Timothy C. Hain, MD • Page last modified: March 12, 2021
Cervical vertigo is a vertigo or dizziness that is provoked by a particular neck posture no matter what the orientation of the head is to gravity. For example, dizziness provoked by turning the head about the vertical axis, while sitting upright. Another definition is "vertigo due to neck disorders" (Ryan and Cope, 1955). We will use the symptom based diagnosis, as we think that the diagnosis base on implication of cause is unrealistic at the present time, given our inability to diagnose cervical vertigo in general at the present writing.
Some poorly informed individuals hold that cervical vertigo does not exist, even persisting in this statement in legal expert testimony. This is an indefensible position, as discussed here.
The precise incidence of cervical vertigo 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 Disequilibrium. In this regard, also note that driving disturbances are common in persons with chronic whiplash associated vertigo (WAD), occurring in 73% according to Takasaki (Takasaki, Johnston et al. 2011). 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 "pathology" (Devaraja, 2018). There should be no hearing symptoms (other than tinnitus) or hearing loss but there may be ear pain (otalgia). A recent review of the topic was essayed by Devaraja (2018). Brandt (1996) has reviewed this topic from a diagnostic perspective, and Wrisely et al (2000) as well as Heikkila (2004) reviewed the physical therapy approach. There is a long history of experimentally induced cervical vertigo, reviewed in several places (de Jong and Bles, 1986; de Jong and de Jong, 1977; Brandt, 1996). While there are many reviews, in the author's opinion, all of these make oversimplification errors, offering schematics based on their opinions, but lacking evidence to back up their assertions, or conclude that things are so complicated, that the entire entity does not exist.
As a comment, here we have two vague words -- "dizziness", and "pathology", with an immense universe of patients who have both. Most authors do agree that "vertigo", meaning a spinning sensation, is generally not found in persons with "cervical vertigo". Rather these patients complain of subjective symptoms involving "light-headedness" (whatever that means), or a disequilibrium (often translating into a fear of falling without any actual falls).
Unfortunately, there is no consensus concerning how one diagnoses cervical vertigo, and the literature is replete with poorly carried out studies as well as publications containing strange suggestions regarding mechanism or treatment. In the following summary, often the author of this page will say that while there are studies suggesting this or that, the author of this page finds their conclusions dubious at best.
|Artists rendition of Vertebral arteries as well as cranial nerves||Normal CTA (CT angiogram) showing how the vertebral arteries traverse the vertebrae in the neck on their way up to the brainstem.||Another view of normal anatomy. This is a reconstruction from another patient's CTA.|
There are many potential causes of cervical vertigo. The situation today (2019), is that we have many potential mechanisms, but don't so far have a good way of separating them out from one another and, more importantly, finding effective treatment. (Hain, 2015)
Generally, when there is nystagmus, it does NOT change with gravity -- but rather with position of the head on neck
1. Vascular compromise (see TIA discussion) -- There are at least 3 distinct mechanisms proposed - - compression, spasm, and dissection.
Movie of vertebral artery compression (head is turned to the right, and there is compression of vertebral artery by a spur), video courtesy of Dr. Dario Yacovino.
Bow hunters -- compression of vertebral arteries on turning of the head on neck:
In Bow-hunter's syndrome, the vertebral arteries in the neck (see above) can be compressed by the vertebrae (which they traverse -- see above), or other structures (Kamouchi, Kishikawa et al. 2003; Sakaguchi, Kitagawa et al. 2003). Arthritis, neck surgery, and chiropractic manipulation are all potential precipitants of neurological symptoms including stroke. According to Bogduk, compression can be due to anomalies of the origin of the vertebral artery, an anomalous course between the fascicles of either longus coli or scalenus anterior, and bands of deep cervical fascia (Bogduk, 1986). All of these mechanisms would presumably be associated with blockage of flow on turning the neck to one side or the other. It is usually of significance only in persons who have a substantial asymmetry in their vertebral circulation -- one being much smaller, or one being absent or terminating in PICA.
It is presently considered a problem when there is mechanical compression during head rotation due to muscular and tendinous insertions, osteophytes, and arthritis around the C1-C2 level. As the vertebral arteries enter the vertebrae around C4, it can also occur at lower levels. As about 50% of cspine rotation occurs around C1, this is likely the reason for the predominance at this level. Araz Server et al (2018) reported reduced flow in the ipsilateral vertebral artery when the head was both hyperextended and rotated. Perhaps a position mainly encountered in dental offices ? Dynamic cerebral angiography is the preferred method of documenting this diagnosis, but this is almost never done as it requires a substantial amount of contrast and radiation, and it rarely results in a positive finding. One would think that MRA done in 3 positions -- head right, head center, head left, would also be diagnostic, but we have not seen any papers of this. In addition, while MRA does not have the radiation issue that CT does, it might require more contrast than reasonable.
