8

J Neurol Neurosurg Psychiatry 2001;71:812

NOSOLOGICAL ENTITIES?

Cervical vertigo
T Brandt, A M Bronstein

Proprioceptive input from the neck participates

in the coordination of eye, head, and body posture as well as spatial orientation. On this basis
it has been argued that a syndrome of cervical
vertigo might exist. However, cervical vertigo is
a controversial clinical entity and patients with
suspected disease often have alternative bases
for their symptoms.1
The neck contains mechanisms directly
involved in balance control (neck aVerents),
cardiovascular control (carotid bodies), and
purely vascular structures (carotid and vertebral arteries). Neck movements are also invariably associated with head movements. Thus,
experiencing unsteadiness or vertigo associated
with neck movements could be due to a disorder in vestibular, visual, vascular, neurovascular, or cervicoproprioceptive mechanisms.
Table 1 summarises the possible diVerential
diagnoses.
Without further specification, however, the
term cervical vertigo is reserved for cases where
the suspected mechanism is proprioceptive.
The reasoning is as follows. The perception of
head rotation is mediated by vestibular,
proprioceptive, or visual receptors. Vertigo
should therefore be induced by stimulation of
any of these systems. Degenerative or traumatic
changes of the spine could induce distorted
sensations of head motion (vertigo). This line
of thought is, however, not as straightforward
as it seems. Clearly, vestibular lesions or
experimental vestibular activation (for exam-

Neurologische Klinik,
Klinik Groshadern,
Ludwig Maximilians
Universitat, Munchen,
Germany
T Brandt
Division of
Neuroscience and
Psychological
Medicine, Imperial
College School of
Medicine, Charing
Cross Hospital,
Fulham Palace Road,
London W6 8RF, UK
A M Bronstein
Correspondence to:
Dr AM Bronstein
[email protected]
Received 2 October 2000
Accepted 29 November 2000

ple, a caloric test) produce powerful illusions of

self motion. Similarly, visually induced illusion
of self motion is readily experiencedfor
example, the feeling that the train we are in has
started to move oV when, in fact, it is the train
next to ours which has done so.
Evoking a clear sensation of head turning by
cervical stimulation is, by contrast, not so
straight forward. To start with, to investigate
neck proprioception, the head must be immobilised while the trunk is rotated. Unless this
technical precaution is taken, any normal or
abnormal sensations of head turning can
always be due to vestibular stimulation. With
this approach, under special conditions of perceptual uncertainty (for example, both the
subjects head and trunk can be independently
rotated in the dark), trunk rotation can induce
sensations of head turning.2 However, when
the subjects head is unambiguously fixed, or in
normal viewing conditions, trunk rotation does
not induce sensations of head turning. This is
so, even in certain pathological conditions
when trunk rotation is capable of inducing
strong nystagmusfor example, bilateral absence of vestibular function,3 or occasionally, in
cerebellar lesions.4
Questions relevant for the discussion of cervical vertigo are: What is the functional
relevance of neck aVerent input and how does
the lack of or distortion of such input lead to
vertigo or disequilibrium? Ataxia and unsteadiness occurring with sensory polyneuropathy

Table 1 DiVerential diagnosis of cervical vertigo: vertigo, unsteadiness, or oscillopsia triggered/aggravated by head-neck
movements
Disorder

Assumed mechanism

Labyrinthine:
Benign paroxysmal positional vertigo
Post-traumatic otolith vertigo
Perilymph fistula
Vestibular nerve:
Unilateral vestibular failure (eg, vestibular neuritis)
Bilateral vestibular failure
Vestibular paroxysmia
Nerve compression by cerebellopontine angle mass
Ocular motor:
Extraocular eye muscle or gaze paresis
Central vestibular:
Central positional nystagmus/vertigo
Migraine without aura
Migraine with aura (basilar migraine, vestibular migraine)
Vestibulocerebellar ataxia
Vascular:
Rotational vertebral artery occlusion
Carotid sinus syndrome
Intoxication:
Positional alcohol nystagmus/vertigo
Drugs (eg, antiepileptics)

