Timothy C. Hain, MD • Page last modified: March 28, 2015


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).


Ataxia, or staggering like a drunk, is the main and well-established effect of cutting dorsal neck muscles in animals (de Jong and Bles, 1986). Nystagmus is a much less pronounced effect. Experimental work has "Firmly established" that acute loss of neck afferent information causes pronounced ataxia and some nystagmus (de Jong and Bles, 1986).

Experimental work has been met with several serious technical difficulties -- these experiments are often accompanied by significant pain. General anesthetics by themselves produce positional nystagmus, and local anesthetics damp the cervico-vestibulo-ocular circuits.


In 1858, Claude Bernard reported on early experients of Magendi and Longet, and in 1838, Magendie had discovered cervical ataxia in the guinea pig. In 1845, Longet confirmed that transverse section of suboccipital muscles elicited ataxia in rabbits, capibaras, cats, dogs, sheep and horses. Bernard added that titmice lost the ability to fly, but could walk and hop normally after neck muscle transection.

According to De Jong and Bles (1986), there was "fairly much" positional nystagmus in the rabbit induced by cervical anesthesia.

Cats and dogs

Abrahams and Falchetto (1969) described hindlimb cervical ataxia in cats in whom the neck muscles were anesthetized, similar to Longet's report (1845)

Manzonni and others (1979) demonstrated that unilateral deafferentation of C1-C3 elicited a similar postural deficit as cutting the 8th nerve on the opposite side. Recovery was complete in 20 days.

According to De Jong and Bles (1986), there was "less" positional nystagmus in the cat induced by cervical anesthesia.


Disturbances of gait have been noted in animals in whom the upper cervical sensory supply was disturbed by cutting the upper cervical dorsal roots (Richmond, 1976).

In 1961, Cohen reported that ataxia and positional nystagmus could be produced in baboons and macaques by local suboccipital anesthesia. According to De Jong and Bles (1986), there was "little" positional nystagmus in the rhesus monkey bby cervical anesthesia.

In 1969 and 1972, Igarashi et al reported that squirrel monkeys underwent a roughly 10-day period of ataxia after unilateral surgical deafferentation of C1 and 2. Igarashi commented that no "spontaneous nystagmus" was seen after anesthesia or section of the afferents, but there was transient reduction of postroatory and OKN slow phases.


De Jong and De Jong (1977) injected local anesthetics into their own necks. Such injections caused unsteadiness and minor amounts of dizziness.

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.