Vestibular

Rehabilitation,
Dizziness, Balance,
and Associated
Issues in Physical
Therapy
Independent Study Course 17.3.3

Cervicogenic Dizziness and

Differential Diagnosis of
Dizziness in the Orthopaedic
Physical Therapy Setting

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, MTC, CSCS,

FAAOMPT, FCAMT
University of St Augustine for Health Sciences
St Augustine, Florida
The Journal of Manual and Manipulative Therapy
Forest Grove, Oregon
Shelbourne Physiotherapy Clinic
Victoria, British Columbia
Dynamic Physical Therapy
Cadillac, Michigan

Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPT

Mercy Rehab Associates
Darby, Pennsylvania
Specialized Physical Therapy, LLC
Cherry Hill, New Jersey
University of St Augustine for Health Sciences
St Augustine, Florida
University of the Sciences in Philadelphia
Philadelphia, Pennsylvania

An Independent Study Course Designed

for Individual Continuing Education
Vestibular Rehabilitation, Dizziness, Balance,
and Associated Issues in Physical Therapy
Christopher Hughes, PT, PhD, OCS—Editor

Dear Colleague,

I am pleased to welcome you to Cervicogenic Dizziness and Differential Diagnosis of Dizziness in

the Orthopaedic Physical Therapy Setting, authored by Peter A. Huijbregts, PT, MSc, MHSc, DPT,
OCS, MTC, CSCS, FAAOMPT, FCAMT, and Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPT,
as part of the Independent Study Course entitled Vestibular Rehabilitation, Dizziness, Balance, and
Associated Issues in Physical Therapy.

Dr Peter A. Huijbregts received a diploma in physiotherapy from the Hogeschool Eindhoven in

1990, an MSc degree in manual therapy from the Vrije Universiteit Brussel in 1994, an MHSc
degree in physical therapy from the University of Indianapolis in 1997, and a DPT degree in 2001
from the University of St Augustine for Health Sciences in St Augustine, Florida. He is currently
clinically employed as a consultant physiotherapist at Shelbourne Physiotherapy Clinic in Victoria,
British Columbia, and is assistant professor of online education at the University of St Augustine
for Health Sciences. He is also Editor-in-Chief of The Journal of Manual and Manipulative Therapy
and serves as a manuscript reviewer for Physiotherapy Canada. He is a member of the scientific
board of the Rehabilitacja Medyczna Journal and also serves as a consulting editor for Jones
and Bartlett Publishers in Sudbury, Massachusetts. He has been a previous author of many other
independent study course monographs for the Orthopaedic Section.

Dr Paul G. Vidal received his MPT degree from Philadelphia College of Pharmacy and Science
and his DPT degree from the University of St Augustine for Health Sciences. His areas of expertise
include orthopaedics, manual physical therapy, and vestibular rehabilitation. He is owner of
Specialized Physical Therapy, LLC, in Cherry Hill, New Jersey, and also is employed at Mercy Rehab
Associates, in Darby, Pennsylvania. He has been a frequent presenter at national conferences on
the topic of physical therapy management of cervicogenic dizziness. He has also published in the
peer-reviewed publications Journal of Orthopaedic and Sports Physical Therapy and Journal of
Manual and Manipulative Therapy.

The authors present a thorough review of the physiology and etiology of cervicogenic dizziness and
other pathologies potentially causing dizziness and present an evaluation scheme that applies a 4-
category diagnostic classification system and leads to the management of cervicogenic dizziness
and other types of dizziness amenable to physical therapy management. The classification system
facilitates proper diagnosis and helps the clinician distinguish between those patients who can
benefit from physical therapy intervention and those who require medical-surgical referral.

The authors also discuss performance, scoring, and interpretation of tests and measures used in
evaluating dizziness. Vertigo, presyncope, and dysequilibrium are specifically defined according
to the structures affected and the presentation of the patient’s symptoms.

After reviewing the monograph, I am sure you will find the information practical and readily
applicable to effectively evaluating and treating your patients who present with dizziness as a
symptom.