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Canalolithiasis, cupulolithiasis
Dislodged otoconia, causing unequal heavy load on macula
Floating labyrinth
Cross coupling eVects with acute vestibular tone imbalance
Defective vestibulo-ocular reflex
Neurovascular cross compression
Conduction block or ectopic discharges
Inappropriate vestibulo-ocular reflex
Cerebellar disinhibition
Motion sickness due to sensory hyperexcitability
Spreading depression involving vestibular structures
Vestibulocerebellar dysfunction
Ischaemic depolarisation
Global cerebral ischaemia
Cerebellar and specific gravity diVerential between cupula
and endolymph (buoyancy mechanism)
Cerebellar and ocular motor

Cervical vertigo

are readily recognised and explained by a deficient sense of position of the lower limb joint.5
Dizziness and unsteadiness suspected to be of
cervical origin could be due either to loss or
inadequate stimulation of neck receptors in
cervical pain syndromes. Thus far this has
never been shown.
Functional relevance of neck aVerents
Proprioception is mostly dependent on the
deep short intervertebral neck muscles, which
are extensively supplied with muscle spindles.6 7 The neck input participates in perceptual functions and reflex responsesnamely,
cervicopostural and cervico-ocular reflexes.
PERCEPTUAL FUNCTIONS

The perception of head or trunk rotation in

space would be erroneous if only vestibular
stimulation or only neck stimulation were
involved. When vestibular and cervical stimuli
are combined (head rotation relative to the
trunk), the perception of both trunk and head
rotation in space reflects the true position.2 8
Vestibular and visual cues produce postural
corrections but these responses change direction with changes in head position.9 When the
head is rotated horizontally by 90 to the right
or leftfor example, horizontal head movements and horizontal retinal slip of the visual
scene (right-left in head coordinates)no longer
indicate lateral body sway; instead, they represent fore and aft movements.10 Consequently,
the compensatory postural adjustments must
be corrected and this function is also mediated
by neck aVerences.11
The perceived straight ahead and the
subjective visual vertical can also be modified by cervical stimulation. Unilateral electrical stimulation of the neck12 causes deviation of
the subjective vertical. Vibration of neck
muscles, which stimulates the primary endings
of the muscle spindles as if the muscle were
being stretched13 elicits an illusion of head tilt
and apparent movement of a visual target.14
Accordingly, subjective straight ahead shifts
toward the side of the vibrated dorsal neck
muscle.15 It has now been clarified that changes
in the subjective straight ahead15 and the
illusory motion of a target light during neck
vibration16 are due to minute slow phase eye
movements. This vibration induced cervicoocular reflex is, in agreement with head/trunk
rotation studies,3 significantly enhanced in
patients with bilateral absence of vestibular
function.16 In unilateral vestibular lesions, the
increase in muscle spindle input (as tested by
vibration) is asymmetric, restricted to the
aVected side, and gradually builds up over
weeks.15 Of note, however, both visual illusions
and postural responses are comparatively
stronger than any illusion of head movement. It
would seem that neck input is important for the
generation of automatic reflexes but less
important for generating conscious perceptions
of head turning.
REFLEX RESPONSES

Two reflexes are mediated by neck proprioceptors: the postural neck reflexes and the cervico-

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ocular reflex. Tonic neck reflexes, studied by

