Page last modified:
December 15, 2007
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Page last modified:
December 15, 2007
Page last modified:
December 15, 2007
Vertigo or dizziness occasionally accompanies a neck injury or is provoked by a neck posture no matter what the orientation of the head is to gravity. The precise incidence is controversial but it is estimated that 20-58% of patients who sustain closed-head injuries or whiplash experience late onset symptoms of dizziness, vertigo and dysequilibrium. Cervical vertigo is matter of considerable concern because of the high litigation related costs of whiplash injuries. Cervical vertigo from other causes is much less common.
When cervical vertigo is diagnosed, the usual symptoms are dizziness associated with neck movement. There should be no hearing symptoms (other than tinnitus) or hearing loss 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 many potential causes of cervical vertigo:
1. Vascular compression (see TIA discussion). This is sometimes called "Bow-hunter's syndrome". The vertebral arteries in the neck (see above) can be compressed by the vertebrae (which they traverse), or other structures (Kamouchi, Kishikawa et al. 2003; Sakaguchi, Kitagawa et al. 2003) . Arthritis, surgery, chiropractic manipulation are all possibilities.
There is a substantial conventional neurological literature showing that chiropractic manipulation of the neck is associated with a substantial increased risk of vertebral artery territory stroke (Rothwell et al, 2001; Smith et al, 2003; Vibert et al, 1993). Chiropractors are often unaware of this association (Haldeman et al, 2002). For this reason, we recommend against chiropractic treatment of vertigo that includes "snapping" or forceful manipulation of the vertebrae in persons with dizziness or unstable necks.
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. (Brandt 1996) 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).
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MRI of person with cervical vertigo associated with cervical stenosis. Arrow points to region of narrowing. |
3. Cervical cord compression (Benito-Leon, Diaz-Guzman et al. 1996; Brandt 1996). In this case, ascending or descending tracts in the spinal cord that interact with the cerebellum, vestibular nucleus or vestibulospinal projections are the culprit. This may be painless. In our opinion, based on clinical observations during videonystagmography, this is the most common mechanism of cervical vertigo. Management is not very successful as surgery is generally not felt to be appropriate, and mobilization of the neck is rarely useful.
4. Cerebrospinal Fluid (CSF) leak due to tear of cervical root sleeve with dizziness and headache (Vishteh, Schievink et al. 1998). For example, a whiplash injury may tear a cervical root sleeve causing low CSF pressure and hearing symptoms. CSF leaks can cause low-tone sensorineural hearing loss, resembling bilateral Meniere's disease.
5. Barré-Liéou "syndrome". (discredited) This entity is controversial at best. Barré (the same French neurologist associated with the well established Guillain Barre syndrome) described a syndrome of the posterior cervical sympathetic nerves and its frequent cause—chronic cervical arthritis. It has not been agreed as a neurological entity, but is used as a repository for undiagnosed symptoms including those succeeding acute neck injuries. (Foster and Jabbour 2006)
6. High cervical disease (i.e. C1-C2). This disorder does exist but it is grossly overdiagnosed, primarily by the chiropractic community. We have encountered occasional patients with platybasia and rheumatoid arthritis who have high-cervical disease. Our estimate is that only about 1/500 patients with cervical vertigo have high-cervical problems.
7. 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.
Injuries to the neck may also damage structures related to the ears. Although blunt neck trauma has been reported to affect hearing (Segal et al, 2003), we feel that in this situation there is likely an additional injury to the inner ear.
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 (see above). 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 should 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 little or no hearing symptoms or findings, other than an occasional low-tone sensorineural hearing reduction (an audiogram and OAE 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.
Use of VNG to diagnose cervical vertigo: Although the idea is logical, the author has not generally 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. While persons with herniated disks often do develop nystagmus when their head is turned while upright (see next section), current ENG technology is usually insufficient to document it. It seems likely to us that a methodology where there was a method of keeping the eye in the center of the orbit (perhaps with a "winking" light, and a method of quantifying head position on the body (perhaps with a still picture grabbed at the right point), would do the job. Nobody has this technology implemented yet in their ENG systems. In the author's practice, this test is done entirely at the bedside.
Often it is helpful to compare nystagmus elicited with the head prone to with the head supine, as if the nystagmus does not reverse, cervical vertigo seems fairly certain.
Head-turning upright test. Another useful maneuver is to turn the head to one side to the limit of range, while the examinee is upright and simply wait for 30 seconds. The figure below shows a weak positive and the movie below in the case section shows a strong positive. Clinically, nystagmus that changes direction according to the direction of the head on neck, rather than with gravity, makes cervical vertigo likely. It is the author's personal observations that persons who are positive on this test nearly always have a disk abutting their cervical cord, generally at C5-6.
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| Cervical nystagmus recorded with head turned to left. |
More detail about this test can be found here.
Laboratory studies: If cervical vertigo still seems likely after excluding reasonable alternatives, one next needs to look for positive confirmation. Routine studies in working up cervical vertigo
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CT angiogram with 3-dimensional reconstruction. Left vertebral (left lower) is large and dominant. Right vertebral (right lower) is small and hypoplastic. |
Angiography: CT-angiography has been rapidly improving in recent years and it is excellent for detection of vertebral hypoplasia -- which is as much as you may be able to determine anyway. Three-dimensional reconstructions can be very helpful.
