European Archives of Oto-Rhino-Laryngology

https://doi.org/10.1007/s00405-018-5088-z

REVIEW ARTICLE

Approach to cervicogenic dizziness: a comprehensive review of its

aetiopathology and management
K. Devaraja1

Received: 29 June 2018 / Accepted: 6 August 2018

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Abstract
Purpose Though there is abundant literature on cervicogenic dizziness with at least half a dozen of review articles, the
condition remains to be enigmatic for clinicians dealing with the dizzy patients. However, most of these studies have studied
the cervicogenic dizziness in general without separating the constitute conditions. Since the aetiopathological mechanism
of dizziness varies between these cervicogenic causes, one cannot rely on the universal conclusions of these studies unless
the constitute conditions of cervicogenic dizziness are separated and contrasted against each other.
Methods This narrative review of recent literature revisits the pathophysiology and the management guidelines of various
conditions causing the cervicogenic dizziness, with an objective to formulate a practical algorithm that could be of clinical
utility. The structured discussion on each of the causes of the cervicogenic dizziness not only enhances the readers’ under-
standing of the topic in depth but also enables further research by identifying the potential areas of interest and the missing
links.
Results Certain peculiar features of each condition have been discussed with an emphasis on the recent experimental and
clinical studies. A simple aetiopathological classification and a sensible management algorithm have been proposed by the
author, to enable the identification of the most appropriate underlying cause for the cervicogenic dizziness in any given case.
However, further clinical studies are required to validate this algorithm.
Conclusions So far, no single clinical study, either epidemiological or interventional, has incorporated and isolated all the
constitute conditions of cervicogenic dizziness. There is a need for such studies in the future to validate either the reliability
of a clinical test or the efficacy of an intervention in cervicogenic dizziness.

Keywords Cervicogenic dizziness · Cervical vertigo · Bow hunter’s syndrome · Barre–Lieou syndrome · Whiplash-
associated disorder · Benign paroxysmal positional vertigo

Introduction of vestibular disorders, the terms ‘vertigo’ and ‘dizziness’

Broadly, the dizziness incorporates four descriptive symp-
toms: namely, ‘vertigo’, which is nothing but a false percep-
tion of movement of self or surrounding; ‘disequilibrium’
or ‘imbalance’ which is an inability to maintain balance;
‘presyncope’, a sense of losing consciousness; and ‘light-
headedness’, defined as a vague symptom of feeling dis-
connected from the environment [1, 2]. However, accord-
ing to the Barany society’s committee for the classification
* K. Devaraja
deardrdr@gmail.com
1
Department of Otorhinolaryngology, Kasturba Medical
College, Manipal Academy of Higher Education, Manipal,
Udupi, Karnataka 576104, India
are non-hierarchical and reflect distinctly separate sets of
symptoms [3]. They define ‘vertigo’ as the false sense of
self-motion without any motion or the feeling of distorted
self-motion with normal movement. Similarly, the dizziness
has been defined as a sense of disturbed or impaired spatial
orientation without a false or distorted sense of motion. They
have further sub-classified vertigo into internal and external,
for separating the vestibular sense of false motion from the
visual sense of false motion, respectively [3]. Nevertheless,
the patients with cervicogenic balance disorder rarely expe-
rience true vertigo; instead, they often complain of light-
headedness and disequilibrium which are included under
dizziness [4–7]. Dizziness is said to be cervicogenic when
it is closely associated with the neck pain, the neck injury,
or the neck pathology, after excluding the other causes of

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dizziness [4]. Though neurologists, neuro-otologists, physi-
cians, and orthopedicians commonly come across patients
with presumptive cervicogenic dizziness in clinics, not
many would stake the claim. The dearth in the awareness
about the constitute conditions contributes at least partly
to this. In addition, most of the existing literature discusses
the cervicogenic dizziness, in general, and provides guide-
lines accordingly. However, cervicogenic dizziness can be
caused by many conditions of separate pathophysiological
backgrounds. Failure to separate these conditions in clinical
practice as well as in research studies may have a negative
impact and hamper the further understanding of the disease.
Apart from discussing the peculiar features of each condi-
tion responsible for the cervicogenic dizziness, this narrative
review proposes a simple aetiopathological classification
and a sensible management algorithm, to enable the appro-
priate diagnosis and management in any suspected case of
cervicogenic dizziness.
Cervical contribution to the balance
and to the dizziness
The sense of balance and orientation of a human being is
dependent on the optimal functioning of multisensory per-
ception and the integration in the nervous system. Visual
and auditory cues sensing the spatial relationship with the
external environment, vestibular organs detecting the inter-
nal signals of motion, and muscles and joints involved in
the proprioception are the three chief sensory preceptors of
one’s sense of orientation [8]. Integration of symmetrical
inputs from these afferent systems is essential for the normal
orientation and the balance, and any dysfunction in these
sensory organs or asymmetry in the afferent inputs would
result in sense of imbalance or dizziness [9, 10]. Further
discussion of these neural networks seems to be inappro-
priate for this clinical narrative of cervicogenic dizziness.
Nevertheless, the proprioceptive signals of neck muscles and
cervical joints play an enormous role in maintaining and
Fig. 1  Proposed classification
of cervicogenic dizziness based
on the predominant aetiopatho-
logical mechanism involved in
dizziness
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European Archives of Oto-Rhino-Laryngology
fine-tuning the person`s orientation at rest and the balance
while motion [11–13], and the alteration in these propriocep-
tive signals seems to be responsible for the majority of cases
of the so-called ‘cervicogenic dizziness’ [14, 15]. The dis-
eased cervical joints are shown to have a significantly higher
concentration of Ruffini corpuscles [16], which, otherwise,
are abundantly found in knee joints [17], and are known to
play a major role in proprioception [18]. Some authors use
the term ‘cervical proprioceptive vertigo’ to describe this
dizziness caused by disharmonic hyperactivity of cervical
mechanoreceptors located in joints, ligaments, and muscle
spindles [9].
Classification of cervicogenic dizziness
After reviewing the literature thoroughly, the author has
classified the cervicogenic dizziness, as shown in Fig. 1,
based on the predominant aetiopathology responsible for it.
It has to be noted, though, that the aetiopathology of some
of these conditions could be overlapping, and also, some of
the conditions can cause dizziness by several independent
mechanisms. Nevertheless, in any given case of cervicogenic
dizziness, identifying the appropriate underlying cause is
relevant both clinically as well for interpreting the results
of the intervention trials. At least differentiating the vas-
cular causes from the neural causes seems sensible as the
management principles of these conditions also vary. The
aetiopathology of these conditions has been narrated below
in the corresponding sections along with their management.
Degenerative cervical spine disorders
Presumptively, the degenerative cervical spine disorder
(DCD), also known as the cervical spondylosis (CS), consti-
tutes the most common cause of cervicogenic dizziness [19,
20]. In 1952, the term ‘cervicogenic vertigo’ was introduced
by Ryan and Cope, who attributed it to the abnormal signals
European Archives of Oto-Rhino-Laryngology
from the degenerated upper cervical joints to the vestibular
nucleus [21]. However, the term ‘cervicogenic dizziness’ is
preferred over the ‘cervicogenic vertigo’ owing to the non-
specific dizziness or feeling of lightheadedness complained
by DCD patients rather than true vertigo [19]. Growing evi-
dence from the experimental and the human studies support
the role of the cervical joints in the maintenance of posture,
and also their contribution to the cervicogenic dizziness
in a diseased state [16, 22–24]. DCD is commonly seen in
older patients [25]. The non-specific dizziness seen in these
patients would be mostly episodic, lasting from minutes to
hours [4, 19]. In some of the DCD patients, the onset of
dizziness can have a temporal relationship to the turning of
the neck [26–29]. Neck stiffness, shoulder pain, headache,
radiculopathy, or myelopathy are the other features of DCD,
which may also be seen in these patients.
Cervical degenerative index (CDI) score is a physician-
rated scale used to quantify the radiological changes seen
in DCD and has good inter-observer and intra-observer
reliability [30, 31]. Disc space narrowing, sclerosis, osteo-
phytes, and olisthesis are the four factors considered in CDI,
each one graded from zero to three depending on the sever-
ity [31]. However, as far as the cervicogenic dizziness is
concerned, correlation with these grades has not been uni-
formly predictable [32, 33]. In fact, there are no structured
clinical studies which have directly evaluated the relation-
ship between severity of CDI scores and the presence or
the absence cervicogenic dizziness. There are studies which
have correlated the severities of cervical spine degeneration
in dizzy patients with the arterial blood flow in their verte-
brobasilar system [32–36]. They have reported a significant
reduction in the vertebral artery flow velocities on turning
the neck in DCD patients with the dizziness, compared to
those DCD patients without the dizziness and to the normal
controls. Many of the authors have attributed the dizziness
seen in these patients of DCD to the dynamic vertebrobasilar
insufficiency [26–29]. In other words, at least in a subset of
dizzy patients with DCD, the cause of dizziness on turning
the neck could be due to the reduced vertebral blood flow.
