The term ‘whiplash’ itself entails 3 different com-
ponents:1
• The ‘whiplash event’ — a biomechanical process
suffered by the occupants of a vehicle that is struck
by another vehicle.
• The ‘whiplash injury’ — this is the impairment
which results from the whiplash event.
• The ‘whiplash syndrome’ — a constellation of
symptoms that are attributed to the supposed
whiplash injury.
Etiology and Pathogenesis
Classical description of the whiplash injury restricts the
definition to movements of the neck in the sagittal plane
only, with forced flexion and extension only.
This firm belief of extension has held sway for over
30 years. However, with further experimentation and
scientific studies, this belief will need to be further re-
considered for it has been revealed that the movements
involved are more complex than was previously
ascertained.
It has been found, that both the axial compression
and the unnatural, double curvature of the cervical spine
are important in the initial response of the cervical spine
to the load.
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Speed of Impact
One common misperception about the whiplash injury
is that if a vehicle does not sustain damage, or if the
damage to the vehicle is minimal, then the occupants
could not have sustained a severe whiplash injury.
However, scientific studies have shown that low-speed
collisions may produce whiplash injuries just as severe as
in high-speed collisions. How can this be explained in
physical terms?
The answer lays in where the force ends up going.
In typical low-speed collisions, the amount of force
sustained by the vehicle is not enough to cause the
crushing of the vehicle itself, which results in most of the
force being transferred to the occupant.2
In higher-speed collisions, the metal of the vehicle
crushes and deforms, which dissipates much of the
energy of the collision.
Normal Volunteers’ Test by McConnell
In an experiment carried out by McConnell et al in
normal volunteers,3 high speed photography was used to
determine in detail the excursions of the neck after rear-
end impacts at 3–8 km/hr.
During the movements and phases that have been
described in previous issues of the CME bulletin, the
top of the neck underwent accelerations ranging from
0.3 to 3.5 g whose vectors changed directions with time
from upwards, to upwards and forwards, downwards and
forwards, backwards and upwards.
It was inferred from this experiment that substantial
compressive forces were exerted on the cervical range of
motion. The threshold for mild injury was taken as 8
km/hr.
Normal Volunteers’ Test by Matsuhita4
Similar observations were reported in an experiment
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Figure 1. Sequential radiographs from normal volunteers’
test by Kaneoka.5
in normal volunteers during simulated collisions of
approximately 5 km/hr.
In this experiment, the subjects reported mild
discomfort and neck pain that lasted 2–4 days, but none
had any long-term sequelae.
Normal Volunteers’ Test by Kaneoka5
In this study, the volunteers were subjected to an 8 km/
hr impact that resulted in 4 g acceleration.
The segments achieved peak initial flexion between
50 and 110 ms after impact and peak extension between
100 and 200 ms after impact. Thus, the overall result
is that the cervical spine assumed an S shaped curve at
about 100 ms, while the lower segments started extension
while the higher segments were still undergoing flexion.
Sequential radiographs were taken and these are
shown in Figure 1.
However, what constitutes a low-speed impact can
vary according to the different authorities performing
the studies. The general rule is that, speed less than 10
mph would be considered as ‘low speed’.
Mode of Injury
The emphasis here is that the axial compression causes
abnormal motion of extension.
In particular, whilst extension occurs about an
abnormally high axis of rotation, the vertebra rotates
which results in abnormal separation of the anterior
elements of the neck and abnormal patterns of
compression posteriorly.
Effect of Seat Belts and Shoulder Harnesses
The National Highway Traffic Safety Administration
(NHTSA) suggests that the use of shoulder and lap belts
reduce the risk of fatal injuries by 45% but these safety
devices increase the number of minor injuries.6
Head restraints have also proved to be effective in
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SPOTLIGHT
preventing whiplash injury only when they are
properly positioned. The standard suggestion is
that the restraint is placed at least 27.5 inches
above the seating reference point. This reference
point, however, varies with the size and gender
of the individual.
Contents of the Neck on Impact
Due to the infolding of the ligamentum flavum
on extension, the cross-sectional area of the
spinal canal actually decreases on extension and increases
on flexion7 (Figure 2).
The nerve tissues within the spinal canal are
incompressible during a typical whiplash injury with
rapid flexion-extension, and so there are changes of the
cerebrospinal fluid (CSF) as well as the blood flow in
order to compensate any change in space.
Hence, in a typical whiplash injury, pressure gradients
in the spinal fluid column form, causing mechanical
stress on the nerve tissues8 (Figure 3).
Uncovertebral Joints
These joints act as a barrier between the intervertebral
disc and the neural contents of the foramen.
Thus, when the head is turned in a whiplash injury,
the rotary forces on the adjacent vertebra may cause
tearing of the annular fibers at the moment of the
impact9 (Figure 4).
Figure 2. Cross-sectional area of the spinal canal.
Figure 3. Pressure gradients in the spinal fluid column.
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SPOTLIGHT
Figure 4. Tearing of the annular fibers at the moment of impact.
Intervertebral Discs
Injuries to the intervertebral disks have been reported
from a number of sources. Typical lesions are those with
avulsion of the disc from the vertebral end-plate and
tears of the annulus fibrosus of the disc.
Separation of the disc from the vertebra or fractures
10
of the end-plates are seen in both the X-rays and MRI.
They are also found during surgery, 11 reproduced in
animal experiments12 and at post-mortem.13
‘Rim lesions’ may also be found without any
degenerative changes. Rim lesions are a separation of the
outer annular fibers of the disc from the outer avascular
cartilage plates, which are connected to the outer, highly
vascular bony endplate14 (Figure 5).
Zygapophyseal Joints
There is compelling evidence to suggest that the
zygapophyseal joints, more commonly known as facet
joints, may be damaged in whiplash injury and give rise
to pain symptoms.15,16,17
Indeed, it is estimated that in around 50% of the
subjects with chronic whiplash syndrome, the pain
Figure 5. Rim lesions.
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actually arises from the facet joints.18
Having said this, facet joints are
notoriously difficult to visualize. They
are in general, poorly seen on X-rays,
CT scans or even MRI scans. However,
tears of the joint capsules have been
confirmed during surgery.19
Thus, patients with suspected facet
joint problems may be diagnosed in a
number of ways:
1. By reproducing the pain from lateral
flexion and extension of the neck.
2. Localized tenderness of the joint.
3. Relieving the pain by injecting local anesthetics
into the joint.
Nociceptor Chemicals
There are a number of nociceptor chemicals which
accumulate at the trauma site. An acronym of
‘inflammatory soup’ is used (Figure 6).
This ‘inflammator y soup’ in turn, sensitizes
the calcium channels of the nerve, with increased
sensitization of the dorsal root ganglia and the dorsal
horn neurons.
Spinal Cord Hyperexcitability
A recent article by Banic et al has suggested that the
spinal cord hyperexcitability of the spinal cord is
allegedly the cause of chronic pain after a whiplash
injury.20
The exact mechanism of spinal cord hyperexcitability
is unknown but it is postulated that the inflammation
produces cyclooxygenase-2 (COX-2) in the spinal cord,
which leads to production of prostaglandin, which
secondarily produces hyperexcitability of the spinal
neurons.
This hyperexcitability is also observed in the entire
spinal cord and the supraspinal centers. Activation of
the glial cells in the spinal cord is also involved in the
Figure 6. Inflammatory soup.
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 SPOTLIGHT