This is not a common syndrome, but there is a substantial literature. About 20 papers in Pubmed have "Bow hunter's stroke" in their title, almost all being case reports from neurosurgeons. According to Choi et al (2005), who reported 4 cases, vertigo, tinnitus and nystagmus are due to labyrinthine ischemia. Logically, one would wonder why an artery that supplies the lower brainstem, would produce findings solely from ischemia of the labyrinth. In their cases, there was a mixed downbeat/torsional/horizontal nystagmus beating towards the compressed vertebral artery (i.e. away from the direction of head turning). In three patients the nystagmus spontaneously reversed direction. The nystagmus appears after a latency of about 5 seconds (the author has seen a patient in which it took 20 seconds). On repeat of head rotation, the nystagmus may be lessened. There seem to be many variants of "bow hunter's stroke", and certainly one cannot rely on all cases to show the same pattern.
Surgical intervention, when the patient is a good candidate, is recommended by neurosurgeons in persons with Bow hunter's syndrome. As it would seem that all of these cases must be congenital, and also many persons function quite well with only one vertebral artery, in our opinion, this should be considered with great care.
Subclavian artery syndromes -- not a likely cause of cervical dizziness.
The subclavian artery feeds the vertebral arteries in the neck, and thus disorders of the subclavian can interact with vertebral blood flow. The thoracic outlet syndrome would be unlikely to affect vertebral blood flow as narrowing of the subclavian in TOS occurs after the vertebral arteries take off from the subclavian.
The subclavian steal syndrome is provoked by movement of the arm, rather than turning the head on neck. Thus it is also an unlikely cause of cervical dizziness. A very narrowed subclavian that reduced blood flow to the vertebral, might cause a vascular type of cervical dizziness but one would think that this syndrome would be dominated by poor blood flow to the arm.
Spasm of vertebral arteries -- speculative
Bogduk (1986) suggested that spasm of the vertebral arteries might occur due to the close relation between the sympathetic trunk and vertebral artery. This idea seems rather difficult to substantiate, and lacking a method of testing the hypothesis, it remains speculation.
Vertebral artery loops
Yenigun et al (2016) reported that vertebral artery loops were frequently seen on MRAs of patients with "cervicogenic dizziness". We are dubious for several reasons -- the difficulty in identifying "cervicogenic vertigo", and the lack of clarity regarding the prevalence of "vertebral artery loops" in normal subjects.
Dissection of the vertebral arteries:
Dissection means that the wall of an artery is torn, and blood enters between two layers of the artery, often causing it to block. With respect to dissection, it is thought that vertebral arteries can be damaged at the points that they are anchored in the upper cervical spine, through a mechanism that involves stretching. Generally speaking, this occurs due to a traumatic event such as a motorcycle accident. Dissection is reportedly more common in individuals who are "double jointed", such as the Ehlers-Danlos syndrome.
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). A recent paper that enrolled a nearly 1000 subjects noted that "cervical manipulation" preceded 7% of strokes caused by cervical artery dissection (Engelter et al, 2013), but only 0.6% of strokes not caused by cervical artery dissection. A 10:1 difference in risk. Other forceful activities such as heavy lifting, extreme head movements, and sports all were highly associated with greater risk of strokes from cervical artery dissection. It seems then that stretching the vertebral artery sometimes causes it to rupture.
On the other hand, a recent large Canadian study reported that the risk of vertebral artery territory stroke was greater for both visits to chiropractors and primary care physicians (Cassidy et al, 2008). The authors of this study inferred in their discussion that this observation meant that visits to chiropractors does not cause strokes, as the same risk of stroke was seen in situations where there was no manipulation of the neck. However, we are not so sure as we think there is a logical fallacy. Another way to interpret this data is that vertebral artery strokes are generally diagnosed by seeing primary care physicians, sometimes later rather than sooner, and that this comparison is simply invalid as a visit to a physician is required for diagnosis of a stroke anyway. A more proper comparison would be with visits to, lets say, a dermatologist and chiropractic visits.