Sincerely,

Christopher Hughes PT, PhD, OCS, CSCS

Editor

2920 East Avenue South, Suite 200 | La Crosse, WI 54601

Office 608-788-3982 | Toll Free 800-444-3982 | Fax 608-788-3965
 TABLE OF CONTENTS

LEARNING OBJECTIVES...................................................................................................................................................1

CERVICOGENIC DIZZINESS............................................................................................................................................1

Dizziness Originating in the Cervical Spine.............................................................................................................1

Cervicogenic Dizziness...........................................................................................................................................2

Diagnostic Criteria and Differential Diagnosis.........................................................................................................2

Physical Therapy Management of Cervicogenic Dizziness........................................................................................3

DIAGNOSTIC CLASSIFICATION SYSTEM.........................................................................................................................4

Vertigo.....................................................................................................................................................................4

Presyncope..............................................................................................................................................................4

Dysequilibrium........................................................................................................................................................4

Other Dizziness.......................................................................................................................................................5

Challenges to the Diagnostic Classification System..................................................................................................5

VERTIGO.........................................................................................................................................................................5

Peripheral Vestibular Disorders................................................................................................................................5

Benign paroxysmal positional vertigo................................................................................................................5

Ménière disease................................................................................................................................................6

Acute peripheral vestibulopathy........................................................................................................................6

Otosclerosis......................................................................................................................................................6

Head trauma.....................................................................................................................................................7

Cerebellopontine angle tumor...........................................................................................................................7

Toxic vestibulopathies.......................................................................................................................................7

Acoustic neuropathy..........................................................................................................................................7

Perilymphatic fistula..........................................................................................................................................7

Autoimmune disease of the inner ear................................................................................................................7

Central Vestibular Disorders.....................................................................................................................................7

Drug intoxication..............................................................................................................................................7

Wernicke encephalopathy.................................................................................................................................8

Inflammatory disorders......................................................................................................................................8

Multiple sclerosis..............................................................................................................................................8

Alcoholic cerebellar degeneration.....................................................................................................................8

 Phenytoin-induced cerebellar degeneration.......................................................................................................9

Hypothyroidism.................................................................................................................................................9

Paraneoplastic cerebellar degeneration..............................................................................................................9

Hereditary spinocerebellar degenerations..........................................................................................................9

Ataxia-telangiectasia.........................................................................................................................................9

Wilson disease..................................................................................................................................................9

Creutzfeldt-Jakob disease..................................................................................................................................9

Posterior fossa tumors........................................................................................................................................9

Posterior fossa malformations............................................................................................................................9

Familial paroxysmal ataxia..............................................................................................................................10

PRESYNCOPE.................................................................................................................................................................10

Pancerebral Hypoperfusion....................................................................................................................................10

Vasovagal presyncope.....................................................................................................................................10

Cardiovascular presyncope..............................................................................................................................10

Migraine..........................................................................................................................................................10

Benign paroxysmal vertigo of childhood..........................................................................................................11

Takayasu disease.............................................................................................................................................11

Carotid sinus syndrome...................................................................................................................................11

Orthostatic hypotension..................................................................................................................................11

Hyperventilation.............................................................................................................................................11

Cough-related syncope....................................................................................................................................11

Micturition syncope........................................................................................................................................11

Glossopharyngeal neuralgia............................................................................................................................12

Hypoglycemia.................................................................................................................................................12

Brainstem Hypoperfusion.......................................................................................................................................12

Vertebrobasilar insufficiency...........................................................................................................................12

Vertebrobasilar infarction................................................................................................................................13

Basilar-type migraine.......................................................................................................................................14

Vertebrobasilar migraine.................................................................................................................................14

Vestibular migraine.........................................................................................................................................14

Subclavian steal syndrome..............................................................................................................................14

DYSEQUILIBRIUM.........................................................................................................................................................14

Visual Impairment.................................................................................................................................................15

Somatosensory Impairment....................................................................................................................................15

Myelopathy.....................................................................................................................................................15

Landsickness and mal de debarquement syndrome.........................................................................................15

Musculoskeletal Impairment..................................................................................................................................16

Basal Ganglia Impairment......................................................................................................................................16

OTHER DIZZINESS........................................................................................................................................................16

Psychogenic Dizziness...........................................................................................................................................16

Panic disorder..................................................................................................................................................16

Phobic postural vertigo....................................................................................................................................16

Tilting of the Environment......................................................................................................................................17

PHYSICAL THERAPY VERSUS MEDICAL DIFFERENTIAL DIAGNOSIS............................................................................17

HISTORY........................................................................................................................................................................19

Symptoms..............................................................................................................................................................20

Symptom description.......................................................................................................................................20

Symptom behavior..........................................................................................................................................28

Pertinent Past and Present Medical History.............................................................................................................29

Patient demographics......................................................................................................................................29

Medical history...............................................................................................................................................29

Family history..................................................................................................................................................30

Medication history..........................................................................................................................................30

PHYSICAL EXAMINATION.............................................................................................................................................30

Observation...........................................................................................................................................................30

Skin.................................................................................................................................................................30

Posture............................................................................................................................................................31

Eyes.................................................................................................................................................................31

Vital Signs..............................................................................................................................................................32

Blood pressure................................................................................................................................................32

Heart rate........................................................................................................................................................32

Auscultation....................................................................................................................................................32
 Gait Assessment.....................................................................................................................................................32