This dynamic compression of the vertebral artery and its
mechanism of causation of dizziness have been discussed in
detail in the subsequent sections. Interestingly, apart from
the abnormal proprioceptive signals from diseased joints and
the reduction in vertebrobasilar flow, the DCD can cause
dizziness by a third mechanism involving the stimulation of
sympathetic system.
Barre–Lieou syndrome
In 1926, Barre and Lieou proposed the neurovascular
hypothesis for the cervicogenic dizziness, in which they
attributed the vertigo and related symptoms to the transient
intracerebral ischemia, secondary to sympathetic fibers’
compression by the diseased cervical joints [37]. However,
subsequent experimental studies by Heisted and his col-
leagues showed that the sympathetic stimulation had little
or no effect on cerebral blood flow [38–41]. Many others
also have questioned and criticized the existence of BLS
[42, 43]. However, the results of some of the recent studies
provide certain corroborative pieces of evidence substantiat-
ing the involvement of sympathetic nervous system in the
aetiopathology of cervicogenic dizziness. Separate studies
have reported the association of sympathetic symptoms like
vertigo in DCD patients and the relief of these symptoms
by the surgical treatment of DCD [44–49]. Both animal and
clinical studies have demonstrated that the degenerated cer-
vical vertebral joints can lead to vertigo via the stimulation
of sympathetic fibers in the adjacent posterior longitudinal
ligament [44, 50]. Researchers have confirmed the distribu-
tion of sympathetic fibers in the human posterior longitudi-
nal ligament [46]. Others have identified bidirectional neural
networks between the cervical spinal and the sympathetic
ganglia re-iterating the possible neuroanatomical hypothesis
for this condition [51]. By the critical review of all these
studies, it seems improbable at this stage to subvert the role
of the sympathetic nervous system in the pathophysiology of
cervicogenic dizziness. Clinically, it is hard to differentiate
the BLS from the dizziness due to proprioceptive defects
of the DCD, and there is no specific diagnostic investiga-
tion available either. However, the association of degenera-
tive changes in cervical spine radiograph with sympathetic
symptoms and the relief of these symptoms upon the treat-
ment of degenerated joints should suggest the diagnosis of
BLS.
Having multiple mechanisms by which it can cause the
dizziness, it is understandable that the DCD is responsible
for the majority of cases of cervicogenic dizziness, and the
management of DCD goes a long way in controlling these
symptoms. Muscle relaxants are effective in reducing the
neck pain and neck stiffness seen in DCD [52]; however, the
effect of these agents on the cervicogenic dizziness is not yet
evident. Though a recent retrospective study claims muscle
relaxants to be effective in the cervicogenic dizziness [7],
there is not enough evidence to support their use to control
the dizziness in DCD patients. Similarly, studies evaluat-
ing the utility of non-steroidal anti-inflammatory drugs in
DCD patients for control of dizziness are non-existent at
present. Finally, considering the recent studies’ affirmation
of the sympathetic system involvement in DCD, it would
not be whimsical to study the role of sympatholytic agents
in controlling the dizziness in these patients. On the other
hand, many studies have separately evaluated the role of
cervical traction and exercise or physiotherapy in control
of the cervicogenic dizziness due to DCD, and have found
them to be effective [53]. Combination of manual therapy
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and physiotherapy is shown to be better than physiotherapy
alone in this regard [54]. Manual therapy involves the use
of therapist’s hands to perform the physiotherapy, whereas
physical therapy is nothing but providing passive assistance
to the patient to enable him or her to exercise. Chiropractic
therapy is a unique form of manual therapy, popularized by
Palmer and Palmer [55]. The primary mode of chiroprac-
tic therapy is spinal manipulation, and the cervical spinal
manipulation has been shown to be effective in controlling
the cervicogenic dizziness [56]. However, this therapy is
surrounded by some controversy and is not entirely safe [57].
Acute compression of the vertebral artery [58], dissection
of the vertebral artery [59, 60], and bilateral diaphragmatic
palsy [61] are some of the reported complications with the
chiropractic therapy. Though the cervical manipulation is
depicted to be safe in healthy young adults [62], it is prefer-
ably to be avoided in elderly patients.
A recent study showed that the surgically treated patients
of DCD do much better than conservatively managed
patients in terms of both the intensities as well as the fre-
quency of cervicogenic dizziness [22]. In another study, total
disc replacement significantly reduced the severity of diz-
ziness and other sympathetic features in DCD [23]. Though
both the studies aimed to evaluate the relief of dizziness in
DCD patients, the surgery was done for radiculopathy and
myelopathy in these studies and not for the dizziness control.
In other words, the results of these studies may not imply
active surgical intervention for the control of dizziness; nev-
ertheless, the surgical intervention may be an optimal thera-
peutic option when the cervicogenic dizziness is associated
with radiculopathy and/or myelopathy. Many other authors
have also reported improved dizziness and other sympathetic
symptoms by surgical treatment of degenerated cervical
joints or discs [45, 46, 48, 49].
Whiplash‑associated disorders
Whiplash injury refers to acceleration–deceleration injury to
the neck resulting commonly from motor vehicle collisions,
but could be due to other modes of trauma also. Mechanism
of injury involves a sudden movement of the head over the
neck or the head and neck over the trunk. This mode of
injury may cause a significant damage to the structures in
the neck, giving rise to a multitude of signs and symptoms
grouped under whiplash-associated disorders (WAD) [63].
The Quebec Task Force classified the WAD into four catego-
ries and redefined its management in 1995 [64]. However,
since this classification does not concern the dizziness seen
in WAD patients, further discussion on it may deviate the
manuscript from its objective. The dizziness-vertigo-imbal-
ance forms one of the significant symptom complexes in the
chronic WAD, other predominate manifestations being the
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neck pain–headache complex, and the paresthesia–sensory
disturbances complex [4, 63, 65, 66].
Dizziness or vertigo in WAD patients could be due to
three causes, the labyrinthine concussion and the benign
paroxysmal positional vertigo (BPPV) and the cervicogenic
cause [67, 68]. The labyrinthine concussion is rare in dizzy
patients of an isolated WAD, but it is common when WAD
is associated with head trauma [68, 69]. On the other hand,
BPPV could be the cause of vertigo in almost one-third of
the WAD patients [70]. The clinicopathological character-
istics of the BPPV in these patients are similar to that of
the idiopathic BPPV, except that the multiple reposition-
ing maneuvers may be required in these WAD associated
cases [70, 71]. By and large, the dizziness in most of the
symptomatic WAD patients is due to the cervicogenic cause
[68]. Nevertheless, in any patient of WAD having dizziness,
it is worth performing a positional test before attributing
it to the cervicogenic cause. The exact aetiopathology of
cervicogenic cause for dizziness in WAD is not fully under-
stood. The abnormal cervical afferent inputs due to mecha-
noreceptor dysfunction, mismatching with the normal ves-
tibular information has been proposed as the most probable
cause for cervical dizziness in WAD patients [15, 72–74]. In
another hypothesis, the hypertonicity of cervical and lum-
bar erector muscles following whiplash injury is thought to
affect the balance perception of the central nervous system
leading to disequilibrium [75].
The clinical characteristics of ‘cervicogenic dizziness’
in WAD patients are similar to the dizziness in DCD and
include episodic lightheadedness or imbalance lasting min-
utes to hours [76]. The affected patients would have signifi-
cantly reduced neck mobility and postural instability com-
pared to the age- and sex-matched normal controls [77, 78].
The postural abnormalities in dizzy patients with WAD can
be of diagnostic significance and could help in separating
cervicogenic dizziness in WAD from malingering [78, 79]
and vestibular causes [80]. One of the clinical signs of the
abnormal cervical proprioception is the ‘cervical nystagmus’
or the ‘neck torsion nystagmus’, which is nothing but the
nystagmus that arises from a neck rotation without labyrin-
thine stimulation [81]. This nystagmus is most appreciated in
patients with bilateral vestibular loss [82]. To attribute this
nystagmus to abnormal cervical signals, one has to examine
it using nystagmography in a dark room while rotating the
trunk in relation to stationary head, rather than the neck rota-
tion over trunk [82]. Though it is observed in some cases of
WAD [83], its pathophysiological mechanism and clinical
relevance have been questionable [63, 81, 82]. Some authors
have also reported spontaneous nystagmus in 30–60% of the
WAD patients with cervicogenic dizziness [83].
Measuring the postural deficit is one of the ways to
confirm cervicogenic cause for dizziness in WAD. In pos-
turography, a computerized stable force platform measures
European Archives of Oto-Rhino-Laryngology
the postural sway and the changes in standing balance,
under the altered visual and support conditions [74]. Pos-
turography has demonstrated significant deficiencies in
the postural responses among the WAD patients having
dizziness compared to the WAD patients not having dizzi-
ness and the healthy controls [73, 74]. Since the results of
posturography are not influenced by age, medication, ves-
tibular compensation status, or anxiety levels at the time of
testing [74], it can be used to differentiate the malingering
patients complaining of vertigo after injury with the mali-
cious intent of claiming compensation [78, 79]. It can also
be used as a quantitative assessment tool for grading the
imbalance in WAD patients with cervicogenic dizziness
[69, 77].
