CERVICAL VERTIGO -- Denying that it exists is not defensible.
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.
Cervical vertigo is matter of considerable concern because of the high litigation related costs of whiplash injuries.
We often encounter physicians, generally orthopedic surgeons or neurosurgeons, who say that dizziness does not "come from the neck". Or in other words, these physicians state that cervical dizziness does not exist. We call this the "head in the sand defense" when we run into it in medicolegal matters.
The purpose of this page is to gently remind these physicians and otherwise interested persons of the overwhelming data that proves that dizziness can come from the neck.
Cervical vertigo can be due to neck artery compression.
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.
Experimentally dizziness can be produced by injections of local anesthetics into the neck. The key reference to read regarding neck afferent ataxia is DeJong and Dejong (1997). They injected local anesthetics into two human volunteers. Such injections caused unsteadiness and minor amounts of dizziness.
DeJong and Dejong also injected the necks of several species of animals.
In cats, a staggering ataxia was produced in about 80%.
In monkeys, ataxia was severe.
In rabbits, unilateral neck injection was followed by falling and rolling to the side of the injection, then by lateropulsion, and finally by hypotonia on the injected side. After bilateral neck injections, rabbits were unwilling to move and had horizontal oscillating head movements.
Disturbances of gait occur 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).
Dejong and Dejong also observed nystagmus after injection of cats, lasting from 4 minutes to an hour. In monkeys, nystagmus was seen when lidocaine was injected very high up, against the later side of the occipital condyle. It was not produced by injection at lower levels. Nystagmus was not observed after injection in the two human subjects.
Nystagmus, a physical manifestation of vertigo, can be produced by stimulating the neck.
Vibration of the neck is a well established source of nystagmus, in persons with vestibular damage. See the page linked above for a discussion.
Case 1. 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.
An 88-year-old white male with diabetes complained 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.
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.
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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Kamouchi, M., K. Kishikawa, R. Matsuo, et al. (2003). "Ultrasonographic detection of extracranial vertebral artery compression in bow hunter's brain ischemia caused by neck rotation." Cerebrovasc Dis16(3): 303-5.
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