Vestibulospinal Examination..................................................................................................................................33

Single-leg stance.............................................................................................................................................33

Romberg and sharpened Romberg...................................................................................................................33

Modified Clinical Test of Sensory Integration of Balance..................................................................................33

Fukuda step test...............................................................................................................................................34

Cranial Nerve Examination....................................................................................................................................34

Oculomotor Examination.......................................................................................................................................34

Observation for spontaneous nystagmus..........................................................................................................35

Saccadic eye movements.................................................................................................................................35

Smooth pursuit testing.....................................................................................................................................35

Hearing Examination.............................................................................................................................................36

Weber test.......................................................................................................................................................36

Rinne test........................................................................................................................................................36

Active Range-of-motion Tests.................................................................................................................................36

Limb Ataxia Tests...................................................................................................................................................36

Passive Range-of-motion Tests................................................................................................................................37

Strength Tests.........................................................................................................................................................37

Reflex Tests............................................................................................................................................................38

Sensation Tests.......................................................................................................................................................38

Vertebrobasilar Insufficiency Tests..........................................................................................................................38

De Kleyn-Nieuwenhuyse test..........................................................................................................................38

Sustained cervical rotation test........................................................................................................................39

Hautant test.....................................................................................................................................................39

Vestibulo-ocular Tests.............................................................................................................................................39

Dynamic visual acuity.....................................................................................................................................39

Autorotation test..............................................................................................................................................40

Doll’s head test................................................................................................................................................40

Head-shaking nystagmus test...........................................................................................................................40

Head-thrust test...............................................................................................................................................40

Benign Paroxysmal Positional Vertigo Tests.............................................................................................................40

 Hallpike-Dix maneuver...................................................................................................................................40

Straight head-hanging test...............................................................................................................................41

Roll test...........................................................................................................................................................41

Walk-rotate-walk test.......................................................................................................................................41

Cervicogenic Dizziness Testing..............................................................................................................................41

Breathing-related Tests...........................................................................................................................................42

Hyperventilation test.......................................................................................................................................42

Valsalva test....................................................................................................................................................42

HISTORY AND PHYSICAL EXAMINATION....................................................................................................................42

CASE STUDIES...............................................................................................................................................................42

Case Study 1..........................................................................................................................................................42

Subjective information.....................................................................................................................................42

Objective findings...........................................................................................................................................43

Physical therapy diagnosis...............................................................................................................................43

Guide to Physical Therapist Practice diagnosis.................................................................................................44

Physical therapy management and outcomes..................................................................................................44

Case Study 2..........................................................................................................................................................44

Subjective information.....................................................................................................................................44

Objective findings...........................................................................................................................................45

Physical therapy diagnosis...............................................................................................................................45

Guide to Physical Therapist Practice diagnosis.................................................................................................46

Physical therapy management and outcomes..................................................................................................46

ACKNOWLEDGEMENTS................................................................................................................................................47

REFERENCES..................................................................................................................................................................47

REVIEW QUESTIONS.....................................................................................................................................................56

Opinions expressed by the authors are their own and do not necessarily reflect the views of the Orthopaedic Section.

The publishers have made every effort to trace the copyright holders for borrowed material.
If we have inadvertently overlooked any, we would be willing to correct the situation at the first opportunity.
© 2007, Orthopaedic Section, APTA, Inc.

Course content is not intended for use by participants outside the scope of their license or regulations. Subsequent use of
management is physical therapy only when performed by a PT or a PTA in accordance with Association policies, posi-
tions, guidelines, standards, and ethical principals and standards.
Cervicogenic Dizziness and Differential
Diagnosis of Dizziness in the Orthopaedic
Physical Therapy Setting
Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, MTC,
CSCS, FAAOMPT, FCAMT
University of St Augustine for Health Sciences
St Augustine, Fla
The Journal of Manual and Manipulative Therapy
Forest Grove, Ore
Shelbourne Physiotherapy Clinic
Victoria, British Columbia
Dynamic Physical Therapy
Cadillac, Mich
Paul G. Vidal, PT, MHSc, DPT, OCS, MTC, FAAOMPT
Mercy Rehab Associates
Darby, Pa
Specialized Physical Therapy, LLC
Cherry Hill, NJ
University of St Augustine for Health Sciences
St Augustine, Fla
University of the Sciences in Philadelphia
Philadelphia, Pa
LEARNING OBJECTIVES
Upon completion of this monograph, the course par-
ticipant will be able to discuss:
1. The underlying pathophysiology, diagnostic criteria,
and physical therapy management of cervicogenic
dizziness.
2. A 4-category diagnostic classification system for the
differential diagnosis of patients complaining of dizzi-
ness.
3. Pathologies organized to conform to this diagnostic
classification system potentially responsible for a pa-
tient report of dizziness.
4. The performance, scoring, and interpretation of tests
and measures used in the history and physical exami-
nation of patients complaining of dizziness.
5. The characteristics of patients that may respond to
conservative interventions within the physical therapy
scope of practice versus patients that require medical-
surgical referral for medical differential diagnosis and
medical-surgical management.
CERVICOGENIC DIZZINESS
Dizziness Originating in the Cervical Spine
Multiple different dysfunctions or diseases of the
cervical spine can result in a patient report of dizziness.
Three pathophysiologic mechanisms have been proposed
for dizziness originating in the cervical spine1-3:
1. Ischemic processes affecting the vertebrobasilar sys-
tem.
2. Vasomotor changes caused by irritation of the cervical
sympathetic nervous system.