Joint position error (JPE) or head repositioning error
(HRE) is another measure to detect the abnormalities in
cervical proprioception. In this test, the blindfolded patients
are asked to perform neck movement within the comfort-
able range and to return to starting position as accurately as
possible [15]. Simple computer-based algorithms have been
found useful and can be of clinical utility [84]. If repeatedly
performed (at least six times), the results can be reliable
[85]. WAD group would have larger JPE compared to the
healthy controls during flexion–extension and reposition-
ing tasks [86, 87]. Among WAD patients, those with dizzi-
ness are shown to have significantly greater JPE than those
without [15]. Interestingly, the amount of JPE seems to be
correlating with the severity of WAD [87]. The vestibular
function influences the JPE results more often [88] than
not [89]. Moreover, the results of JPE are dependent on the
behavior of the subject undergoing the test [86, 88] and have
to be interpreted accordingly.
The smooth pursuit neck torsion (SPNT) test has a sensi-
tivity of 90% and specificity of 91% in WAD patients having
the cervicogenic dizziness [72]. In this test, the patients are
asked to follow the moving object/light as closely as possible
by keeping the head still. These smooth pursuit eye move-
ments are checked in the neutral position, in 45° head turned
to the right, and then in head turned to the left [72, 88]. In
patients of WAD with cervicogenic dizziness, the smooth
pursuit gain has been shown to reduce significantly in the
torsion positions compared to that in the neutral position.
Such differences in smooth pursuit gains were observed nei-
ther in normal subjects nor in patients with central or periph-
eral vestibular pathologies [72]. Though many authors have
been able to reproduce the similar SPNT test results [90],
some have reported the statistically insignificant differences
[91–93], and this is probably because of the methodologi-
cal differences between these studies [94]. In addition, the
results of SPNT test may get influenced by age, presence or
absence of neck pain, sedation, and examination conditions
like the predictability of the moving target [95, 96] making
this a less reliable test in isolation.
In fact, a combination of JPE, posturography, and SPNT
test can better predict the possibility of cervicogenic diz-
ziness in WAD [97]. More than 2/3 of WAD patients hav-
ing cervicogenic dizziness would have an abnormality in
two out of three and more than 1/3 would yield abnormal
results in all three tests. Abnormal cervical JPE score has a
high positive predictive value (88%) for predicting abnormal
scores in one or both of the other postural control tests in
WAD; however, as an isolated test, it has a low sensitivity
(60%) and specificity (54%) to determine the abnormality
in balance [97]. The JPE is one of the manifestations of the
cervical motor system dysfunction seen in WAD patients.
Two other signs of the cervical motor system dysfunction
include the restricted neck movement and the increased
activity of superficial neck flexors, which can be investigated
respectively, by ‘cervico-ocular-reflex (COR) gain measures’
and ‘craniocervical flexion test (CCFT)’ [87, 98]. During
the rotation of the trunk with a stationary head in the dark,
the COR measured by an electronystagmography shows an
increased gain in WAD patients [99, 100]. Similar to ‘the
cervical nystagmus’ described previously, this increased
COR gain can be attributed to WAD-related cervicogenic
dizziness only after negating the influence of the vestibu-
lar system. Furthermore, clinicians have to keep in mind
that both ‘the cervical nystagmus’ and ‘the increased COR
gain’ are apparent signs in bilateral vestibular hypofunction.
Accordingly, these signs are of limited value for diagnosing
the cervical contribution to dizziness in patients who are
also having vestibular deficits. In fact, the workup for diag-
nosing the cervicogenic dizziness is to be considered only
after excluding the vestibular as well as the central causes.
In addition, in the course of the diagnostic workup for cer-
vicogenic cases, nystagmography has to be done in a dark
room, by making the patient turn his/her trunk against the
stationary head to prevent the stimulation of intact vestibu-
lar system. Nevertheless, the COR gain also has a potential
to be an objective test to diagnose WAD [100]. In CCFT,
the patient is asked to progressively increase the craniocer-
vical flexion range, while the contraction of longus coli is
monitored by electromyography, and in patients with WAD,
instead of the deep flexors like longus coli, the superficial
flexors like sternocleidomastoid and trapezius are stimulated
[87, 98]. However, this test is not specific for WAD [101].
The cervicogenic dizziness in WAD patients can be effec-
tively treated by cervical physiotherapy [69, 102]. Reviews
have also found enough evidence to support the manual
therapy in patients with cervicogenic dizziness [103, 104].
However, the studies included have not categorized the exact
cause for cervicogenic dizziness and seem to contain the
mixed cohort of DCD as well as WAD; accordingly, the
usefulness of manual therapy in specific patients of WAD
is still not apparent. Nevertheless, since the physiotherapy
is the preferred treatment modality in WAD and the manual
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therapy is a form of physiotherapy, its role in controlling the
cervicogenic dizziness in WAD patients cannot be ruled out.
The recent review by Lystad et al. did not find supportive
evidence to combine the vestibular rehabilitation with the
manual therapy. However, they have highlighted enough
rationale to back the vestibular rehabilitation in cervico-
genic dizziness [103]. Patient education is another effective
treatment modality in WAD [105]. The patient education
integrated into exercise programs, and behavioral programs
not only reduce the pain and the dizziness but also enhance
the recovery and the mobility in chronic WAD patients [106,
107]. One session of patient education and subsequent tel-
ephonic support is shown to be as effective as 20 sessions
of comprehensive physiotherapy exercise programs [108].
However, this study does not imply to discontinue the exer-
cise therapy in the chronic WAD, but it reinforces the physi-
otherapists on the importance of patient education in reha-
bilitating such patients [109]. There are very few trials on
pharmacotherapy in the chronic WAD, and thus, no specific
recommendations exist for drug therapy [110]. The role of
muscle relaxants and NSAIDs in controlling cervicogenic
dizziness due to WAD is yet another potential research ques-
tion for further studies. Similarly, the utility of surgical pro-
cedures in WAD patients is also not apparent, owing to the
contradictory evidence in the literature [111]. Among many
invasive procedures tried in WAD, the existing evidence sup-
ports only the radiofrequency neurotomy in chronic WAD
patients, who are not responding to the conventional therapy
[111].
Bow hunter’s syndrome
Sorenson in 1978 named the condition of ‘symptomatic
vertebral artery insult with dynamic neck posture’ as ‘Bow
hunter’s stroke’ [112], which then became popular as bow
hunter’s syndrome (BHS) due to the multitude of possible
symptoms in the affected individuals. Sorenson description
was related to the mechanical occlusion of vertebral artery
at the level of the atlantoaxial joint during neck turning.
Though C1–C2 is the most common site of symptomatic
compression, followed by C4–C5 [113–115], the vertebral
artery narrowing anywhere in the neck can also produce
the classical symptoms of BHS [27, 116–119]. BHS is
commonly diagnosed in older patients, in their VI or VII
decades [115], but can also be seen in young individuals
[119–123]. Men are more commonly affected than women
[115]. Vertigo is one of the predominant symptoms in BHS,
but the clinical manifestations may vary from syncope to
posterior circulation stroke [27, 113, 124–128]. Commonly
seen accompanying symptoms include tinnitus, headache,
vision loss, ataxia, double vision, tinnitus, and/or head-
ache [27, 113, 129, 130]. Typically, the affected individuals
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European Archives of Oto-Rhino-Laryngology
present with vertigo and other symptoms on turning the neck
anywhere between 45° and 90° [122, 131–133], and these
symptoms disappear on bringing the head back to the neutral
position.
Vertigo in BHS is most often due to dynamic compres-
sion of the dominant vertebral artery, and since the left ver-
tebral artery is dominant in most individuals, it is respon-
sible for BHS in the majority [113, 114, 121, 129]. Rarely
compression of the non-dominant vertebral artery can also
lead to BHS symptoms [29, 120, 131, 134, 135]. Pre-existing
narrowing in the contralateral vertebral artery may predis-
pose to vertigo when the normal ipsilateral vertebral artery
gets compressed by neck turn. The direction of neck turn
producing the symptoms in BHS can reasonably suggest the
side and site of the vertebral artery compression. Vertigo on
turning the neck to one side may either be due to the ipsilat-
eral vertebral artery compression at or below C4 [117–119]
or due to the contralateral vertebral artery compression at
or above C3 [114]. Sometimes, turning on to either side can
produce symptoms, which is seen in the bilateral vertebral
artery compression or stenosis [27, 119, 136]. The sympto-
mology in BHS is attributed to reduced vertebral artery flow
resulting in transient hypoperfusion of the ipsilateral laby-
rinth or the lateral medulla or the inferior cerebellum [135]
and resultant neural excitation [130, 137, 138]. The transient
ischemia in these organs can also give rise to typical nystag-
mus which may accompany the vertigo in some of the BHS
patients [29, 130, 131, 135]. The nystagmus is a mixed type,
with horizontal and torsional down beating components, and
the direction of nystagmus is generally towards the side of
the compressed vertebral artery [139]. This nystagmus may
also have latency, and it may change the direction on bring-
ing the head back to neutral [29]. As discussed in the earlier
paragraphs, many patients of BHS are predisposed by the
degenerative joints of the cervical spine. Other predispos-
ing conditions for BHS include malformed vertebrae [116],
bony stenosis of vertebral canal [128], accessory osseous
canal in the transverse process [119], hypertrophied neck
musculature [122], and trauma [140].
