Eur Arch Otorhinolaryngol. 2018 (Oct); 275 (10): 2421–2433 ~ FULL TEXT
Department of Otorhinolaryngology,
Kasturba Medical College,
Manipal Academy of Higher Education,
Manipal, Udupi, Karnataka, 576104, India.
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' understanding 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: Barre–Lieou syndrome; Benign paroxysmal positional vertigo; Bow hunter’s syndrome; Cervical vertigo; Cervicogenic dizziness; Whiplash-associated disorder
From the FULL TEXT Article:
Broadly, the dizziness incorporates four descriptive symptoms:
‘vertigo’, which is nothing but a false perception of movement of self or surrounding;
‘disequilibrium’ or ‘imbalance’ which is an inability to maintain balance;
‘presyncope’, a sense of losing consciousness; and
‘lightheadedness’, defined as a vague symptom of feeling disconnected from the environment. [1, 2]
to the Barany society’s committee for the classification
of vestibular disorders, the terms ‘vertigo’ and ‘dizziness’
are non-hierarchical and reflect distinctly separate sets of
symptoms.  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.  Nevertheless,
the patients with cervicogenic balance disorder rarely experience
true vertigo; instead, they often complain of lightheadedness
and disequilibrium which are included under
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
dizziness.  Though neurologists, neuro-otologists, physicians,
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 guidelines
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 condition
responsible for the cervicogenic dizziness, this narrative
review proposes a simple aetiopathological classification
and a sensible management algorithm, to enable the appropriate
diagnosis and management in any suspected case of
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 perception
and the integration in the nervous system. Visual
and auditory cues sensing the spatial relationship with the
external environment, vestibular organs detecting the internal
signals of motion, and muscles and joints involved in
the proprioception are the three chief sensory preceptors of
one’s sense of orientation.  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 inappropriate
for this clinical narrative of cervicogenic dizziness.
Nevertheless, the proprioceptive signals of neck muscles and
cervical joints play an enormous role in maintaining and
fine-tuning the person`s orientation at rest and the balance
while motion [11–13], and the alteration in these proprioceptive
signals seems to be responsible for the majority of cases
of the so-called ‘cervicogenic dizziness’. [14, 15] The diseased
cervical joints are shown to have a significantly higher
concentration of Ruffini corpuscles , which, otherwise,
are abundantly found in knee joints , and are known to
play a major role in proprioception.  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
Classification of cervicogenic dizziness
After reviewing the literature thoroughly, the author has
classified the cervicogenic dizziness, as shown in Figure 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 vascular
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), constitutes
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
from the degenerated upper cervical joints to the vestibular
nucleus.  However, the term ‘cervicogenic dizziness’ is
preferred over the ‘cervicogenic vertigo’ owing to the nonspecific
dizziness or feeling of lightheadedness complained
by DCD patients rather than true vertigo.  Growing evidence
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.  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 physicianrated
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, osteophytes,
and olisthesis are the four factors considered in CDI,
each one graded from zero to three depending on the severity.  However, as far as the cervicogenic dizziness is
concerned, correlation with these grades has not been uniformly
predictable. [32, 33] In fact, there are no structured
clinical studies which have directly evaluated the relationship
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 vertebrobasilar
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
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.  However,
subsequent experimental studies by Heisted and his colleagues
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 substantiating
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 cervical
vertebral joints can lead to vertigo via the stimulation
of sympathetic fibers in the adjacent posterior longitudinal
ligament. [44, 50] Researchers have confirmed the distribution
of sympathetic fibers in the human posterior longitudinal
ligament.  Others have identified bidirectional neural
networks between the cervical spinal and the sympathetic
ganglia re-iterating the possible neuroanatomical hypothesis
for this condition.  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 investigation
available either. However, the association of degenerative
changes in cervical spine radiograph with sympathetic
symptoms and the relief of these symptoms upon the treatment
of degenerated joints should suggest the diagnosis of
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 ; 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 ,
there is not enough evidence to support their use to control
the dizziness in DCD patients. Similarly, studies evaluating
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.  Combination of manual therapy
and physiotherapy is shown to be better than physiotherapy
alone in this regard.  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 is a unique form of manual therapy, popularized by
Palmer and Palmer.  The primary mode of chiropractic
therapy is spinal manipulation, and the cervical spinal
manipulation has been shown to be effective in controlling
the cervicogenic dizziness.  However, this therapy is
surrounded by some controversy and is not entirely safe. 