widespread hyperexcitability of the spinal cord neurons

(Figure 7).

CLINICAL EXAMINATION
The most common symptoms that occur after a whiplash
injury include:
• Neck pain
• Neck stiffness
• Cervicogenic headaches
• Interscapular pain and tenderness
• Upper extremity pain, paraethesia and weakness
• Dizziness
• Cognitive impairment
• Tinnitus
• Temporomandibular joint (TMJ) pain. Figure 8. Nociceptive sites of pain.

Neck Pain Neck Stiffness

In a whiplash injury, the following nociceptive sites can The term ‘muscle spasm’ has proved to have poor
be the site of pain (Figure 8): reliability because of the apparent reason that there is a
• Nerve root huge inter-observer discrepancy.
• Facet joint Abnormal stretch reflex is likely a major cause of
• Outer layer of disc annulus muscular symptoms after a whiplash injury. A stretch
• Posterior longitudinal ligament reflex is initiated by the passive, unexpected stretch of
• Vertebral artery a voluntary muscle that causes the spindle system to
• Erector spinae muscle discharge (Figure 9).
• Interspinous ligament.
Cervicogenic Headaches
Cephalalgia may be present and the discomfort is
felt around the scalp area, or at the base of the occiput
(Figure 10).

Figure 7. Hyperexcitability of the spinal cord neurons. Figure 9. Stretch reflex.

www.hkmacme.org HKMA May 2008 

SPOTLIGHT

Cloward, as early as the 1950’s, had already demonstrated

that interscapular pain may be produced by intranuclear
discograms, where there is irritation of the anterior part
of the disc23 (Figure 12).
Spurling’s sign is a useful test for additional
information. It is performed while placing the head
laterally and turned towards the affected side with axial
compression. It is considered to be positive if there is
reproduction of the radicular pain (Figure 13).

Figure 10. Base of the occiput.

Greater Superior Occipital Neuralgia

Figure 12. Interscapular pain.
The anatomy of the greater superior occipital nerve has
been well described.21,22
The nerve initially courses downward, then laterally
and posteriorly. After reaching the inferior oblique
muscle, it bends and then courses in a medial and
superior direction through the semispinalis muscle
forming the 2nd bend. It then transverses between the
trapezius muscle and travels upward and laterally (Figure
11).
Treatments involve various modalities such as oral
analgesics, heat, massage, local injection of anesthetics
and steroids. Surgery may be indicated which involves
releasing the nerve by dividing the inferior oblique
muscle. Figure 13. Spurling’s sign.