The transcranial Doppler (TCD) or the cervical arterial
duplex ultrasonography (CDU) is used to demonstrate the
reduction in posterior circulation velocity on turning the
patient’s head, corresponding to his or her symptoms [141,
142]. Even the pulsed-wave Doppler of the cervical region
could also be sufficient for screening the patients with cervi-
cogenic dizziness [143]. However, as the most common site
of vertebral artery compression in BHS is above the level
of C3 vertebra, the reduced flow distal to this obstruction is
unlikely to be picked up by the cervical Doppler. Neverthe-
less, neither of these investigations can precisely account for
the site and the extent of vertebral artery compression. These
can be achieved through dynamic digital subtraction angio-
gram (d-DSA), which is the current investigation of choice
European Archives of Oto-Rhino-Laryngology
for diagnosing BHS [144]. In all these tests, care should be
taken to avoid the sustained end-of-range rotation and quick-
thrust rotational manipulations [145]. The three dimension
computed tomography integrated with angiography would
provide the detailed bony as well as soft-tissue anatomy in
topographic relation to the course of the vertebral artery
[128]. It can also delineate the precise cause for dynamic
compression like a fibrous band, osteophyte, or narrowing of
the bony canal, and thus may assist in the surgical planning.
BHS can be best treated by surgical intervention and the
two most effective surgical procedures are vertebral artery
decompression [113, 114, 119, 124, 125, 128, 140, 141] and
fusion of the vertebrae [123, 126, 127, 131, 133]. Though
both the approaches have shown to be effective, the isolated
fusion of the vertebrae is useful primarily in the vertebral
instabilities, and these patients may eventually lose up to
50°–70° of rotational movement postoperatively [121].
Accordingly, vascular decompression is the most preferred
treatment [115], and it can be done by anterior approach or
posterior approach [113]. Considering the ease of accessing
the vertebral artery, for lesions at or below C4, the ante-
rior approach is preferred, and the posterior approach is for
lesions at or above C3 [113, 114]. The posterior approach
seems to have relatively higher morbidity, which can be
minimized by a novel minimally invasive approach [113].
Though some authors have reported nearly 33% re-occlu-
sion rate after successful vascular decompression [121], this
unfavorable outcome is attributed to possibly missed ante-
rior fibrous bands during posterior approach decompression
[128]. Nevertheless, surgical intervention needs to be indi-
vidualized to each patient depending on the site of the occlu-
sion, the extent of the occlusion, and the exact cause of the
occlusion. Often, the combination of vascular decompres-
sion and intervertebral fusion would be required to achieve
the desired clinical outcomes [27, 29, 116–118, 128, 136,
141]. At times, fusion may be required in the later stage
to correct the instability caused by prior decompression
[114]. Similar success rates have been reported with iso-
lated decompression and decompression with fusion [146].
Irrespective of the approach and type of surgery, it is impera-
tive to have a sound anatomical understanding and to exer-
cise extreme caution intraoperatively to prevent the surgical
morbidity. Any of the dynamic vascular studies like TCD,
CDU, or d-DSA can be used for intraoperative assistance
in decompression surgeries, and these studies can also be
handy for the post-operative follow-up [128, 140, 141, 146,
147]. Some surgeons have tried endovascular treatments like
stenting [120, 148] with or without angioplasty [132] of the
stenosed segment, but the practical value of such approaches
in the long term is not yet proven. Conservative management
has also been reported to be useful in BHS, especially when
there is no identifiable structural abnormality compressing
the vertebral artery [137]. Avoiding the head rotation, use
of the cervical collar and use of anticoagulants are some
of the conservative maneuvers to have produced favorable
outcomes [112, 122, 149].
Other rare causes
Beauty parlor stroke syndrome
Beauty parlor stroke syndrome (BPSS) was first reported
by Weintraub in 1993 [150]. This condition is similar to the
BHS in many of the aetiopathology as well as the clinical
aspects, but probably gets this name due to its occurrence
in beauty parlors. However, unlike BHS, the vertebrobasilar
insufficiency in BPSS is not always due to the external com-
pression of the arteries and could also be due to dissection of
the vertebral artery or some systemic conditions [151]. The
onset of symptoms in BPSS is associated with the extension
of the neck and is related to the external compression of the
posterior neck due to hanging the head behind the head-
rest while hairdressing or hair massage [152]. The patients
may manifest with varied symptoms ranging from vertigo
to evolved stroke [151–153]. Age more than 50 years [154],
female sex [151] and hyperextension of the neck [153, 154]
are some of the risk factors associated with this syndrome.
Color Doppler or angiogram may reveal the vascular pathol-
ogy, and magnetic resonance imaging may show the area of
ischemia in the brain. The treatment varies from case to case
depending on the nature of vascular compromise and the
volume of stroke. Restriction of neck movements and anti-
platelet medications form the basis for the treatment of BPS
along with the other supportive measures [153]. Surgical
correction of external compression or vertebral arterial wall
defect may help in relieving the symptoms in the affected
patients [152].
Cervical myofascial pain syndrome
Cervical myofascial pain syndrome (CMPS) includes a
group of disorders of cervical skeletal muscle characterized
by the presence of trigger points. Dizziness is seen in 35% of
the CMPS patients [155], and it correlates with the symptom
of pain [156]. It is commonly seen in young individuals, in
fourth decade of life, and females are affected more often
[155]. Trapezius muscle would have trigger points in half
of the affected patients [155]. There may be associated fea-
tures like skin flushing, lacrimation, and other autonomic
symptoms. CMPS is commonly associated with cervical
trauma, fibromyalgia, and joint hypermobility syndrome
[155]. Apart from the typical clinical features, the needle
electromyography findings can help in diagnosing this con-
dition. The affected muscles fatigue faster than the rest, and
this active focus is depicted as spontaneous endplate activity
13

in electromyography [157]. Exercise therapy is the treatment
for cervicogenic dizziness and other complaints in CMPS
patients [158]. Along with stretching and strengthening reha-
bilitation programs, the trigger point injections are also use-
ful in treating the cervicogenic dizziness caused by CMPS
[156, 157]. The combination of manual therapy with needle
therapy [159] and added vestibular rehabilitation [160] is
shown to provide the maximum benefit and even complete
regression of dizziness in these patients.
Approach to cervicogenic dizziness
By the above discussion, it is clear that some of the con-
ditions causing cervicogenic dizziness have overlapping
aetiopathology, and in addition, they can cause dizziness by
several separate mechanisms. Both the DCD and WAD can
cause cervicogenic dizziness by affecting the propriocep-
tive signals, from joints and muscle spindles, respectively.
However, the DCD can lead to dizziness also by the vas-
cular compression or by the sympathetic stimulation, and
on the other hand, in many of the patients with WAD, the
dizziness can be attributed to benign paroxysmal positional
Fig. 2  Approach to suspected case of cervicogenic dizziness. BPPV
Benign paroxysmal positional vertigo, BHS bow hunter’s syndrome,
DCD degenerative cervical spine disorder, BLS Barre–Lieou syn-
13
European Archives of Oto-Rhino-Laryngology
vertigo. Separating these clinical conditions, and identify-
ing the exact cause for cervicogenic dizziness in a given
case is essential clinically and is relevant for research stud-
ies. However, due to the overlapping symptomology and the
lack of specific diagnostic investigations [161], many of the
high-quality studies and the reviews have not separated these
conditions [103, 104, 107]. One cannot rely on the univer-
sal conclusions of these studies unless the constitute condi-
tions of cervicogenic dizziness are separated and contrasted
against each other. So far, no single clinical study, either epi-
demiological or interventional, has incorporated and isolated
all these conditions in its methodology. There is a need for
such studies in the future to validate either the reliability of a
clinical test or the efficacy of an intervention in cervicogenic
dizziness. After a thorough review exercise, an algorithm
has been formulated, as shown in Fig. 2, on how to approach
a patient with suspected cervicogenic dizziness. The objec-
tive of this flowchart is to help the clinicians and therapists
to identify the most appropriate, if not the actual, underlying
cause for the cervicogenic dizziness in any given case. By
this approach, each of the above-discussed causes for cervi-
cogenic dizziness can be ruled in or out in a systematic man-
ner. Nevertheless, one can proceed with the given algorithm
drome, WAD Whiplash-associated disorder, Hash: positional test
is better to be performed after ruling out cervical spine diseases in
patients above 40 years [162, 163]
European Archives of Oto-Rhino-Laryngology
only after the vestibular, neural, and systemic causes for the
dizziness are excluded beyond the reasonable doubt. The
algorithm is incorporated with the elements from the his-
tory, the examination, and the investigations, in a particular
pattern to maximize the clinical utility and to minimize the
morbidity as well as the wastage of resources.