Magnus,17 innervate limb muscles asymmetrically. In humans, tonic postural neck reflexes
can be elicited only in the newborn18 19for
example, ipsilateral flexion and contralateral
extension of the limbs with head rotation
(fencing posture). Neck input not only
modulates body posture, but also stabilises the
head with respect to the trunk by cervicocollic
reflexes, interacting with vestibulocollic reflexes which stabilise the head in space.20 21 In
healthy human beings, neck reflexes form a
part of the multisensory intersegmental postural control mechanism thus making it
virtually impossible for the clinician to carry
out a selective test of neck function by simple
postural manoeuvres.
It was Brny22 who first demonstrated tonic
cervico-ocular reactions in rabbits, elicited by
motion of the trunk relative to the head. In
humans, this tonic neck-eye reflex can only be
seen in the newborn18 or in rare patients with
gross CNS lesions.23 Bikeles and Ruttin24 were
the first to report nystagmus during head rotation in patients with complete vestibular loss,
which they ascribed to sensory input from neck
joints. More recent studies of the cervicoocular reflex, elicited by rotating the trunk
about the stationary head, have shown that this
reflex is weak in normal subjects.3 A low velocity nystagmus, however, can be elicited in some
normal subjects.3 25 26 This reflex is adaptively
enhanced in acquired vestibular loss, thereby
partially substituting the vestibulo-ocular reflex
deficit in the monkey27 and in humans.3 2830
Thus, attempts to define cervical vertigo on the
basis of cervical nystagmus31 are impractical:
cervical nystagmus occurs in healthy subjects
and can be particularly strong in patients with
no cervical vertigo.3 4
Experimental cervical vertigo
In animals, transverse section of suboccipital
muscles, surgical deaVerentation of C1-C3, or
suboccipital anaesthesia results in locomotor
ataxia.3235 Local anaesthesia of deep posterolateral neck tissue in humans35 36 usually elicits a
transiently increased ipsilateral and decreased
contralateral extensor muscle tone with a
tendency to fall, gait deviation, and pastpointing towards the injected side. Dieterich et
al37 confirmed this in patients with cervicogenic
headache investigated before and after bilateral
therapeutic anaesthetic C2 blockades; however, they found no specific abnormality with
static posturography, or subjective visual vertical or routine electronystagmography. The
weak horizontal spontaneous nystagmus, directed away from the injected side as seen by
Barr,36 is not a typical feature in humans.35 37
Biemond38 reported positional nystagmus due
to upper cervical root section in the rabbit but
Cohen39 showed that this positional nystagmus
is species specific: most pronounced in rabbits,
less in the cat, and subtle in the rhesus monkey.
Positional nystagmus cannot be attributed to a
disturbance of the cervical sympathetic chain36;
animal experiments35 40 indicate that it most
probably represents a tone imbalance of upper
cervical roots.

10

Brandt, Bronstein

Clinical evidence for cervical vertigo?

Because section or anaesthesia of cervical roots
or muscles causes an asymmetry in somatosensory input, unilateral irritation or deficit of
neck aVerents could create a cervical tone
imbalance, thus disturbing integration of vestibular and neck inputs. However, it has not
been shown that whiplash injuries or cervical
pain syndromes produce such a tone imbalance
with ataxia and vertigo. Rotational vertigo and
nystagmus associated with pain arising from
the cervical spine with tenderness and limitation of neck movement should not be called
cervical vertigo; indeed, when post-traumatic,
vertebral artery dissection should be ruled
out.41
Symptoms of cervical vertigo, if it exists,
would be a sensation of lightheadedness or
floating unsteadiness and slight ataxia of stance
and gait, perhaps more on head turns. This can
be inferred from the experimental unsteadiness
induced in humans by unilateral suboccipital
local anaesthesia.35 37 As somatosensory cervical input converges with vestibular input to
mediate multisensory control of orientation,
gaze in space, and posture, the clinical
syndrome of cervical vertigo could theoretically include perceptual symptoms of disorientation, postural imbalance, and ocular motor
signs although the last looks particularly
unlikely. Consequently, further clinical studies
seeking to define cervical vertigo should focus
on establishing reliable measures for it. These
could include psychophysics, oculography,
posturography, and measurements of cervicospinal reflexes but, as assessment under static
conditions has so far proved inconclusive,
further investigations should focus on dynamic
somatosensory studies. If vestibular function is
tested by vestibular stimuli and visual function
by visual stimuli, then somatosensory cervical
function should be tested with selective somatosensory stimulation. Complains of vertigo or
unsteadiness on turning the head are much
more likely to imply vestibular rather that cervical dysfunction.
Some of the more conscientious studies have
been based on posturography data.4245 Patients
with chronic cervicobrachial pain (not selected
for complaints of vertigo) had poorer postural
control, based on vibration induced and
galvanically induced body sway, than normal
controls.42 It was also noted that physiotherapy
was of value in reducing neck pain as well as
dizziness and postural balance.44 The findings,
however, are not specific enough to establish a
diagnosis of cervical vertigo.
Hypothetical mechanisms
Firstly, it is not known how traumatic,
degenerative, inflammatory, or rheumatic diseases aVect neck sensory input. In such
uncharted regions, various hypotheses thrive
for example, the hypothesis of cervical vertigo
after whiplash injury. Suggestions have included neuromuscular46 and neurovascular
mechanisms47 and mechanical obstruction of
the vertebral artery.48 Longet32 very early made
the incidential finding that post-traumatic vertigo and ataxia improve with the use of a neck

