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The term "whiplash" is generally used to describe neck injuries that follow a rear-end collisions. Vertigo in this situation is usually attributed to "Cervical vertigo", and headaches, to "cervical headache", but there are other potential causes (see below). Whiplash is classically attributed to soft tissue injury caused by hyperextension of the neck (Carroll et al, 1985). Injuries may include rupture of the anterior longitudinal ligament, muscle hemmorhage and tear, disk rupture and bulge, and occasionally, brain injury (Davis et al, 1991). Visual disturbances as well as inner ear disturbances are classically attributed to vertebrobasilar artery injury (Carroll et al, 1985). The vertebral arteries might be injured by movement of the vertebrae, or elongation of the vertebral arteries (Panjabi et al, 1998: Eck et al, 2001). In the latter situation, one would not expect to find any abnormalities of vertebral motion on imaging.
Some authors have suggested a role for acquired Chiari malformation, as well as CSF leaks (Freeman et al, 2010)
Whiplash clinically is similar to postconcussion syndrome, but with the addition of neck complaints. It is possibly related to cervical vertigo. Dizziness occurs in 20-60%. Dizziness associated with whiplash can persist for years. Fortunately about 75% of patients with whiplash are recovered by 1 year (Radanov et al, 1994).
Although concussion can occur as a result of whiplash, there is a marked difference in the threshold of force required to injure the brain vs. the neck. The lowest threshold to cause brain trauma in animals is about 60 g of force, but the limit of tolerance to whiplash is an acceleraiton of about 14g. Thus whiplash-type motion can cause injury at force levels far below those required to injure the brain (Mallison et al, 1998).
Regarding prognosis, long term studies show that cervical stiffness pain may persist in 20 to 45% of patients with significant whiplash. Degenerative problems develop after injury in about 40% of patients (Dufton et al, 2012; Rodriquez et al, 2004; Schofferman et al, 2007). They are more common in persons with more severe collisions.
It is difficult to see how there could be a substantial inner ear damage after whiplash. Nevertheless, balance and hearing problems are commonly reported after whiplash. Mallinson and Longridge reviewed the literature up to 1998. Hinoki reported that 85% of his patients were dizzy after a T-bone type accident. Oosterveld also reported that 85% of his whiplash subjects were "dizzy".
According to Tranter and Graham, (2008), explanations include transient ischemia or hemmorage in the labyrinth as a result of transient compression of the vertebral artery, direct labyrinthine concussion, brain stem concussion, the noise of the collision, and psychological triggering. These explanations all seem rather far fetched to us for an injury confined to the neck. We would be willing to accept, however, triggering of migraine as a reasonable conjecture for some of these cases. In some instances, we also would accept the possibility that whiplash caused a spinal fluid leak triggering hearing symptoms, as well as that damage to the neck might cause tinnitus.
Hearing complaints are common in persons with whiplash, but in most cases the hearing impairment is not associated with the whiplash injury (Tjell et al, 1999).
Non-organic hearing loss is an exaggerated or fabricated hearing loss. With current diagnostic technology, simulated hearing loss can nearly always be easily recognized.
Rowlands et al (2009) reported that in 109 patients, 4 patients reported a short-lived dizziness acutely after whiplash. No patients reported persistent vestibular symptoms.
Vibert and associates (2003) reported three cases of peripheral ear type vertigo (1 BPPV, 2 vestibular nerve injury) after whiplash. They suggested that dizziness associated with whiplash may be more often due to vestibular injury rather than neck or brain trauma. Similarly, Dispenza reported that 39% of whiplash injuries with vertigo, had BPPV (Dispenza et al, 2010). Their study consisted of patients referred to their ENT practice, and for this reason might contain substantially more patients with BPPV than would occur in whiplash injury patients referred to, for example, an orthopedic service. It seems highly unlikely that 39% of all patients with whiplash injury have BPPV.
Whiplash may be increased by use of seat-belts. Seat-belts limit body injury, but can paradoxically increase cervical injuries as they restrict movement of the trunk. Testing for this condition may include X-rays of the neck. Active flexion and extension lateral views can be helpful in documenting dynamic stability. A CT scan of the cervical spine may help in better defining bony injuries. An MRI and MRA scan of the neck may be helpful with disks, vascular syndromes, and other soft tissue injuries.
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