Vantage and limitations of the study
In this narrative review, the various conditions causing
cervicogenic dizziness have been discussed systematically,
incorporating and segregating the existing literature as per
the different categories. The classification of cervicogenic
dizziness described is simple yet practical. The algorithm
provided here for evaluating the suspected cases of cervico-
genic dizziness seems appropriate and sensible. Neverthe-
less, since the algorithm is based on the extrapolation of
facts from the literature, it needs further validation by clini-
cal studies. Moreover, in some patients, dizziness could be
due to a combination of cervicogenic cause and vestibular
or neural deficits, the scenario which has been not addressed
in the given algorithm.
Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.
Research involving human participants and/or animals Not applicable.
Informed consent Not applicable.
References
1. Lee AT (2012) Diagnosing the cause of vertigo: a practical
approach. Hong Kong Med J 18:327–332
2. Post RE, Dickerson LM (2010) Dizziness: a diagnostic approach.
Am Fam Physician 82:361–369
3. Bisdorff A, Von Brevern M, Lempert T, Newman-Toker DE
(2009) Classification of vestibular symptoms: towards an interna-
tional classification of vestibular disorders. J Vestib Res Equilib
Orientat 19:1–13
4. Wrisley DM, Sparto PJ, Whitney SL, Furman JM (2000) Cervi-
cogenic dizziness: a review of diagnosis and treatment. J Orthop
Sports Phys Ther 30:755–766
5. Yacovino DA, Hain TC (2013) Clinical characteristics of cervi-
cogenic-related dizziness and vertigo. Semin Neurol 33:244–255
6. Jung FC, Mathew S, Littmann AE, MacDonald CW (2017)
Clinical decision making in the management of patients with
cervicogenic dizziness: a case series. J Orthop Sports Phys Ther
47:874–884
7. Takahashi S (2018) Importance of cervicogenic general dizzi-
ness. J Rural Med JRM 13:48–56
8. St George RJ, Fitzpatrick RC (2011) The sense of self-motion,
orientation and balance explored by vestibular stimulation. J
Physiol 589:807–813
9. Grgić V (2006) Cervicogenic proprioceptive vertigo: etiopatho-
genesis, clinical manifestations, diagnosis and therapy with spe-
cial emphasis on manual therapy. Lijec Vjesn 128:288–295
10. Karnath H-O, Reich E, Rorden C, Fetter M, Driver J (2002) The
perception of body orientation after neck-proprioceptive stimula-
tion. Exp Brain Res 143:350–358
11. Wyke B (1979) Cervical articular contribution to posture
and gait: their relation to senile disequilibrium. Age Ageing
8:251–258
12. Maravita A, Spence C, Driver J (2003) Multisensory integration
and the body schema: close to hand and within reach. Curr Biol
CB 13:R531–R539
13. Pettorossi VE, Schieppati M (2014) Neck proprioception shapes
body orientation and perception of motion. Front Hum Neurosci
8:895
14. Grande-Alonso M, Moral Saiz B, Mínguez Zuazo A, Lerma Lara
S, La Touche R (2018) Biobehavioural analysis of the vestibular
system and posture control in patients with cervicogenic dizzi-
ness. A cross-sectional study. Neurol Barc Spain 33:98–106
15. Treleaven J, Jull G, Sterling M (2003) Dizziness and unsteadiness
following whiplash injury: characteristic features and relation-
ship with cervical joint position error. J Rehabil Med 35:36–43
16. Yang L, Yang C, Pang X, Li D, Yang H, Zhang X et al (2017)
Mechanoreceptors in diseased cervical intervertebral disc and
vertigo. Spine 42:540–546
17. Hirasawa Y, Okajima S, Ohta M, Tokioka T (2000) Nerve dis-
tribution to the human knee joint: anatomical and immunohisto-
chemical study. Int Orthop 24:1–4
18. Abraira VE, Ginty DD (2013) The sensory neurons of touch.
Neuron 79:618–639
19. Yahia A, Ghroubi S, Jribi S, Mâlla J, Baklouti S, Ghorbel A et al
(2009) Chronic neck pain and vertigo: is a true balance disorder
present? Ann Phys Rehabil Med 52:556–567
20. Morinaka S (2009) Musculoskeletal diseases as a causal factor
of cervical vertigo. Auris Nasus Larynx 36:649–654
21. Ryan GM, Cope S (1955) Cervical vertigo. Lancet Lond Engl
269:1355–1358
22. Peng B, Yang L, Yang C, Pang X, Chen X, Wu Y (2018) The
effectiveness of anterior cervical decompression and fusion for
the relief of dizziness in patients with cervical spondylosis: a
multicentre prospective cohort study. Bone Jt J 100:81–87
23. Sun Y-Q, Zheng S, Yu J, Yan K, Tian W (2013) Effect of total
disc replacement on atypical symptoms associated with cervical
spondylosis. Eur Spine J 22:1553–1557
24. Ren L, Guo B, Zhang J, Han Z, Zhang T, Bai Q et al (2014)
Mid-term efficacy of percutaneous laser disc decompression
for treatment of cervical vertigo. Eur J Orthop Surg Traumatol
24:S153–S158
25. Garfin SR (2000) Cervical degenerative disorders: etiology, pres-
entation, and imaging studies. Instr Course Lect 49:335–338
26. Nishikawa H, Miya F, Kitano Y, Mori G, Shimizu S, Suzuki H
(2017) Positional occlusion of vertebral artery due to cervical
spondylosis as rare cause of wake-up stroke: report of two cases.
World Neurosurg 98:877.e13–877.e21
27. Fleming JB, Vora TK, Harrigan MR (2013) Rare case of bilateral
vertebral artery stenosis caused by C4–5 spondylotic changes
manifesting with bilateral bow hunter’s syndrome. World Neu-
rosurg 79:799.E1–799.E5
28. Piñol I, Ramirez M, Saló G, Ros AM, Blanch AL (2013) Sympto-
matic vertebral artery stenosis secondary to cervical spondylolis-
thesis. Spine 38:E1503–E1505
29. Iida Y, Murata H, Johkura K, Higashida T, Tanaka T, Tateishi K
(2018) Bow Hunter’s syndrome by nondominant vertebral artery
compression: a case report, literature review, and significance of
downbeat nystagmus as the diagnostic clue. World Neurosurg
111:367–372
13

30. Gore DR, Sepic SB, Gardner GM (1986) Roentgenographic
findings of the cervical spine in asymptomatic people. Spine
11:521–524
31. Ofiram E, Garvey TA, Schwender JD, Denis F, Perra JH, Trans-
feldt EE et al (2009) Cervical degenerative index: a new quan-
titative radiographic scoring system for cervical spondylosis
with interobserver and intraobserver reliability testing. J Orthop
Traumatol 10:21–26
32. Bayrak IK, Durmus D, Bayrak AO, Diren B, Canturk F, Canturk
F (2009) Effect of cervical spondylosis on vertebral arterial flow
and its association with vertigo. Clin Rheumatol 28:59–64
33. Machaly SA, Senna MK, Sadek AG (2011) Vertigo is associated
with advanced degenerative changes in patients with cervical
spondylosis. Clin Rheumatol 30:1527–1534
34. Cevik R, Bilici A, Nas K, Demircan Z, Tekin RC (2010) Non-
invasive evaluation of vertebral artery blood flow in cervical
spondylosis with and without vertigo and association with degen-
erative changes. Clin Rheumatol 29:541–546
35. Olszewski J, Majak J, Pietkiewicz P, Luszcz C, Repetowski M
(2006) The association between positional vertebral and basilar
artery flow lesion and prevalence of vertigo in patients with cer-
vical spondylosis. Otolaryngol Head Neck Surg 134:680–684
36. Strek P, Reroń E, Maga P, Modrzejewski M, Szybist N (1998) A
possible correlation between vertebral artery insufficiency and
degenerative changes in the cervical spine. Eur Arch Oto-Rhino-
Laryngol 255:437–440
37. Barre J (1926) On a posterior cervical sympathetic syndrome
and its frequent cause: cervical arthritis [in French]. Rev Neurol
(Paris) 45:1246–1248
38. Heistad DD, Marcus ML, Gross PM (1978) Effects of sympa-
thetic nerves on cerebral vessels in dog, cat, and monkey. Am J
Physiol 235:H544–H552
39. Heistad DD, Marcus ML (1978) Evidence that neural mecha-
nisms do not have important effects on cerebral blood flow. Circ
Res 42:295–302
40. Faraci FM, Heistad DD (1990) Regulation of large cerebral arter-
ies and cerebral microvascular pressure. Circ Res 66:8–17
41. Baumbach GL, Heistad DD, Siems JE (1989) Effect of sympa-
thetic nerves on composition and distensibility of cerebral arte-
rioles in rats. J Physiol 416:123–140
42. Pearce JMS (2004) Barré-Liéou “syndrome”. J Neurol Neurosurg
Psychiatry 75:319
43. Foster CA, Jabbour P (2007) Barré–Lieou syndrome and the
problem of the obsolete eponym. J Laryngol Otol 121:680–683
44. Li J, Gu T, Yang H, Liang L, Jiang D, Wang Z et al (2014)
Sympathetic nerve innervation in cervical posterior longitudinal
ligament as a potential causative factor in cervical spondylo-
sis with sympathetic symptoms and preliminary evidence. Med
Hypotheses 82:631–635
45. Hong L, Kawaguchi Y (2011) Anterior cervical discectomy and
fusion to treat cervical spondylosis with sympathetic symptoms.
