Critical Reviews™ in Physical and Rehabilitation Medicine

ISSN for PRINT: 0896-2960

For Online Access

2005, Volume17

Issue 4

90 pages

DOI: 10.1615/CritRevPhysRehabilMed.v17.i4

Issue price - $163.00

James Taylor
Curtin University of Technology, Perth, Western Australia 6845

Lance Twomey, PhD
Curtin University of Technology, Perth, Western Australia 6845

Whiplash injury, resulting in whiplash-associated disorder (WAD), has increased in prevalence in recent decades concomitant with the rise in use of motor vehicles. The use of seat belts has decreased fatalities but increased the likelihood of the more severe forms of WAD, with chronic pain and significant disability. The neck pain, headache, and brachialgia of WAD are well recognized, but the pathological basis of these symptoms remains a matter of controversy. This is partly because X-rays are notoriously inefficient at demonstrating soft tissue lesions, and even magnetic resonance imaging (MRI) underestimates or misses some injuries. MRI demonstrates traumatic disc herniations but probably misses disc avulsions and many zygapophyseal joint lesions in well-aligned spines. Most of the evidence describing the possible injuries is indirect, coming from simulated whiplash in cadavers and animals and from studies of injuries in fatal accidents, but careful assessment of patients with severe WAD may reveal similar injuries. The concurrence of the evidence from all of the studies reviewed strongly suggests that in severe whiplash injuries there is an objective pathological basis for WAD. The human neck, with its small anterior muscles, is vulnerable to extension sprain, with anterior disc tears and posterior compressive injuries to the synovial folds and articular surfaces of facet joints. The slender female neck is more vulnerable to injury than the average male neck. Rear-end crashes are more likely to cause WAD than frontal impacts, though compression extension sprain can result from a blow to the front or the crown of the head. It is suggested that the depression and other psychosocial problems often associated with chronic WAD are results of chronic pain rather than their cause. There is good evidence for hypersensitivity in the central and peripheral nervous systems in chronic pain but these nervous system changes alone cannot explain all the symptoms of chronic WAD, especially when there is good evidence for nociceptive pain from organic pathology.

DOI: 10.1615/CritRevPhysRehabilMed.v17.i4.30 Download article, 285-300 pages

Article price - $35.00

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