CME (May 2008)
Monthly Self-Study Series

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 components: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 reconsidered 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.

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 rearend 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 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'.

Figure 1. Sequential radiographs from normal volunteers' test by Kaneoka.⁵

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 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).

Figure 2. Cross-sectional area of the spinal canal.

Figure 3. Pressure gradients in the spinal fluid column.

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 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 of the end-plates are seen in both the X-rays and MRI.¹⁰ 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).

Figure 5. Rim lesions.

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 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 'inflammatory soup' in turn, sensitizes the calcium channels of the nerve, with increased sensitization of the dorsal root ganglia and the dorsal horn neurons.

Figure 6. Inflammatory soup.

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 widespread hyperexcitability of the spinal cord neurons (Figure 7).

Figure 7. Hyperexcitability of the spinal cord neurons.

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.

Neck Pain

In a whiplash injury, the following nociceptive sites can be the site of pain (Figure 8):

• Nerve root
• Facet joint
• Outer layer of disc annulus
• Posterior longitudinal ligament
• Vertebral artery
• Erector spinae muscle
• Interspinous ligament.

Figure 8. Nociceptive sites of pain.

Neck Stiffness

The term 'muscle spasm' has proved to have poor reliability because of the apparent reason that there is a huge inter-observer discrepancy.

Abnormal stretch reflex is likely a major cause of muscular symptoms after a whiplash injury. A stretch reflex is initiated by the passive, unexpected stretch of a voluntary muscle that causes the spindle system to discharge (Figure 9).

Figure 9. Stretch reflex.

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 10. Base of the occiput.

Greater Superior Occipital Neuralgia

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).

Figure 11. Greater superior occipital neuralgia.

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.

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).

Figure 12. Interscapular pain.

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 13. Spurling's sign.

References

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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. US Depar tment of Transpor tat ion. Head rest raints — identification of issues relevant to regulation, design and effectiveness. Washington DC; NHTSA Office of Crashworthiness Standards; 1996.

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8. Shea M et al. Variations of stiffness and strength along the main cervical spine. J Biomechanics 1991;24:95–107.

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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.