Interscapular Pain
References
1. Malanga GA, Nadler SF. ‘Whiplash’. Hanley & Belfus Inc, 2002; p.
41–78.
2. Blumenfeld F, Jerome A. Advanced whiplash care: a manual for
patients and professionals. Center Path Publishing, 2006; p. 5–6.
3. McConnell WE et al. Analysis of human subject kinematic
responses to low velocity rear end impacts. Proceedings of the
37th STAPP Car Crash Conference. Warrendale, PA, Society for
Automobile Engineers, 1993; p. 21–30.
4. Matsushita T et al. XR study of human neck motion due to
head inertia loading. Proceedings of the 38th STAPP Car Crash
Conference. Warrendale, PA, Society for Automobile Engineers,
1994; p. 55–64.
5. Kaneoka K et al. Abnormal segmental motion of the cervical
spine during simulated whiplash loading. J Jap Orth Ass
1997;71:S 1680.
6. U S D e p a r t m e n t o f Tr a n s p o r t a t i o n . H e a d re s t r a i n t s —
Figure 11. Greater superior occipital neuralgia. identification of issues relevant to regulation, design and

 HKMA May 2008 www.hkmacme.org

 SPOTLIGHT

effectiveness. Washington DC; NHTSA Office of Crashworthiness
Standards; 1996.
7. Kaneoka K et al. Notion analysis of cervical vertebra during
whiplash lading. Spine 1999;24(8):763–70.
8. Shea M et al. Variations of stiffness and strength along the main
cervical spine. J Biomechanics 1991;24:95–107.
9. Cailliet R. Whiplash-associated diseases. AMA 2006;38–9.
10. Keller RH. Traumatic displacement of the cartilaginous vertebral
rim: a sign of intervertebral disc prolapse. Radiology 1974;110:
21–4.
11. MacNab I. Whiplash injuries of the neck. Manit Med Rev 1966;46:
172–4.
12. La Rocca H. Acceleration injuries of the neck. Clin Neurosurg
1978;25:209–17.
13. Johnson H et al. Hidden cervical spine injuries in traffic accident
victims with skull fractures. J Spinal Disord 1991;4:251–63.
14. Foreman SM, Croft AC. Whiplash injuries: the cervical
acceleration/deceleration syndrome. 3rd Ed. LWW, 2002; p. 346.
15. Aprill C, Bogduk N. The prevalence of cervical zygapophyseal
joint pain: a first approximation. Spine 1991;744–7.
16. Aprill C et al. Cervical zygapophyseal joint patterns I: a study in
normal volunteers. Spine 1990;15:453–7.
17. Bogduk N et al. The cervical zygapophyseal joints as a source of
neck pain. Spine 1988;13:610–7.
18. Schofferman J et al. Chronic whiplash and whiplash-associated
disorders: an evidence-based approach. JAAOS 2007;15:596–
606.
19. Craig JB et al. Superior facet fractures of the axis vertebrae.
Spine 1991;16:875–7.
20. Banic B et al. Evidence for spinal cord hyperexcitability in chronic
pain after whiplash injury and in fibromyalgia. Pain 2004;107:7–
15.
21. Bogduk N. The anatomy of occipital neuralgia. Clin Exp Neurol
1980;17:167–84.
22. Gille O et al. Surgical treatment of greater occipital neuralgia by
neurolysis of the greater occipital nerve and sectioning of the
inferior oblique muscle. Spine 2004;29(7):828–32
23. Cloward RB. Cervical discography: a contribution to the etiology
and mechanism of neck, shoulder and arm pain. Ann Surg
1959;150:1052.

Answer these on page 16 or

make an online submission at:
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Please indicate whether the following questions are true or false
1. ‘Whiplash’ consists of 3 elements. 8. ‘Rim lesions’ are usually found with co-existing
2. Only sagittal flexion and extension movements degenerative changes of the spine.
are involved in the whiplash injury. 9. Cervicogenic headache after whiplash injury may be
3. Low-speed collisions are classified as collisions caused by irritation of the greater superior occipital nerve.
below 10 mph. 10. Prolapsed cervical discs may cause interscapular pain.
4. Seat belts help to reduce fatal injuries.
5. Head restraints are useful in preventing whiplash ANSWERS TO April 2008
injury irrespective of their positions. Chronic Kidney Disease (CKD) — Old diseases with
6. The volume of the spinal canal increases on new global challenges
extension of the neck. 1. False 2. True 3. True 4. False 5. True
7. Uncovertebral joints are facet joints. 6. False 7. True 8. True 9. False 10. True

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