3. Altered proprioceptive input from the upper cervical
region.
Mechanical compression, tension, dissection, or steno-
sis of one or both vertebral arteries as they course through
the cervical spine will cause decreased vertebrobasilar
blood flow and may cause hindbrain and brainstem isch-
emia resulting in dizziness. Faulty head and neck posture,
congenital cervical deformities, cervical thrust manipula-
tion, and traumatic or degenerative instabilities are among
the causes that have been implicated for the mechanical
compromise leading to vertebrobasilar ischemia.1,2,4-6
The previous monograph has discussed vertebral artery
compromise in detail.
The cervical sympathetic ganglia are located along-
side the blood vessels and muscles anterolateral to the
vertebral bodies. The superior cervical ganglion, located
at the level of C2-C3, is the largest of the cervical sympa-
thetic ganglia. It is formed by coalescence of the cranial
4 sympathetic ganglia.7 Upper cervical dysfunction has
been hypothesized to negatively impact this ganglion.1,2
This might affect the sympathetic innervations of both the
vertebral and internal carotid arteries with subsequent
hypoperfusion of the brain resulting in a report of dizzi-
ness.7,8 However, Bogduk et al9 noted no effect of electri-
cal stimulation of the cervical sympathetic trunk and the
vertebral nerve on vertebral artery blood flow in monkeys.
Likewise, Brandt and Bronstein10 discounted this proposed
pathophysiologic mechanism and reported that there is no
scientific support for this proposed cervical sympathetic
irritation in the etiology of cervicogenic dizziness.
There are extensive efferent and afferent connections
between especially the upper cervical spine and other
structures involved in balance control.11 The vestibulocer-
vical reflex counteracts angular rotation of the head by
reflexively producing opposite head and neck rotation.12
The hair cells in the semicircular canals (SCCs) provide
afferent information for the vestibulocervical reflex to the
neck and proximal trunk muscles.12 The otolithic maculae
may also contribute to this vestibulocervical reflex by
supplying afferent information to the sternocleidomastoid
muscle.13 The upper cervical spine contains a great den-
sity of muscle and joint mechanoreceptors with a role in
postural control.14,15 Muscle spindle density is especially
high in the deep, short intervertebral neck muscles.10 Af-
ferent input from these mechanoreceptors into the central
vestibular system and integration with vestibular (and
visual) afferent information allows for a true perception
of head and trunk position in space.10 Abnormal stimu-
lation of these proprioceptors due to cervical whiplash
trauma, spondylosis, disk herniations, and head trauma
has been hypothesized to lead to a sensory mismatch at
the level of the central vestibular apparatus of the cervi-
cal proprioceptive with the vestibular and visual input.6
Ryan and Cope16 also implicated iatrogenic injury in the
form of cervical traction. Muscle spasms and active trig-
ger points in the neck muscles, specifically in the sterno-
cleidomastoid muscles, have also been suggested in the
etiology of proprioceptive cervicogenic dizziness.9,11,17
The sensory mismatch discussed above may result in a
conscious awareness of balance and thereby a feeling
of dysequilibrium.6 It is this proprioceptive cervicogenic
dizziness, defined by Furman and Cass18 as a nonspecific
sensation of altered orientation in space and dysequilib-
rium originating from abnormal afferent activity from the
neck, that is the topic of this monograph.
Cervicogenic Dizziness
The rationale for implicating aberrant information from
cervical mechanoreceptors in the etiology of cervicogenic
dizziness is based on the anatomical connections between
the cervical spine and the balance control systems, on
studies on experimentally induced cervicogenic dizzi-
ness, and on proposed clinical evidence.10 We described
above the anatomical connections and their possible
etiologic role in producing cervicogenic dizziness.
There is also research evidence linking the upper
cervical region to a patient report of dizziness. Injection
of a local anesthetic agent in the upper cervical spine of
humans created a strong sensation of imbalance and of
being pulled to the same side as the injection, as well
as a postinjection gait ataxia.19 Similar experiments have
produced transient increased ipsilateral and decreased
contralateral extensor muscle tone, a tendency to fall, gait
deviation, and past pointing toward the injected side.10
Application of a unilateral electrical or vibratory stimulus
to neck muscles resulted in a modification of the visual
vertical orientation as perceived by the test subjects.10
These experiments would seem to support a role for aber-
rant afferent proprioceptive cervical information in the
etiology of cervicogenic dizziness.
There is also some clinical support for this proposed
proprioceptive cervicogenic dizziness. Dizziness, vertigo,
and dysequilibrium are symptoms in 20% to 58% of indi-
viduals that have sustained a whiplash-type injury of the
cervical spine or a closed head injury.17 Between 40%
and 70% of patients with chronic whiplash-associated
disorder (WAD) complain of dizziness and unsteadiness
often resulting in loss of balance and falls.20 Treleaven et
al20 reported significantly greater cervical joint reposi-
tioning errors in subjects with WAD when compared to
asymptomatic controls. These authors also found a signifi-
cantly greater joint repositioning errors in right rotation
(P = 0.006) and a near-significant difference in left rota-
tion (P = 0.06) when comparing subjects with WAD and
complaints of dizziness to those not reporting dizziness.
They implicated cervical mechanoreceptor dysfunction as
the likely cause for cervicogenic dizziness. Heikkilä and
Wenngren21 also reported significantly greater cervical
joint repositioning errors in patients with WAD as com-
pared to healthy controls. They also found significantly
greater cervical joint repositioning errors in patients with
WAD and dizziness as compared to those patients with
WAD who did not report dizziness. They also noted a
significant correlation between joint repositioning errors
and abnormalities in smooth pursuit and saccadic eye
movements, and suggested that restricted cervical range