J Spinal Disord Tech 24:11–14
46. Li H, Ma X, Wu X, Liu F, Yu T, Yue B et al (2014) Morpho-
logical observation of sympathetic nerve fibers in the human
posterior longitudinal ligament. Spine 39:2119–2126
47. Zhong Z, Hu J, Zhai J, Tian Y, Qiu G, Weng X et al (2015)
Therapeutic effect and mechanism of the surgical treatment for
cervical vertigo with cervical spondylosis. Zhonghua Yi Xue Za
Zhi 95:2014–2017
48. Muheremu A, Sun Y, Yan K, Yu J, Zheng S, Tian W (2016)
Effect of anterior cervical discectomy and fusion on patients with
atypical symptoms related to cervical spondylosis. J Neurol Surg
A Cent Eur Neurosurg 77:395–399
49. Li J, Jiang D-J, Wang X-W, Yuan W, Liang L, Wang Z-C (2016)
Mid-term outcomes of anterior cervical fusion for cervical spon-
dylosis with sympathetic symptoms. Clin Spine Surg 29:255–260
13
European Archives of Oto-Rhino-Laryngology
50. Wang Z, Wang X, Yuan W, Jiang D (2011) Degenerative patho-
logical irritations to cervical PLL may play a role in presenting
sympathetic symptoms. Med Hypotheses 77:921–923
51. Zuo J, Han J, Qiu S, Luan F, Zhu X, Gao H et al (2014) Neural
reflex pathway between cervical spinal and sympathetic ganglia
in rabbits: implication for pathogenesis of cervical vertigo. Spine
J 14:1005–1009
52. Bose K (1999) The efficacy and safety of eperisone in patients
with cervical spondylosis: results of a randomized, double-blind,
placebo-controlled trial. Methods Find Exp Clin Pharmacol
21:209–213
53. Moustafa IM, Diab AA, Harrison DE (2017) The effect of nor-
malizing the sagittal cervical configuration on dizziness, neck
pain, and cervicocephalic kinesthetic sensibility: a 1-year rand-
omized controlled study. Eur J Phys Rehabil Med 53:57–71
54. Galm R, Rittmeister M, Schmitt E (1998) Vertigo in patients with
cervical spine dysfunction. Eur Spine J 7:55–58
55. Homola S (2006) Chiropractic: history and overview of theories
and methods. Clin Orthop 444:236–242
56. Ndetan H, Hawk C, Sekhon VK, Chiusano M (2016) The role
of chiropractic care in the treatment of dizziness or balance dis-
orders: analysis of national health interview survey data. J Evid
Based Complement Altern Med 21:138–142
57. Ernst E (2008) Chiropractic: a critical evaluation. J Pain Symp-
tom Manag 35:544–562
58. Young Y-H, Chen C-H (2003) Acute vertigo following cervical
manipulation. Laryngoscope 113:659–662
59. Frumkin LR, Baloh RW (1990) Wallenberg’s syndrome follow-
ing neck manipulation. Neurology 40:611–615
60. Albuquerque FC, Hu YC, Dashti SR, Abla AA, Clark JC, Alkire
B et al (2011) Craniocervical arterial dissections as sequelae of
chiropractic manipulation: patterns of injury and management.
J Neurosurg 115:1197–1205
61. John S, Tavee J (2015) Bilateral diaphragmatic paralysis due to
cervical chiropractic manipulation. Neurologist 9:65–67
62. Quesnele JJ, Triano JJ, Noseworthy MD, Wells GD (2014)
Changes in vertebral artery blood flow following various head
positions and cervical spine manipulation. J Manip Physiol Ther
37:22–31
63. Fischer AJ, Verhagen WI, Huygen PL (1997) Whiplash injury. A
clinical review with emphasis on neuro-otological aspects. Clin
Otolaryngol Allied Sci 22:192–201
64. Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J,
Suissa S et al (1995) Scientific monograph of the Quebec Task
Force on Whiplash-Associated Disorders: redefining “whiplash”
and its management. Spine 20:1S–73S
65. Evans RW (1992) Some observations on whiplash injuries. Neu-
rol Clin 10:975–997
66. Claussen CF, Claussen E (1995) Neurootological contributions
to the diagnostic follow-up after whiplash injuries. Acta Oto-
Laryngol Suppl 520:53–56
67. Ernst A, Basta D, Seidl RO, Todt I, Scherer H, Clarke A (2005)
Management of posttraumatic vertigo. Otolaryngol Head Neck
Surg 132:554–558
68. Vibert D, Häusler R (2003) Acute peripheral vestibular deficits
after whiplash injuries. Ann Otol Rhinol Laryngol 112:246–251
69. Nacci A, Ferrazzi M, Berrettini S, Panicucci E, Matteucci J,
Bruschini L et al (2011) Vestibular and stabilometric findings in
whiplash injury and minor head trauma. Acta Otorhinolaryngol
Ital 31:378–389
70. Dispenza F, De Stefano A, Mathur N, Croce A, Gallina S (2011)
Benign paroxysmal positional vertigo following whiplash injury:
a myth or a reality? Am J Otolaryngol 32:376–380
71. Gordon CR, Levite R, Joffe V, Gadoth N (2004) Is posttrau-
matic benign paroxysmal positional vertigo different from the
idiopathic form? Arch Neurol 61:1590–1593
European Archives of Oto-Rhino-Laryngology
72. Tjell C, Rosenhall U (1998) Smooth pursuit neck torsion test: a
specific test for cervical dizziness. Am J Otol 19:76–81
73. Yu L-J, Stokell R, Treleaven J (2011) The effect of neck torsion
on postural stability in subjects with persistent whiplash. Man
Ther 16:339–343
74. Treleaven J, Jull G, Lowchoy N (2005) Standing balance in per-
sistent whiplash: a comparison between subjects with and with-
out dizziness. J Rehabil Med 37:224–229
75. Hinoki M (1985) Vertigo due to whiplash injury: a neurotological
approach. Acta Oto-Laryngol Suppl 419:9–29
76. Treleaven J (2017) Dizziness, unsteadiness, visual disturbances,
and sensorimotor control in traumatic neck pain. J Orthop Sports
Phys Ther 47:492–502
77. Madeleine P, Prietzel H, Svarrer H, Arendt-Nielsen L (2004)
Quantitative posturography in altered sensory conditions: a way
to assess balance instability in patients with chronic whiplash
injury. Arch Phys Med Rehabil 85:432–438
78. Endo K, Suzuki H, Yamamoto K (2008) Consciously pos-
tural sway and cervical vertigo after whiplash injury. Spine
33:E539–E542
79. Vonk J, Horlings CGC, Allum JHJ (2010) Differentiating malin-
gering balance disorder patients from healthy controls, com-
pensated unilateral vestibular loss, and whiplash patients using
stance and gait posturography. Audiol Neurootol 15:261–272
80. Karlberg M, Johansson R, Magnusson M, Fransson PA (1996)
Dizziness of suspected cervical origin distinguished by posturo-
graphic assessment of human postural dynamics. J Vestib Res
Equilib Orientat 6:37–47
81. Norré ME (1987) Cervical vertigo. Diagnostic and semiological
problem with special emphasis upon “cervical nystagmus”. Acta
Otorhinolaryngol Belg 41:436–452
82. Brandt T, Bronstein AM (2001) Cervical vertigo. J Neurol Neu-
rosurg Psychiatry 71:8–12
83. Oosterveld WJ, Kortschot HW, Kingma GG, de Jong HA, Saatci
MR (1991) Electronystagmographic findings following cervical
whiplash injuries. Acta Otolaryngol (Stockh) 111:201–205
84. Basteris A, Pedler A, Sterling M (2016) Evaluating the neck joint
position sense error with a standard computer and a webcam.