Acute compression of the vertebral artery , dissection
of the vertebral artery [59, 60], and bilateral diaphragmatic
palsy  are some of the reported complications with the
chiropractic therapy. Though the cervical manipulation is
depicted to be safe in healthy young adults , it is preferably
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 frequency
of cervicogenic dizziness.  In another study, total
disc replacement significantly reduced the severity of dizziness
and other sympathetic features in DCD.  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; nevertheless,
the surgical intervention may be an optimal therapeutic
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 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). 
The Quebec Task Force classified the WAD into four categories
and redefined its management in 1995.  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-imbalance
forms one of the significant symptom complexes in the
chronic WAD, other predominate manifestations being the
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.  The clinicopathological characteristics
of the BPPV in these patients are similar to that of
the idiopathic BPPV, except that the multiple repositioning
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.  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 understood.
The abnormal cervical afferent inputs due to mechanoreceptor
dysfunction, mismatching with the normal vestibular
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 lumbar
erector muscles following whiplash injury is thought to
affect the balance perception of the central nervous system
leading to disequilibrium. 
The clinical characteristics of ‘cervicogenic dizziness’
in WAD patients are similar to the dizziness in DCD and
include episodic lightheadedness or imbalance lasting minutes
to hours.  The affected patients would have significantly
reduced neck mobility and postural instability compared
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.  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 labyrinthine
stimulation.  This nystagmus is most appreciated in
patients with bilateral vestibular loss.  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 rotation
over trunk.  Though it is observed in some cases of
WAD , 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. 
Measuring the postural deficit is one of the ways to
confirm cervicogenic cause for dizziness in WAD. In posturography,
a computerized stable force platform measures
the postural sway and the changes in standing balance,
under the altered visual and support conditions.  Posturography
has demonstrated significant deficiencies in
the postural responses among the WAD patients having
dizziness compared to the WAD patients not having dizziness
and the healthy controls. [73, 74] Since the results of
posturography are not influenced by age, medication, vestibular
compensation status, or anxiety levels at the time of
testing , it can be used to differentiate the malingering
patients complaining of vertigo after injury with the malicious
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 comfortable
range and to return to starting position as accurately as
possible.  Simple computer-based algorithms have been
found useful and can be of clinical utility.  If repeatedly
performed (at least six times), the results can be reliable.  WAD group would have larger JPE compared to the
healthy controls during flexion–extension and repositioning
tasks. [86, 87] Among WAD patients, those with dizziness
are shown to have significantly greater JPE than those
without.  Interestingly, the amount of JPE seems to be
correlating with the severity of WAD.  The vestibular
function influences the JPE results more often  than
not.  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 sensitivity
of 90% and specificity of 91% in WAD patients having
the cervicogenic dizziness.  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 movements
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 neither
in normal subjects nor in patients with central or peripheral
vestibular pathologies.  Though many authors have
been able to reproduce the similar SPNT test results ,
some have reported the statistically insignificant differences [91–93], and this is probably because of the methodological
differences between these studies.  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 dizziness
in WAD.  More than 2/3 of WAD patients having
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.  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 vestibular
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 diagnosing
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 cervicogenic
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 vestibular
system. Nevertheless, the COR gain also has a potential
to be an objective test to diagnose WAD.  In CCFT,
the patient is asked to progressively increase the craniocervical
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. 
The cervicogenic dizziness in WAD patients can be effectively
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
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 cervicogenic
dizziness.  Patient education is another effective
treatment modality in WAD.  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 telephonic
support is shown to be as effective as 20 sessions
of comprehensive physiotherapy exercise programs. 
However, this study does not imply to discontinue the exercise
therapy in the chronic WAD, but it reinforces the physiotherapists
on the importance of patient education in rehabilitating
such patients.  There are very few trials on
pharmacotherapy in the chronic WAD, and thus, no specific
recommendations exist for drug therapy.  The role of
muscle relaxants and NSAIDs in controlling cervicogenic
dizziness due to WAD is yet another potential research question
for further studies. Similarly, the utility of surgical procedures
in WAD patients is also not apparent, owing to the
contradictory evidence in the literature.  Among many
invasive procedures tried in WAD, the existing evidence supports
only the radiofrequency neurotomy in chronic WAD
patients, who are not responding to the conventional therapy. 