of motion and altered proprioceptive afferent input might
affect oculomotor function. Abnormal visual as well as
proprioceptive input would seem to have an even greater
potential to produce a sensory mismatch, as discussed
above, and subsequent complaints of dizziness. Ernst et
al22 reported dizziness, tinnitus, and hearing loss in pa-
tients with neck and closed head injury. Information on
the prevalence of dizziness in patients with other types of
neck dysfunction is limited to case reports.17
However, we have to question the value of these
clinical findings in linking dizziness after neck trauma
to cervical proprioceptive dysfunction. Head trauma
and whiplash injury can, of course, also affect structures
other than the cervical spine including the brain, the
brainstem and the cranial nerve nuclei located there,
and the peripheral vestibular apparatus.10,22 In their case
series of patients with dizziness after neck and closed
head injury, Ernst et al22 reported both peripheral and
central vestibular dysfunction. Grimm23 described either
a damaged peripheral labyrinth or cochlea in 90% and
both in 69% of a cohort of 227 patients with whiplash
presenting for a neurology evaluation. Of these patients,
92% met the diagnostic criteria for inner ear contusion.
Of this subgroup, 63% were diagnosed with benign
paroxysmal positional vertigo (BPPV), 64% with second-
ary endolymphatic hydrops, and 21% with unilateral
or bilateral perilymphatic fistulae. Oostendorp et al24
reported a 25% prevalence of BPPV in 273 consecutive
patients with rear-end impact whiplash injury without
head injury. Cervical joint repositioning errors as tested
by Treleaven et al20 and Heikkilä et al21 might, of course,
also have been affected by injuries to structures other
than the cervical mechanoreceptors. Other studies have
reported abnormalities in saccadic and smooth pursuit
eye movements in patients with chronic WAD but have
either linked these oculomotor abnormalities to prefron-
tal cortical dysfunction25 or have found no relationship
with cervical positioning, making a proprioceptive origin
for these oculomotor abnormalities less likely.26
Diagnostic Criteria and Differential Diagnosis
There is no gold standard test for cervicogenic dizzi-
ness, making it a diagnosis of exclusion.6 As discussed
above, a clinician might suspect cervicogenic dizziness if
the patient history includes a report of cervical whiplash
trauma, spondylosis, disk herniations, head trauma, or
cervical traction treatment.
Signs and symptoms proposed as indicative of cervi-
cogenic dizziness include1,3,10,17:
• Cervical region pain or discomfort, especially follow-
ing trauma
• Dizziness described as lightheadedness or floating
unsteadiness
• Dizziness provoked by certain head positions or
movements
• Dizziness of short duration and decreasing intensity
• Persistent occipital headache
• Limited cervical range of motion
• Temporomandibular pain
• Radicular symptoms in the arm
• Episodic or persistent slight ataxia of stance and gait
• Hearing loss associated with neck pain
• Earache
Although seemingly the most relevant, dizziness
provoked by certain head positions or movements has
only limited value as a diagnostic criterion specific for
cervicogenic dizziness. The cervical spine contains
structures providing afferent input to the balance control
system (cervical joint and muscle mechanoreceptors) but
also structures that are part of the output portion of this
system (spinal cord, nerve roots, and muscles). The neck
also has structures relevant to cardiovascular control
(carotid barosensors) and vascular structures (carotid and
vertebral arteries). In addition, neck movements invari-
ably produce head movements, thereby involving the
vestibular and visual systems.10
The clinician should also consider that dizziness has a
high prevalence. Dizziness accounts for 7% of physician
visits for patients over the age of 45;27 for adults over 65,
it is the number one reason to visit a physician.28 Diz-
ziness is more common in women than in men,29 and
the prevalence of dizziness increases with increasing
age.30 However, only some of the 15% to 30% of people
experiencing dizziness will seek medical attention.30 The
complaint of dizziness that brought the patient to seek
treatment after a recent trauma or other etiology linked to
cervicogenic dizziness may have been, at least to some
extent, preexisting but not previously reported and related
to another pathology capable of causing dizziness.
To further complicate matters, patients reporting diz-
ziness may mean lightheadedness, blurry vision, loss of
balance, or a feeling of weakness in the legs. Dizziness is
also used for various sensations of body orientation and
position that are often difficult for patients to describe.31
In summary, there are no history items or physical ex-
amination tests and measures specific for the diagnosis of
cervicogenic dizziness. Neck movements have an effect
not only on cervical joint and muscle systems but also
on the vestibular, visual, vascular, and cardiovascular
systems.10 Dizziness is highly prevalent among the gen-
eral population and may be, to some extent, a preexist-
ing complaint that, therefore, may have a multifactorial
etiology that needs to be explored during the differential
diagnostic process. Finally, most patients have great dif-
ficulty expressing their problem in terms helpful to the
clinician’s effort at differential diagnosis. This indicates
the need for a comprehensive differential diagnostic
process for every patient presenting with a complaint of
dizziness.
Physical Therapy Management of Cervicogenic
Dizziness
Historically, physical therapy interventions for patients
with cervicogenic dizziness have included thrust and
nonthrust manipulation, mechanical traction, physical
modalities, posture reeducation, active range-of-motion