Man Ther 26:231–234
85. de Vries J, Ischebeck BK, Voogt LP, van der Geest JN, Janssen
M, Frens MA et al (2015) Joint position sense error in people
with neck pain: a systematic review. Man Ther 20:736–744
86. Feipel V, Salvia P, Klein H, Rooze M (2006) Head repositioning
accuracy in patients with whiplash-associated disorders. Spine
31:E51–E58
87. Sterling M, Jull G, Vicenzino B, Kenardy J, Darnell R (2003)
Development of motor system dysfunction following whiplash
injury. Pain 103:65–73
88. Jansen GB, Edlund C, Grane P, Hildingsson C, Karlberg M, Link
H et al (2008) Whiplash injuries: diagnosis and early manage-
ment. The Swedish Society of Medicine and the Whiplash Com-
mission Medical Task Force. Eur Spine J 17:S355–S417
89. Malmström E-M, Karlberg M, Fransson P-A, Lindbladh J, Mag-
nusson M (2009) Cervical proprioception is sufficient for head
orientation after bilateral vestibular loss. Eur J Appl Physiol
107:73–81
90. Gimse R, Tjell C, Bjørgen IA, Saunte C (1996) Disturbed eye
movements after whiplash due to injuries to the posture control
system. J Clin Exp Neuropsychol 18:178–186
91. Dispenza F, Gargano R, Mathur N, Saraniti C, Gallina S (2011)
Analysis of visually guided eye movements in subjects after
whiplash injury. Auris Nasus Larynx 38:185–189
92. Prushansky T, Dvir Z, Pevzner E, Gordon CR (2004) Electro-
oculographic measures in patients with chronic whiplash and
healthy subjects: a comparative study. J Neurol Neurosurg Psy-
chiatry 75:1642–1644
93. Kongsted A, Jørgensen LV, Bendix T, Korsholm L, Leboeuf-
Yde C (2007) Are smooth pursuit eye movements altered in
chronic whiplash-associated disorders? A cross-sectional
study. Clin Rehabil 21:1038–1049
94. Ischebeck BK, de Vries J, Van der Geest JN, Janssen M, Van
Wingerden JP, Kleinrensink GJ et al (2016) Eye movements
in patients with Whiplash Associated Disorders: a systematic
review. BMC Musculoskelet Disord 17:441
95. Treleaven J, Jull G, LowChoy N (2005) Smooth pursuit neck
torsion test in whiplash-associated disorders: relationship to
self-reports of neck pain and disability, dizziness and anxiety.
J Rehabil Med 37:219–223
96. Janssen M, Ischebeck BK, de Vries J, Kleinrensink G-J, Frens
MA, van der Geest JN (2015) Smooth pursuit eye movement
deficits in patients with whiplash and neck pain are modulated
by target predictability. Spine 40:E1052–E1057
97. Treleaven J, Jull G, LowChoy N (2006) The relationship of
cervical joint position error to balance and eye movement dis-
turbances in persistent whiplash. Man Ther 11:99–106
98. Jull GA, O’Leary SP, Falla DL (2008) Clinical assessment of
the deep cervical flexor muscles: the craniocervical flexion test.
J Manip Physiol Ther 31:525–533
99. Montfoort I, Van Der Geest JN, Slijper HP, De Zeeuw CI, Frens
MA (2008) Adaptation of the cervico- and vestibulo-ocular
reflex in whiplash injury patients. J Neurotrauma 25:687–693
100. Kelders WP, Kleinrensink GJ, Geest JNVD, Schipper IB,
Feenstra L, Zeeuw CID et al (2005) The cervico-ocular
reflex is increased in whiplash injury patients. J Neurotrauma
22:133–137
101. Jull G, Kristjansson E, Dall’Alba P (2004) Impairment in the
cervical flexors: a comparison of whiplash and insidious onset
neck pain patients. Man Ther 9:89–94
102. Teasell RW, McClure JA, Walton D, Pretty J, Salter K, Meyer
M et al (2010) A research synthesis of therapeutic interventions
for whiplash-associated disorder (WAD): part 4—noninvasive
interventions for chronic WAD. Pain Res Manag 15:313–322
103. Lystad RP, Bell G, Bonnevie-Svendsen M, Carter CV (2011)
Manual therapy with and without vestibular rehabilitation for
cervicogenic dizziness: a systematic review. Chiropr Man Ther
19:21
104. Yaseen K, Hendrick P, Ismail A, Felemban M, Alshehri MA
(2018) The effectiveness of manual therapy in treating cervico-
genic dizziness: a systematic review. J Phys Ther Sci 30:96–102
105. Van Oosterwijck J, Nijs J, Meeus M, Truijen S, Craps J, Van den
Keybus N et al (2011) Pain neurophysiology education improves
cognitions, pain thresholds, and movement performance in peo-
ple with chronic whiplash: a pilot study. J Rehabil Res Dev
48:43–58
106. Meeus M, Nijs J, Hamers V, Ickmans K, Oosterwijck JV (2012)
The efficacy of patient education in whiplash associated disor-
ders: a systematic review. Pain Physician 15:351–361
107. Minguez-Zuazo A, Grande-Alonso M, Saiz BM, La Touche
R, Lara SL (2016) Therapeutic patient education and exercise
therapy in patients with cervicogenic dizziness: a prospective
case series clinical study. J Exerc Rehabil 12:216–225
108. Michaleff ZA, Maher CG, Lin C-WC, Rebbeck T, Jull G, Latimer
J et al (2014) Comprehensive physiotherapy exercise programme
or advice for chronic whiplash (PROMISE): a pragmatic ran-
domised controlled trial. Lancet Lond Engl 384:133–141
109. Nijs J, Ickmans K (2014) Chronic whiplash-associated disorders:
to exercise or not? Lancet Lond Engl 384:109–111
110. Sterling M (2014) Physiotherapy management of whiplash-asso-
ciated disorders (WAD). J Physiother 60:5–12
111. Teasell RW, McClure JA, Walton D, Pretty J, Salter K, Meyer
M et al (2010) A research synthesis of therapeutic interventions
for whiplash-associated disorder (WAD): part 5—surgical and
13

injection-based interventions for chronic WAD. Pain Res Manag
15:323–334
112. Sorensen BF (1978) Bow hunter’s stroke. Neurosurgery
2:259–261
113. Lu DC, Zador Z, Mummaneni PV, Lawton MT (2010) Rota-
tional vertebral artery occlusion—series of 9 cases. Neurosur-
gery 67:1066–1072
114. Zaidi HA, Albuquerque FC, Chowdhry SA, Zabramski JM,
Ducruet AF, Spetzler RF (2014) Diagnosis and management of
bow hunter’s syndrome: 15-year experience at barrow neurologi-
cal institute. World Neurosurg 82:733–738
115. Jost GF, Dailey AT (2015) Bow hunter’s syndrome revisited: 2
new cases and literature review of 124 cases. Neurosurg Focus
38:E7
116. Tsutsumi S, Ito M, Yasumoto Y (2008) Simultaneous bilateral
vertebral artery occlusion in the lower cervical spine manifesting
as bow hunter’s syndrome. Neurol Med Chir (Tokyo) 48:90–94
117. Buchanan CC, McLaughlin N, Lu DC, Martin NA (2014) Rota-
tional vertebral artery occlusion secondary to adjacent-level
degeneration following anterior cervical discectomy and fusion.
J Neurosurg Spine 20:714–721
118. Miele VJ, France JC, Rosen CL (2008) Subaxial positional ver-
tebral artery occlusion corrected by decompression and fusion.
Spine 33:E366–E370
119. Lee V, Riles TS, Stableford J, Berguer R (2011) Two case pres-
entations and surgical management of Bow Hunter’s syndrome
associated with bony abnormalities of the C7 vertebra. J Vasc
Surg 53:1381–1385
120. Darkhabani MZ, Thompson MC, Lazzaro MA, Taqi MA, Zaidat
OO (2012) Vertebral artery stenting for the treatment of bow
hunter’s syndrome: report of 4 cases. J Stroke Cerebrovasc Dis
21:908.e1–908.e5
121. Matsuyama T, Morimoto T, Sakaki T (1997) Comparison of
C1–2 posterior fusion and decompression of the vertebral artery
in the treatment of bow hunter’s stroke. J Neurosurg 86:619–623
122. Sarkar J, Wolfe SQ, Ching BH, Kellicut DC (2014) Bow hunter’s
syndrome causing vertebrobasilar insufficiency in a young man
with neck muscle hypertrophy. Ann Vasc Surg 28:1032.e1–1032.
e10
123. Saito K, Hirano M, Taoka T, Nakagawa H, Kitauchi T, Tanizawa
E et al (2010) Artery-to-artery embolism with a mobile mural
thrombus due to rotational vertebral artery occlusion. J Neuro-
imaging 20:284–286
124. Tominaga T, Takahashi T, Shimizu H, Yoshimoto T (2002) Rota-
tional vertebral artery occlusion from occipital bone anomaly: a
rare cause of embolic stroke. J Neurosurg 97:1456–1459
125. Citow JS, Macdonald RL (1999) Posterior decompression of the
vertebral artery narrowed by cervical osteophyte: case report.