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collar.49 But head trauma and whiplash injury

aVect not only neck structures. Whiplash injuries often damage the brain,50 51 making the
interpretation of abnormal vestibulo-ocular
tests diYcult.52 53 The otoliths are highly
vulnerable to accelerations; damage to them
may cause otolith vertigo,54 characterised by a
benign course similar to that of neck pain. In
addition, dislodged otoconia often also enter
the lumen of the semicircular canals, resulting
in canal lithiasis and post-traumatic benign
paroxysmal positional vertigo (BPPV).55 It
must be borne in mind that canal lithiasis can
involve not only the posterior canal (classic
BPPV) but also the horizontal and anterior
canals, thus explaining atypical presentations
which would have been previously confused
with cervical vertigo or nystagmus.
A convincing mechanism of cervical vertigo
would have to be based on altered upper cervical somatosensory input associated with neck
tenderness and limitation of movement. Interstitial inflammatory mediators have been postulated to sensitise muscle spindles,56 and myofascial trigger points exhibit spontaneous EMG
activity, which is compatible with hyperactive
muscle spindles.57 If the firing characteristics
(symmetric or asymmetric) of the cervical
somatosensors change due to neck pain, a sensory mismatch between vestibular and cervical
inputs would be expected to result in cervical
vertigo. Particularly, this would occur during
active head movements, when expected and
actual reaVerent input would not match.
DiVerential diagnosis
DiVerential diagnosis of vertigo associated with
cervical symptoms or head-neck movement
avoidance is broad (table 1). If it is posttraumatic or follows cervical whiplash injuries,
then post-traumatic otolith vertigo,54 or benign
paroxysmal positioning vertigo,58 central vestibular dysfunction secondary to brainstem
concussion, vertebral artery dissection, and
perilymph fistulas should be considered.55 In
non-traumatic cases, psychogenic vertigo59 60
can have similar symptomatology but cerebellar or spinal ataxia, vestibular paroxysmia,61
and bilateral vestibulopathy62 63 should be considered first, before psychogenic or cervical
origin is assumed. Not uncommonly, cervical
pain is actually secondary to a genuine vestibular disorder, such as vestibular neuritis, and
probably develops as patients stiVen up their
neck muscles to avoid head movements. This
feature is well recognised by physiotherpapists
working with vestibular patients.64 Lesions of
the extracranial portion of the vertebral
arteries, as it travels the cervical column within
the transverse foramina (portion V2) and loops
from C2 into the foramen magnum (portion
V3), have to be considered in the diVerential
diagnosis. As this part of the vertebral artery is
relatively free from atherosclerosis, occlusions
due to neck movements/positions, neck manipulations, osteophyte compression, trauma,
and spontaneous dissection can occur.65
More widespread posterior circulation features
should be the norm but some cases with fairly
selective vestibular symptoms have been well

11

Cervical vertigo

documented.66 By contrast, there seems to be

no scientific basis for the syndrome of cervicalsympathetic irritation.36 It is likely that most
cases of this syndrome are pure vestibular disease, vertebral artery compression, vestibular
parxysmia, or basilar migraine.
In summary, vertigo can be accompanied by
cervical pain, associated with head injury,
whiplash injury, or cervical spine disease. In
some cases it can improve dramatically with
physiotherapy. None of these instances provides convincing evidence of a cervical mechanism, and alternative explanations are almost
always possible. All clinical studies on cervical
vertigo to date have three weak points: (1) the
inability to confirm the diagnosis, (2) the lack
of a specific laboratory test, and (3) the
unexplained discrepancy between patients with
severe neck pain without vertigo and patients
complaining of disabling vertigo with moderate
neck pain. If cervical vertigo exists, appropriate
management is the same as that for the cervical
pain syndrome, and this management should
not be denied any patient. As such therapy is
carried out in any case, the debate on the
relevance and mechanism of cervical vertigo is
more of theoretical interest than of practical
relevance.
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