(AROM) exercises, massage, balance retraining, trig-
ger point treatment, and the use of a soft collar during
the acute phase.17 However, perhaps as a result of the
absence of specific diagnostic criteria for cervicogenic
dizziness, the research on the physical therapy manage-
ment is limited.
Karlberg et al32 reported on 17 patients with suspected
cervicogenic dizziness. Noncervical causes of dizziness
had been excluded in all patients. Patients were random-
ized into 2 groups: immediate and delayed (2 months)
treatment. Outcome measures included body sway mea-
sured by way of posturography, neck pain and dizziness
intensity, and dizziness frequency. There were no pretest
between-group differences and all patients demonstrated
significantly poorer postural control as compared to a
healthy population (P < 0.05). Treatment consisted of soft
tissue and joint manipulation, cervical spine stabilization
exercises, relaxation techniques, home exercises, and
ergonomic changes at work. Treatment significantly im-
proved postural performance (P < 0.05) and significantly
reduced neck pain intensity and dizziness intensity and
frequency (P < 0.01).
Galm et al33 reported on 50 patients with cervicogenic
dizziness. The diagnosis was established by exclusion of
otorhinolaryngologic and otoneurologic pathology. Of
these patients, 31 had cervical segmental restrictions and
were treated with manipulation and unspecified physi-
cal therapy; 19 patients had no evidence of segmental
dysfunction and received only physical therapy. A signifi-
cantly greater number of the patients in the manipulation
group reported improvement in dizziness symptoms (P =
0.0005).
Bracher et al34 reported on 15 patients with cervico-
genic dizziness. A negative otorhinolaryngologic and
otoneurologic medical examination, the presence of a
rotary cervical nystagmus, and the presence of signs and
symptoms suggestive of cervical dysfunction were used
to establish the diagnosis. Treatment consisted of soft tis-
sue and joint manipulation, electrical modalities for pain
control, labyrinth-sedating medication, biofeedback, and
upper quadrant range-of-motion exercises. After a mean
number of 5 visits (range 3 to 10) over a median of 41
days (range 15 to 77 days), 9 patients reported complete
resolution, 3 reported consistent improvement, and 3
reported no change.
Reid and Rivett35 performed a systematic review of the
literature on the outcomes with manual therapy treatment
of patients with cervicogenic dizziness. They identified 1
randomized clinical trial and 8 nonrandomized clinical
trial studies including the 3 studies above. They noted
that all studies of manual therapy intervention in patients
complaining of cervicogenic dizziness resulted in signifi-
cant posttreatment improvements in signs and symptoms
of dizziness. However, they also noted that all studies
reviewed were of low methodological quality.
Exercises to strengthen the upper cervical deep flexor
muscles may be indicated for the treatment of patients
with cervicogenic headache.36-38 Jull et al37 demon-
strated consistently poor endurance of these muscles in
patients with cervicogenic headache. In these patients,
this decreased deep flexor muscular endurance was
often associated with increased upper trapezius, leva-
tor scapulae, and scalenes recruitment.37,38 Jull39 also
showed this decreased activity of the deep neck flexors
and increased activity in more global neck flexors such
as the sternocleidomastoid in patients with WAD. A study
comparing various combinations of orthopaedic manual
physical therapy and an exercise program consisting of
deep cervical flexor endurance training, scapular retrac-
tion exercises, postural education, and low-load cervical
flexion and extension resistive exercises in 200 patients
with cervicogenic headache showed that the 3 active
treatments (orthopaedic manual physical therapy, exer-
cise therapy, and orthopaedic manual physical therapy
combined with exercise) reduced headache frequency
and intensity more than the control therapy immediately
after intervention and after 12 months.36 The combined
treatment showed clinically but not statistically relevant
increased effect sizes over the other 2 treatment groups
at 12 months.
The research above36-39 involved patients with cervico-
genic headache. However, deep cervical flexor exercises
may also be indicated for patients with cervicogenic
dizziness. Hypertonicity of the sternocleidomastoid and
upper trapezius muscles has been implicated in the etiol-
ogy of cervicogenic dizziness.6,17 By way of reciprocal
inhibition, deep cervical flexor exercises may play a
role in decreasing this global neck flexor and suboc-
cipital muscle hypertonicity. In addition, these exercises
involve voluntary contraction and holding of the deep
neck flexors that are heavily lined with mechanorecep-
tors. This may improve mechanoreceptor function and
thereby positively affect the complaints of proprioceptive
dysfunction hypothesized to be the cause of cervicogenic
dizziness. However, it should be noted that, at this time,
the appropriateness of cervical spine stabilization exer-
cises for patients with cervicogenic dizziness is based
solely on a pathophysiologic rationale.
Treatment for cervicogenic dizziness may also need to
include kinesthetic exercises for the cervical spine. We
discussed the greater cervical joint repositioning errors
in subjects with WAD when compared to asymptomatic
controls and also in subjects with WAD and complaints of
dizziness as compared to those with WAD not reporting
dizziness.20 This finding contrasts with the nonsignificant
differences found40 between patients with nontraumatic
cervical pain and asymptomatic controls, and would
seem to indicate the need for a different management
for patients with cervicogenic dizziness of traumatic and
nontraumatic origin.
Based on a pathophysiologic rationale, the clinician
could choose interventions to affect cervical range of
motion, upper quadrant muscle length and tone, and
posture. One could consider soft tissue and joint manipu-
lation, trigger point techniques, exercise interventions,
modalities, ergonomic advice and modification, and pa-

