Timothy C. Hain, MD Spanish version Page last modified: April 15, 2013
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 hold that cervical vertigo does not exist, even 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 dysequilibrium. 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 movement. There should be no hearing symptoms (other than tinnitus) or hearing loss but there may be ear pain (otalgia). 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.
Unfortunately, there is no consensus concerning how one diagnoses cervical vertigo, and the literature is replete with poorly carried out studies as well as studies 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.
There are many potential causes of cervical vertigo. The situation today (2013), 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.
1. Vascular compression (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.
Regarding compression, in 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, 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 vertberal artery, an anomalous course between the fasciles 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.
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.
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.
In this regard, 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).
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). Although the issue remains controversial, we recommend against chiropractic treatment of vertigo that includes "snapping" or forceful manipulation of the vertebrae in persons with dizziness or unstable necks.
Whiplash (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.
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).
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.
On the other hand, 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.
|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 the most 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 is irrational.
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. 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". (discredited)
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.
6. High cervical disease (i.e. C1-C2) associated with cervical vertigo.
This disorder does exist but it is 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. In other words, again a dubious mechanism.
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).
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.
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. We think this is another very likely mechanism for cervical vertigo. This mechanism might improve with physical therapy that made the neck more predictable.
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, and 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.
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 physician in the United States, including the author of this page, who has written anything substantial on cervical vertigo. 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. 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 (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.
|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 include:
|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. 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.
Posturography with the head held in different angles on the neck has been used in an attempt to diagnose cervical vertigo (Kogler et al, 2000). This process, to us, 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).
As should be apparent from the previous discussion, cervical vertigo is difficult to diagnose. Nevertheless, in dizziness, there are many other common disorders that have no "test" that proves that their diagnosis is correct -- e.g. Migraine associated vertigo, Chronic subjective dizziness, and Mal de Debarquement syndrome. So, clearly the "lack of a test" is logically not the same as "the diagnosis does not exist".
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 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.
There are very bizarre treatments that have been reported for cervical vertigo, that we will mention briefly. In recent years, the general population has gotten the idea that lasers are good for nearly any medical problem. We have encountered, for example, situations where lasers to the external ear are suggested as treatment for tinnitus. This seems to us simple fraud. In a similar way, some have suggested that "laser acupuncture" is effective for cervical vertigo. This is implausible as lasers have no mechanism of manipulating the neck. The literature substantiates that laser acupuncture is ineffective for cervical vertigo (Aigner et al, 2004).
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.
Cervical vertigo is poorly defined, and due to this, no relevant studies exist of prognosis. In the author's clinical practice, his impression is that cervical vertigo is a poor prognosis condition. The reason for this is that the musculoskeletal conditions that are associated with cervical vertigo - neck stiffness, pain, disk disease and facet arthropathy, are also slow to resolve. A second reason may be that the patients seen in the author's clinic usually have already had symptoms for many months.
With respect to the chronicity of whiplash injuries, Dufton et al (2012), recently found in a very large study that about 25% of persons after whiplash injury develop chronic symptoms. Another recent metanalysis reported that somewhere between 14 and 42% of patients with WAD will develop chronic neck pain (Rodriquez, Barr et al. 2004). In the same study, it pointed out that roughly 75% of all persons with injury, had previous neck pain.
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 positive 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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