Bow hunter’s syndrome
Sorenson in 1978 named the condition of ‘symptomatic
vertebral artery insult with dynamic neck posture’ as ‘Bow
hunter’s stroke’ , 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 , but can also be seen in young individuals. [119–123] Men are more commonly affected than women.  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 headache. [27, 113, 129, 130]Typically, the affected individuals
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
Vertigo in BHS is most often due to dynamic compression
of the dominant vertebral artery, and since the left vertebral
artery is dominant in most individuals, it is responsible
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 predispose
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 ipsilateral
vertebral artery compression at or below C4 [117–119]
or due to the contralateral vertebral artery compression at
or above C3.  Sometimes, turning on to either side can
produce symptoms, which is seen in the bilateral vertebral
artery compression or stenosis [27, 119, 136]. The symptomology
in BHS is attributed to reduced vertebral artery flow
resulting in transient hypoperfusion of the ipsilateral labyrinth
or the lateral medulla or the inferior cerebellum 
and resultant neural excitation. [130, 137, 138]
ischemia in these organs can also give rise to typical nystagmus
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.  This nystagmus may
also have latency, and it may change the direction on bringing
the head back to neutral.  As discussed in the earlier
paragraphs, many patients of BHS are predisposed by the
degenerative joints of the cervical spine. Other predisposing
conditions for BHS include malformed vertebrae ,
bony stenosis of vertebral canal , accessory osseous
canal in the transverse process , hypertrophied neck
musculature , and trauma. 
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 cervicogenic
dizziness.  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. Nevertheless,
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 angiogram
(d-DSA), which is the current investigation of choice
for diagnosing BHS.  In all these tests, care should be
taken to avoid the sustained end-of-range rotation and quickthrust
rotational manipulations.  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.  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. 
Accordingly, vascular decompression is the most preferred
treatment , and it can be done by anterior approach or
posterior approach.  Considering the ease of accessing
the vertebral artery, for lesions at or below C4, the anterior
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. 
Though some authors have reported nearly 33% re-occlusion
rate after successful vascular decompression , this
unfavorable outcome is attributed to possibly missed anterior
fibrous bands during posterior approach decompression.  Nevertheless, surgical intervention needs to be individualized
to each patient depending on the site of the occlusion,
the extent of the occlusion, and the exact cause of the
occlusion. Often, the combination of vascular decompression
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.  Similar success rates have been reported with isolated
decompression and decompression with fusion. 
Irrespective of the approach and type of surgery, it is imperative
to have a sound anatomical understanding and to exercise
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  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.  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.  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 compression
of the arteries and could also be due to dissection of
the vertebral artery or some systemic conditions.  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 headrest
while hairdressing or hair massage. 
may manifest with varied symptoms ranging from vertigo
to evolved stroke. [151–153] Age more than 50 years ,
female sex  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 pathology,
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 antiplatelet
medications form the basis for the treatment of BPS
along with the other supportive measures.  Surgical
correction of external compression or vertebral arterial wall
defect may help in relieving the symptoms in the affected
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 , and it correlates with the symptom
of pain.  It is commonly seen in young individuals, in
fourth decade of life, and females are affected more often.  Trapezius muscle would have trigger points in half
of the affected patients.  There may be associated features
like skin flushing, lacrimation, and other autonomic
symptoms. CMPS is commonly associated with cervical
trauma, fibromyalgia, and joint hypermobility syndrome.  Apart from the typical clinical features, the needle
electromyography findings can help in diagnosing this condition.
The affected muscles fatigue faster than the rest, and
this active focus is depicted as spontaneous endplate activity
in electromyography. 
Exercise therapy is the treatment
for cervicogenic dizziness and other complaints in CMPS
patients.  Along with stretching and strengthening rehabilitation
programs, the trigger point injections are also useful
in treating the cervicogenic dizziness caused by CMPS. [156, 157] The combination of manual therapy with needle
therapy  and added vestibular rehabilitation  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 conditions
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 proprioceptive
signals, from joints and muscle spindles, respectively.
However, the DCD can lead to dizziness also by the vascular
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
vertigo. Separating these clinical conditions, and identifying
the exact cause for cervicogenic dizziness in a given
case is essential clinically and is relevant for research studies.
However, due to the overlapping symptomology and the
lack of specific diagnostic investigations , many of the
high-quality studies and the reviews have not separated these
conditions. [103, 104, 107]
One cannot rely on the universal
conclusions of these studies unless the constitute conditions
of cervicogenic dizziness are separated and contrasted
against each other. So far, no single clinical study, either epidemiological
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 Figure 2, on how to approach
a patient with suspected cervicogenic dizziness. The objective
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 cervicogenic
dizziness can be ruled in or out in a systematic manner.
Nevertheless, one can proceed with the given algorithm
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 history,
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 cervicogenic
dizziness seems appropriate and sensible. Nevertheless,
since the algorithm is based on the extrapolation of
facts from the literature, it needs further validation by clinical
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.
Conflict of interest
The authors declare that they have no conflict of interest.
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