tient education. Some authors1,17 have also suggested that
a combination of these treatment options with vestibular
rehabilitation techniques would provide for a superior
outcome. However, it is clear that the research basis for
management of patients with cervicogenic dizziness is
at present very limited and that the clinician still has to
heavily depend upon a pathophysiologic rationale when
it comes to treatment of these patients.
DIAGNOSTIC CLASSIFICATION SYSTEM
We explained above the need for a comprehensive
differential diagnosis for every patient presenting with a
complaint of dizziness. To enable the clinician to per-
form this necessary differential diagnostic process, we
need to discuss in detail not only the history and physical
examination for a patient presenting with dizziness with
an interpretation of the findings on all our tests and mea-
sures, but we also need to review in sufficient detail the
pathologies that may be responsible for a patient report
of dizziness. Dizziness can have an extremely varied
etiology. The consistent use of a diagnostic classifica-
tion system may serve to minimize confusion regarding
a patient’s dizziness symptoms and possible causative
pathologies. Patients with complaints of dizziness can be
classified into 4 subtypes: vertigo, presyncope, dysequi-
librium, and other dizziness.31,41
Vertigo
Vertigo is a false sensation of movement of either the
body or the environment, usually described as spinning,
which suggests vestibular system dysfunction.29,30,42,43 It is
usually episodic with an abrupt onset and often associ-
ated with nausea or vomiting.41 The causative dysfunc-
tion can be located in the peripheral or central vestibular
system.42,44 Peripheral vestibulopathies account for about
35% to 55% of all cases of dizziness.30 Central vestibular
disorders are less frequent and are responsible for only
about 5% of cases of dizziness.30
Presyncope
Presyncope is described as a sensation of an impend-
ing faint or loss of consciousness and is not associated
with an illusion of movement.29,41,43 It may begin with
diminished vision or a roaring sensation in the ears.41 This
subtype of dizziness results from conditions that compro-
mise the brain’s supply of blood, oxygen, or glucose.43
The frequency reported for presyncopal dizziness varied
from 2% in a dizziness clinic to 16% in an emergency
room.45,46 This type of dizziness may be accompanied by
transient neurological signs (eg, dysarthria, visual distur-
bances, and extremity weakness).47,48
Dysequilibrium
Dysequilibrium is a sense of imbalance without ver-
tigo that is generally attributed to neuromuscular prob-
lems.29 This condition is also characterized by the feeling
that a fall is imminent.41 The unsteadiness or imbalance
occurs only when erect and disappears when lying or
sitting.41 This subtype of dizziness may result from visual
impairment, peripheral neuropathy, and musculoskel-
etal disturbances, and may include ataxia. Prevalence of
dysequilibrium among patients complaining of dizziness
varies from 1% to 15%.29
Other Dizziness
Other dizziness is dizziness described as a vague
or floating sensation with the patient having difficulty
relating the specific feeling to the clinician.29 It includes
descriptions of vague lightheadedness, heavy-headed-
ness, or wooziness and cannot be classified as any of the
3 previous subtypes.41 Psychiatric disorders are the main