Chiropractors often seem unaware that visits to a chiropractor are associated with stroke (Haldeman et al, 2002). We usually recommend against chiropractic treatment of vertigo that includes "snapping" or forceful manipulation of the cervical vertebrae.
Occasionally vertebral artery dissections occur, sometimes in a delayed fashion, after a whiplash injury.
Additionally, flexion-extension injuries to the neck, usually associated with an auto accident involving a rear end collision has also been reported to be associated with asymmetrical vertebral artery flow as documented by sophisticated MRA (Kendo et al, 2006). The significance of this observation is presently unclear, but again the suggested mechanism is stretching of the upper portions of the vertebral arteries. Neck injuries have increased in the US in recent years with auto accidents, presumably due to interaction between use of seat-belts and chest restraints. While chest restraints reduce the risk of death, mechanically by restraining the trunk, they can be associated with greater relative movement of the unrestrained head on neck due to simple biomechanics involving momentum transfer.
Whiplash is simply a description of the mechanism of a neck injury. Whiplash might cause cervical "vertigo" in diverse ways, including proprioceptive injury, or injury to the cervical spinal cord. Whiplash is not a subcategory of "proprioception", as suggested by Devaraja (2018) in his review.
2. Abnormal sensory input from neck proprioceptors.
Sensory information from the neck may be unreliable, too much, 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).
Disturbances of gait have been noted in animals in whom the upper cervical sensory supply was disturbed (Longet, 1845), in whom the neck muscles were anesthetized (Abrahams and falchetto, 1969), and by cutting the upper cervical dorsal roots (Cohen 1961, Richmond, 1976). Supporting this general idea, Loudon et al (1997) found that persons with whiplash injury had deficits in reproducing neck position after whiplash injury and inaccuracy in assessing neutral position. Similarly, Heikkila et al, 2000) found similar results in persons with dizziness/vertigo of cervical origin. This would suggest a deficit in proprioception as one of the potential causes of "cervical vertigo".
On the other hand, Koskimies et al (1997) reported that individuals with "tension neck", had greater postural deviations induced by vibration of their neck than persons without a stiff neck. They suggested that this association might contribute to vertigo. In other words, a tight neck might increase input from muscle proprioceptors, and dizziness due to too much proprioception. Magnussen et al (2006) similarly reported that when the neck is activated, cervical input is switched to become dominant over vestibular input. One could hypothesize that in cervical vertigo could occur when neck input became dominant over vestibular, due to neck pain or stiffness.
|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 and associations between cervical MRI and symptoms, this is a common mechanism of cervical vertigo. Management is not very successful as surgery is generally not felt to be appropriate by neurosurgeons, and mobilization of the neck, such as is favored by physical therapists and chiropractors, is irrational.
After cervical fusions, balance problems and dizziness are very frequent 10 years later (Hermansen et al, 2019). Still, it our impression that this surgery can sometimes convert someone who cannot drive back to a driver, presumably because it is an internal cervical collar.
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. This is certainly possible. It is difficult to know how frequently this occurs.
There is a substantial literature mainly generated by Bjorne (2003), suggesting that symptoms resembling Meniere's disease are associated with or caused by cervical spine lesions or TMJ lesions. We are frankly rather dubious as we don't see how either cervical spine lesions or TMJ disorders could regularly cause hearing loss.
5. Barré-Liéou "syndrome".
This entity is controversial. In 1926, 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). In this syndrome, it is hypothesized that the sympathetic plexus surrounding the vertebral arteries are irritated by arthritis in the cervical area, and this causes reflex vasoconstriction. Irritation of the cervical sympathetics. Similarly, according to Shenk ( 2006), damage to the superior cervical ganglion, located at the C2-C3 level, may cause posterior circulation hypoperfusion. The author of this page find this idea very dubious. Some authors find it remains plausible however (Dvararaja, 2018).
6. High cervical disease (i.e. C1-C2) associated with cervical vertigo.
This disorder does exist but it is over diagnosed, primarily by the chiropractic community. We have encountered occasional patients with platybasia and rheumatoid arthritis who have high-cervical disease. We have also encountered a few patients with anomalies of C1/C2 who have an activity dependent dizziness - -the more that they move their head (usually up/down), the dizzier they get. Nevertheless, this is not common -- our estimate is that only about 1/500 patients with cervical vertigo have high-cervical problems.
