Timothy C. Hain, MD
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Content last updated: 12/02
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Vertigo or dizziness occasionally accompanies a neck injury. The precise incidence is controversial but it is estimated that 20-58% of patients who sustain closed-head injuries or whiplasy experience late onset symptoms of dizziness, vertigo and dysequilibrium. Nevertheless, cervical vertigo is matter of considerable concern because of the high litigation related costs of whiplash injuries.
When cervical vertigo is diagnosed, the usual symptoms are dizziness associated with neck movement. There should be no hearing symptoms or findings but there may be ear pain (otalgia). Brandt (1996) has recently reviewed this topic from a diagnostic perspective, and Wrisely et al (2000) recently reviewed the physical therapy approach.
Physiologically, there are two well recognized causes of cervical vertigo:
1. Vascular compression (see TIA discussion). The vertebral arteries in the neck can be compressed by the vertebrae (which they traverse), or other structures. Arthritis, surgery, chiropractic manipulation are all possibilities. The most common cause of vertebral dissection is chiropractic manipulation (Vibert et al, ORL, 1993). For this reason, we recommend against chiropractic treatment of vertigo that includes "snapping" or forceful manipulation of the vertebrae.
2. Abnormal sensory input from neck proprioceptors. Sensory information from the neck may be unreliable or absent. Sensory information from the neck is combined with vestibular and visual information to determine the position of the head on the neck, and space. This mechanism was investigated by DeJong and DeJong (1977) who injected local anesthetics into their own necks. Such injections caused unsteadiness and minor amounts of dizziness. It is possible that some individuals are more sensitive than others, and also that neck inputs interact with other causes of vertigo (see below).
The neck also interacts with other types of vertigo. Neck input may be used as sensory input to assist in stabilizing vision. This can be easily demonstrated by eliciting ocular nystagmus from vibration of the neck, in individuals who are otherwise well compensated.
The process is generally uncertain and frustrating.
There is no consensus on how to diagnose cervical vertigo (Brandt, 1996). The author of this page uses a combination of criteria. First, one excludes other causes of vertigo such as vestibular neuritis (with an ENG), and BPPV (with a positional test). Other entities that need to be ruled out including inner ear disease such as Meniere's syndrome, central vertigo, psychogenic vertigo (often including malingering when there are legal issues), and medical causes of vertigo. As cervical vertigo often is associated with a head injury, in this situation, the various causes of post-traumatic vertigo shoud be considered. .There should be a sufficient cause of neck injury (whiplash injury or severe arthritis). Symptoms elicited by massage of the neck or vibration to the neck add to the clinical suspicion.
There should be no hearing symptoms or findings (an audiogram is recommended). There may be ear pain (otalgia), as part of the ear is supplied by sensory afferents from the high cervical nerve roots. On physical examination, there should be no spontaneous nystagmus, but there may be positional nystagmus. Many patients who have vertigo in the context of neck disease have a BPPV type nystagmus on positional testing. This suggests that the neck afferents may interact strongly with vestibular inputs derived from the posterior canal.Although the idea is logical, the author has not found it helpful clinically to compare positional results with the head kept constant on body to positional tests where there is head on trunk movement.
If cervical vertigo still seems likely after excluding reasonable alternatives, one next needs to look for positive confirmation. The "gold standard test" for the vertebral arteries is vertebral angiography. Because this is a risky procedure by itself, often it is decided not to proceed to this step. Ordinary MRA and vertebral doppler procedures are rarely abnormal, and sometimes are used as a screening procedure to decide whether vertebral angiography is necessary. An MRI scan of the neck and flexion-extension X-ray films of the neck are suggested in all. Fluroscopy of the neck may be used in persons with abnormal flexion-extension views. ENG testing is recommended, largely to exclude alternative causes.
As should be apparent from the previous discussion, cervical vertigo is difficult to diagnose. Usually conditions that are difficult to diagnose also respond poorly to treatment. For the usual person in whom cervical vertigo is a diagnosis of exclusion, physical therapy treatment is recommended, possibly combined with medication to relieve pain and reduce spasm. Physical therapy includes gentle mobilization, exercise, and instruction in proper posture and use of the neck (Karlberg et al, 1996). Some authors recommend trigger point injection or traction. The prognosis is good in that 75% of patients treated this way have improvement of symptoms.
Medical management may include muscle relaxants such as tizanidine (Zanaflex), cyclobenzaprine (10 mg), and baclofen (Lioresal).
For pain, tramadol (Ultram) and non-steroidals are sometimes useful. Nonsteroidals are particularly useful when arthritis is present.
Antidepressants, may be used for chronic pain and the reactive depression that often accompanies it.(Borg-Stein et al, 2001).
There can be an interaction between migraine (which can include vertigo) and neck pain, and for this reason, it is often useful to empirically try medication with migraine prophylactic medications.
There is presently considerable interest in the use of botulinum toxin injections to reduce painful muscle spasm. Whether this treatment will prove useful in cervical vertigo remains to be seen. Similarly, facet blocks are sometimes used to control neck pain. Again, whether or not this treatment is useful in cervical vertigo is unclear.
An otherwise healthy man was involved in a severe auto accident. On awakening, he was dizzy and he developed severe neck pain over ensuing days. Evaluation in the hospital revealed a BPPV type positional nystagmus, which responded to physical treatment. He had persistent unsteadiness. After discharge from the hospital, on shaking his head forcefully to shake off some raindrops, he suddenly lost vision in one half of his visual field. Vison returned, but at that point a diagnosis of vertebral basilar compression was made. He continues to have unusual visual symptoms, attributed to poor circulation to the back of the brain.