World Neurosurg 51:495–499
126. Inamasu J, Nakatsukasa M (2013) Rotational vertebral artery
occlusion associated with occipitoatlantal assimilation, atlanto-
axial subluxation, and basilar impression. Clin Neurol Neurosurg
115:1520–1523
127. Safain MG, Talan J, Malek AM, Hwang SW (2014) Spontaneous
atraumatic vertebral artery occlusion due to physiological cervi-
cal extension: case report. J Neurosurg Spine 20:278–282
128. Cornelius JF, George B, Oka DN, Spiriev T, Steiger HJ, Hänggi
D (2012) Bow-hunter’s syndrome caused by dynamic vertebral
artery stenosis at the cranio-cervical junction—a management
algorithm based on a systematic review and a clinical series.
Neurosurg Rev 35:127–135
129. Yenigun A, Ustun ME, Tugrul S, Dogan R, Ozturan O (2016)
Classification of vertebral artery loop formation and association
with cervicogenic dizziness. J Laryngol Otol 130:1115–1119
130. Strupp M, Planck JH, Arbusow V, Steiger HJ, Brückmann H,
Brandt T (2000) Rotational vertebral artery occlusion syndrome
13
European Archives of Oto-Rhino-Laryngology
with vertigo due to “labyrinthine excitation”. Neurology
54:1376–1379
131. Matsuyama T, Morimoto T, Sakaki T (1997) Bow Hunter’s stroke
caused by a nondominant vertebral artery occlusion: case report.
Neurosurgery 41:1393–1395
132. Sugiu K, Agari T, Tokunaga K, Nishida A, Date I (2009) Endo-
vascular treatment for bow hunter’s syndrome: case report.
Minim Invasive Neurosurg MIN 52:193–195
133. Yoshimura K, Iwatsuki K, Ishihara M, Onishi Y, Umegaki M,
Yoshimine T (2011) Bow hunter’s stroke due to instability at the
uncovertebral C3/4 joint. Eur Spine J 20:S266–S270
134. Yeh J-F, Lin Y-J, Po HL, Wang S-F, Pan P-Y, Cheng S-J et al
(2005) A case of bow hunter’s stroke caused by non-dominant
vertebral artery. Acta Neurol Taiwanica 14:69–73
135. Noh Y, Kwon O-K, Kim H-J, Kim JS (2011) Rotational vertebral
artery syndrome due to compression of nondominant vertebral
artery terminating in posterior inferior cerebellar artery. J Neurol
258:1775–1780
136. Healy AT, Lee BS, Walsh K, Bain MD, Krishnaney AA (2015)
Bow hunter’s syndrome secondary to bilateral dynamic vertebral
artery compression. J Clin Neurosci 22:209–212
137. Choi K-D, Choi J-H, Kim J-S, Kim HJ, Kim M-J, Lee T-H et al
(2013) Rotational vertebral artery occlusion: mechanisms and
long-term outcome. Stroke 44:1817–1824
138. Kim H-A, Yi H-A, Lee C-Y, Lee H (2011) Origin of isolated
vertigo in rotational vertebral artery syndrome. Neurol Sci
32:1203–1207
139. Choi K-D, Shin H-Y, Kim JS, Kim S-H, Kwon O-K, Koo J-W
et al (2005) Rotational vertebral artery syndrome: oculographic
analysis of nystagmus. Neurology 65:1287–1290
140. Whitmore RG, Simon SL, Hurst RW, Nisenbaum HL, Kasner SE,
Zager EL (2007) Bow hunter’s syndrome caused by accessory
cervical ossification: posterolateral decompression and the use of
intraoperative Doppler ultrasonography. Surg Neurol 67:169–171
141. Vilela MD, Goodkin R, Lundin DA, Newell DW (2005) Rota-
tional vertebrobasilar ischemia: hemodynamic assessment and
surgical treatment. Neurosurgery 56:36–45
142. Iguchi Y, Kimura K, Shibazaki K, Iwanaga T, Ueno Y, Inoue T
(2006) Transcranial doppler and carotid duplex ultrasonography
findings in Bow hunter’s syndrome. J Neuroimaging 16:278–280
143. Shum GL, Cinnamond S, Hough AD, Craven R, Whittingham
W (2017) Test–retest reliability of measuring the vertebral arte-
rial blood flow velocity in people with cervicogenic dizziness. J
Manip Physiol Ther 40:255–262
144. Rastogi V, Rawls A, Moore O, Victorica B, Khan S, Saravanapa-
van P et al (2015) Rare etiology of bow hunter’s syndrome and
systematic review of literature. J Vasc Interv Neurol 8:7–16
145. Mitchell J (2009) Vertebral artery blood flow velocity changes
associated with cervical spine rotation: a meta-analysis of the
evidence with implications for professional practice. J Man
Manip Ther 17:46–57
146. Strickland BA, Pham MH, Bakhsheshian J, Russin JJ, Mack WJ,
Acosta FL (2017) Bow hunter’s syndrome: surgical management
(video) and review of the literature. World Neurosurg 103:953.
e7–953.e12
147. Velat GJ, Reavey-Cantwell JF, Ulm AJ, Lewis SB (2006) Intraop-
erative dynamic angiography to detect resolution of Bow Hunt-
er’s syndrome: technical case report. Surg Neurol 66:420–423
148. Chastain HD, Campbell MS, Iyer S, Roubin GS, Vitek J, Mathur
A et al (1999) Extracranial vertebral artery stent placement: in-
hospital and follow-up results. J Neurosurg 91:547–552
149. Horowitz M, Jovin T, Balzar J, Welch W, Kassam A (2002) Bow
hunter’s syndrome in the setting of contralateral vertebral artery
stenosis: evaluation and treatment options. Spine 27:E495–E498
150. Weintraub MI (1993) Beauty parlor stroke syndrome: report of
five cases. JAMA 269:2085–2086
European Archives of Oto-Rhino-Laryngology
151. Correia PN, Meyer IA, Eskandari A, Michel P (2016) Beauty par-
lor stroke revisited: an 11-year single-center consecutive series.
Int J Stroke 11:356–360
152. Kameda T, Otani K, Tamura T, Konno S (2018) Beauty parlor
stroke syndrome due to a bone fragment from an osteophyte of
the atlas: case report. J Neurosurg Spine 28:389–394
153. Endo K, Ichimaru K, Shimura H, Imakiire A (2000) Cervical
vertigo after hair shampoo treatment at a hairdressing salon: a
case report. Spine 25:632–634
154. Heckmann JG, Heron P, Kasper B, Dorfler A, Maihofner C
(2006) Beauty parlor stroke syndrome. Cerebrovasc Dis Basel
Switz 21:140–141
155. Sahin N, Karataş O, Ozkaya M, Cakmak A, Berker E (2008)
Demographics features, clinical findings and functional status
in a group of subjects with cervical myofascial pain syndrome.
Agri 20:14–19
156. Krabak BJ, Borg-Stein J, Oas JA (2000) Chronic cervical myo-
fascial pain syndrome: Improvement in dizziness and pain with
a multidisciplinary rehabilitation program. A pilot study. J Back
Musculoskelet Rehabil 15:83–87
157. Giamberardino MA, Affaitati G, Fabrizio A, Costantini R (2011)
Myofascial pain syndromes and their evaluation. Best Pract Res
Clin Rheumatol 25:185–198
158. Thompson JM (2012) Exercise in muscle pain disorders. PM R
4:889–893
159. Aydin T, Dernek B, Sentürk Ege T, Karan A, Aksoy C (2018)
The effectiveness of dry needling and exercise therapy in patients
with dizziness caused by cervical myofascial pain syndrome;
prospective randomized clinical study. Pain Med Malden Mass.
https​://doi.org/10.1093/pm/pny07​2
160. Jaroshevskyi OA, Payenok OS, Logvinenko AV (2017) Evalution
of the effectiveness of multimodal approach to the management
of cervical vertigo. Wiad Lek 70:571–573
161. Reneker JC, Clay Moughiman M, Cook CE (2015) The diagnos-
tic utility of clinical tests for differentiating between cervicogenic
and other causes of dizziness after a sports-related concussion:
an international Delphi study. J Sci Med Sport 18:366–372
162. Rashad UM (2010) Patients with benign paroxysmal positional
vertigo and cervical spine problems: is Epley’s manoeuvre con-
traindicated, and is a proposed new manoeuvre effective and
safer? J Laryngol Otol 124:1167–1171
163. Humphriss RL, Baguley DM, Sparkes V, Peerman SE, Moffat
D (2003) Contraindications to the Dix–Hallpike manoeuvre: a
multidisciplinary review. Int J Audiol 42:166–173
13