Some have suggested that damage to the alar ligament is associated with cervical vertigo, and that furthermore such damage can be identified with high-resolution MRI. The alar ligaments connect the dens axis to the occipital condyles. The main function of the alar ligaments is to limit the axial rotation of the head. Injury to these ligaments may cause rotational instability in the craniocervical junction (Dvorak and Panjabi, 1987; Panjabi et al, 1991). Neuroradiological studies suggest that whiplash does not change imaging of these ligaments (Rigmar et al, 2008), and also that neuroradiological evidence of damage to these ligaments is not related to outcome of whiplash (Vetti et al, 2010).
High cervical disease can be associated with a radiculopathy of C1-C2, and result in occipital neuralgia. The mechanism of dizziness in this situation is likely migrainous.
The os odontoideum syndrome -- where the top of the dens is separated from the remainder, would seem likely to be low risk for vertigo. There is a single case report of this situation (2001).
These anomalies nearly always need a CT scan of the cervical spine to define the bony changes.
7. The neck 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 with unilateral vestibular lesions who are otherwise well compensated. Similarly, tonic neck stimulation modulates caloric nystagmus in individuals with unilateral vestibular lesions (Kobayashi et al, 1991). Similarly, It seems likely (but entirely unexplored) that asymmetrical injury to the neck could interact with other types of vertigo and cause dizziness. We think this is a very likely mechanism.
Illustration from Brandt/Huppert, 2016. Internal model theory to explain cervical vertigo. The "expected" afferences are the output of the brain's internal model.
Somewhat along the same lines, one can bring in "internal model theory". When one attempts to move one's head, one's cortex expects that a given motor input to the head will result in an expected displacement of the head on neck. When the head/neck is stiff and painful, local factors and spinal cord reflexes may prevent the head from moving as far as expected. Mismatch between expected and observed movement is disturbing and can induce motion sickness (Brandt and Huppert, 2016) . We think this is another very likely mechanism for cervical vertigo. This mechanism might improve with physical therapy that made the neck more predictable (i.e. improves internal model).
8. Cervicogenic migraine -- neck pain can trigger migraine, and migraine can cause vertigo.
While this idea seems reasonable to us, the main worker in this area, Sjaastad, suggests that migraine and cervical headaches have little overlap (2007). We are dubious about Sjaastad's conclusion ourselves, as we have encountered patients who have classic migraines triggered by neck perturbations. Additionally, with migraine, basically "anything goes", and we don't think one can easily rule out "migraine" from nearly any type of head pain. This is because migraine (like many other illnesses, including most of psychiatry) is a "committee disease", based on "checking off the boxes" on surveys or similar symptom inventories. Anyone that can google migraine, and remember the right boxes to endorse, can be diagnosed with migraine.
We ourselves coauthored a paper on diagnosing cervical vertigo with a questionnaire, and found that the cervical vertigo patients overlapped considerably with migraine. (Thompson Harvey et al, 2019)
That is not to say that we discount the existence of cervicogenic migraine at all. We just think it is best to keep one's mind open. We think it is a good idea to attempt treatment for migraine in almost all situations where head/neck pain is combined with vertigo.
9. 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. Practically , there is almost nothing in the neck that is directly related to the inner ear.
10. Cervicoocular reflex.
There is such a thing as the cervico-ocular reflex (COR), meaning that neck movement, about a still body, can produce eye movements. This is much stronger in lower animals, although monkey's are pretty close to humans. Perhaps the COR causes cervical vertigo. We don't believe it, because the COR is unmeasurable in normal human subjects (Schubert et al, 2004). This suggests that the neck does not have a simple and linear relationship to eye movements. This may be the reason that tests for cervical vertigo are far and few.
We are often asked about who can be seen locally to diagnose and treat cervical vertigo in the United States. The short answer is there does not seem to be any clinician in the United States who has written anything substantial on cervical vertigo. We are trying ourselves (e.g. Yacovino and Hain, 2013; Hain, 2015).
Furthermore, as noted above, the world literature about cervical vertigo is full of strange and peculiar ideas and suggestions, and we would be hard pressed to recommend someone outside of the US either.
Otoneurology (i.e. a neurologist that specializes in dizziness and hearing disorders) is the specialty that seems most reasonable for cervical vertigo - -but there are very few otoneurologists in the world. Practically, the safest thing to do to us seems to be to locate a sympathetic and thoughtful physician to be the "captain of the ship", see appropriate specialists to exclude alternatives involving the ear (e.g. BPPV) , and brain (e.g. migraine), and take reasonable measures to decrease neck pain and stiffness (e.g. physical therapy, and pain clinic if this fails).