The "gold standard test" for the cervical vertigo due to compression of the vertebral arteries is selective vertebral angiography with the head turned to either side. Vertebral angiography is preferred for head-turning tests because there is less dye put into the body than for CT-angiography. However, because selective vertebral angiography is a risky procedure by itself, often it is decided not to proceed to this step. There is also another problem --
Catch 22: A basic flaw with any "head turned" radiographic procedures is the "Catch 22" problem -- if there is a risk of head turning -- it may not be detectable. The reason is that if there is even a tiny risk of a stroke during a radiographic procedure, radiologists may simply not turn the head. Or to put this another way - - a risk averse radiologist will be unable to diagnose a vertebral occlusion associated with head turning because they will refuse to turn the head sufficiently to diagnose it. Practically, it is generally impossible to monitor one's radiology department sufficiently to be sure that they do turn the head to end rotation. Thus, in some settings, it may be simply impossible to diagnose vertebral artery occlusion because of radiologist risk aversion.
Our position is that one should not attempt vertebral angiography, but simply do CT-angiography as long as kidney function is adequate.
Ordinary MRA and vertebral doppler procedures are rarely abnormal, and sometimes are used as a screening procedure to decide whether vertebral angiography is necessary. We are unenthusiastic about this as it seems unreasonable to us to use methods that are unreliable as screening procedures.
An MRI scan of the neck and flexion-extension X-ray films of the neck are suggested in all. We strongly advise against "open MRI", or "stand up MRI", as the image quality from these procedures is not as good as higher field methods.
Fluoroscopy of the neck may be used in persons with abnormal flexion-extension views. ENG testing is recommended, largely to exclude alternative causes. Vertebral artery doppler may be helpful in some. (Sakaguchi et al. 2003), but we presently prefer CT-angiography.
Posturography with the head held in different angles on the neck has been used in an attempt to diagnose cervical vertigo. This process, to us, seems to have too many free variables.
Static posturography does not appear to be useful. Dynamic posturography, incorporating sway referencing, may be more sensitive (Alund et al, 1991).
As should be apparent from the previous discussion, cervical vertigo is difficult to diagnose. Treatment is also problematic. When a specific cause can be identified (from above list), there may be a specific treatment available, sometimes involving surgery.
We generally think that chiropractic treatment is not a good idea for vertigo of any type, including cervical vertigo. We realize that this may not set well with the chiropractic community, but this is simply the author's opinion. There are two reasons: 1). Chiropractic treatment is associated with stroke in young people (Rothwell et al). This is very likely due to compression of the vertebral arteries at the top of the spine (Mann, Refshauge, 2001). 2). There is no mechanism listed above in which chiropractic treatment is more likely to help than physical therapy.
For the usual person in whom cervical vertigo is a diagnosis of exclusion, and pain is prominent, physical therapy treatment is recommended, possibly combined with medication to relieve pain and reduce spasm.
Case 1. Vascular. 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. Vision 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.
Case 2. Vascular. An otherwise healthy woman complained of positional vertigo elicited by turning the head to the left. On positional testing, after roughly a 20 second latency, she developed an extremely powerful right-beating nystagmus, which persisted as long as the head was turned to the left, and was accompanied by additional symptoms such as ear fullness, and at one point, a spot in the vision. She did not get nauseated. When she was tested upright with the head turned to the left side, after 20 seconds she developed a powerful right-beating nystagmus (see below). CT-angiography only revealed an aberrant right subclavian. Nevertheless, we attribute her symptoms to vascular compression in as much as no other mechanism would be likely to cause a 20 second delayed nystagmus.
Case 2b. Vascular (vertebro-basilar insufficiency)
An 88-year-old white male with diabetes complains of dizziness and imbalance for the last six months. In particular, he complains of spinning, lightheadedness, trouble with his hearing, and attacks once or twice per day. Standing up, rapid head movements, walking in a dark room, not eating, exercise, and coughing or sneezing can trigger symptoms. A brain MRI scan, showed tiny chronic infarctions involving the right side of the thalamus and the left cerebellar hemisphere. Hemoglobin A1c was 8.6.
Under video Frenzel's goggles, there is no spontaneous nystagmus but with the vertebral artery test, when his head is turned to the right and left there for about 10-15 seconds, he reproducibly develops a weak down-beating nystagmus.
(on site DVD) Movie of postive Vertebral artery Test (10 meg download)
Case 3. Herniated disk. Another otherwise healthy man was involved in an auto accident. He was wearing a seat belt, and while his head rotated forward and backward, there was no substantial trauma to the head. A disabling vertigo ensued, characterized by nausea and motion intolerance. Physical examination revealed a weak horizontal nystagmus that could be elicited by turning the head to one side (positive "vertebral artery test"). MRI of the neck revealed a C5-C6 disk herniation, abutting the thecal sac. Comment: Nystagmus in this case does not begin immediately but starts after about 10 seconds of head turning. This is the most common association between neck injury and dizziness.
(on site DVD) Movie of cervical vertigo (30 meg download)
Case 4. Cervical afferents. An otherwise healthy 32 year old woman developed neck pain, dizziness, and inability to drive due to visual sensitivity. Audiometry was normal. An MRI/A showed a small vertebral on the left but a CT-angiogram was completely normal. MRI of the neck showed some mild disk disease. On examination there was significant tenderness to the posterior neck muscles. Positional testing revealed a weak direction changing positional nystagmus, which did not reverse with head prone. Comment: the nystagmus in this case as well as other similar ones was weak and came on immediately with positioning.
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