The process is generally uncertain and frustrating. Cervical vertigo is reported to be most common in the 30-50 year old age group, as well as being more common in the female population (Heikkila, 2004). As is common in poorly defined syndromes, criteria for diagnosis are inconsistent and these criteria must be taken as being tentative at best.
According to Heikkila (2004), neck pain must be present. The author of this review does not agree with this statement -- as it would obviously exclude several mechanisms above (e.g. vascular, cord compression). Heikkila also suggests that tinnitus and low-frequency hearing loss are possible. We would disagree that these symptoms are diagnostic. Heikkala suggested that there may be photophobia and blurred vision. We would generally attribute these sorts of symptoms to migraine, ocular disturbances (e.g. post cataract removal), concussion, or much more remotely, vertebral insufficiency.
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/or rotatory chair test), 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. More precisely, there is an upbeating nystagmus supine. (Hozl et al, 2009). This suggests that the neck afferents may interact strongly with vestibular inputs derived from the posterior canal. It is known that neck input interacts with caloric responses (Kobayshi et al, 1991). In our experience however, we also find that persons with Migraine may have BPPV type nystagmus, and the literature suggests that Migraine commonly is associated with positional nystagmus.
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 (neck torsion nystagmus). Another potentially 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 (Cherchi and Hain, 2010). 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. Similar to Devaraja (2018), we feel that this test is not especially useful. Our observations is that it is neither sensitive nor specific for cervical vertigo.
The craniocervical flexion test (CCFT) are difficult ones implement as well as accept as rational. The both involve using EMG. The related "COR" test is discussed separately below.
Posturography with the head held in different angles on the neck has been used in an attempt to diagnose cervical vertigo (Dejong and Bles 1986; Kogler et al, 2000). This process, seems to have too many free variables -- in other words, people can simply sway more due to anxiety or voluntarily sway more, in situations where there is benefit to be obtained from being diagnosed as having cervical vertigo. This situation, of course, naturally arises in people litigating after an auto accident.
Static posturography does not appear to be useful. Dynamic posturography, incorporating sway referencing, may be more sensitive (Alund et al, 1991).
Joint position error. The physical therapy literature has numerous enthusiastic reports concerning this test for cervical vertigo. Like posturography, this test is vulnerable to intent, bias, and malingering. Furthermore, this test presumes a mechanism (proprioception), which may be true in some patients, but certainly not in all. It may be helpful though in a subset of patients with cervical vertigo (i.e. the subset that has proprioceptive loss rather than vertebral artery compromise or cervical stenosis).
Smooth pursuit neck torsion (SPNT) test is another procedure favored by papers in the literature produced by physical therapists. This is a strange procedure where a smooth pursuit is measured with the head turned on 45 degrees to either side. Logically, the connection between neck torsion and smooth pursuit is very difficult to follow, and we think that it is likely overly enthusiastic investigators and overly cooperative subjects. .
|Cervical nystagmus recorded with head turned to left.|
Cervico-ocular reflex (COR) testing
This is a difficult endeavor involving turning the body while recording the eyes. The most practical method is to have the patient sit on a swivel stool, wearing video Frenzel goggles, with vision denied (i.e. in total darkness). Then the patient turns themselves about 30 deg to either side, while the examiner holds the head still in space and watches on the video monitor. This process is nearly always unproductive of any visible eye deviation in persons with complete bilateral vestibular loss. So the straightforward approach doesn't work.
Kelders et al (2005) reported that the COR is increased in whiplash patients. Schubert et al (2004) reported that it is weak, unreliable, and is not increased in patients with unilateral vestibular loss. Bronstein and Hood (1986) reported that it is increased in patients with absent vestibular function. In our clinic, we have not found the COR to be very helpful or reliable. All together, the COR does not seem to be a good way to diagnose cervical vertigo.
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 include:
CT angiogram with 3-dimensional reconstruction. Left vertebral (left lower) is large and dominant. Right vertebral (right lower) is small and hypoplastic.
Note that reconstructions are not nearly as reliable as simple images, as reconstructions are done by computers that may have their own ideas about what is a blood vessel and what is noise.
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. Our position is that one should not attempt vertebral angiography, but simply do CT-angiography as long as kidney function is adequate.
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 choose not to 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.
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.