cause for this subtype and account for about 10% to 25%
of dizziness cases.29,31 Anxiety, depression, and hyperven-
tilation are often at the root of this dizziness.29,49 Changes
in vision and tilting of the environment are included in
the subtype of other dizziness, as is psychogenic or psy-
chosomatic dizziness due to panic disorder.29,50
Challenges to the Diagnostic Classification System
The classification of dizziness into these 4 subtypes
attempts to differentiate complaints of dizziness by symp-
toms and pathophysiology. The clinician should note that
this classification system is challenged when an individual
complains about more than 1 subtype of dizziness. Diz-
ziness may result from disorders in the musculoskeletal,
vestibular, cardiovascular, neurological, and metabolic
systems as well as from psychiatric disorders.30 The term
geriatric syndrome was proposed to describe dizziness in
older adults occurring as a result of multisystem impair-
ment.51 The problem with this term, however, is that it
suggests that dizziness is due to old age. In contrast, re-
cent studies have demonstrated that dizziness is prevalent
in all adult populations.29,31 The system is also challenged
by symptoms of ataxia, a dyscoordination or clumsiness
of movement not associated with muscular weakness.
Ataxia can be the result of neuromuscular or peripheral
proprioceptive disorders, but also of cerebellar and ves-
tibular disorders with these latter 2 groups of disorders
potentially occurring with or without symptoms of ver-
Table 1. Differential Diagnostic Characteristics of Central Versus Peripheral Vertigo*
Central Lesions
Vertigo • Often constant
• Less severe
Nystagmus • Sometimes absent
• Unidirectional or multidirectional
• May be vertical
Hearing Loss or Tinnitus • Rarely present
Brainstem Signs† • Typically present
*Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.
Brainstem signs may include motor and sensory deficits, hyperreflexia, positive Babinski sign, dysarthria, and limb
†
ataxia.

tigo.43 Using the above classification system, we will now
define and discuss pathologies that may be responsible
for a patient who reports dizziness.
VERTIGO
As previously noted, vertigo is the misperception of
movement of the body or of the environment.43 Vertigo is
often accompanied by other signs and symptoms, includ-
ing27,43:
• Impulsion (ie, the sensation that the body is being
hurled or pulled in space)
• Oscillopsia (ie, the visual illusion of moving back and
forth or up and down)
• Nystagmus (ie, the rhythmic oscillation of the eye-
balls)
• Gait ataxia (ie, dyscoordinated gait not resulting from
muscle weakness)
• Nausea
• Vomiting
Together, these symptoms are highly indicative of a
peripheral or central vestibular dysfunction as discussed
below. Table 1 summarizes the general differential
diagnostic criteria for central and peripheral vestibular
lesions.
Peripheral Vestibular Disorders
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo is considered
the most common peripheral vestibular disorder.52,53
Annual incidence in the general US population has
been estimated at 64 per 100 000. Benign paroxysmal
positional vertigo accounts for 17% to 30% of all new
patients presenting to vestibular clinics. It is generally
seen in people over the age of 40 and is rare in people
under 20.53 Idiopathic BPPV has a peak incidence of on-
set in the sixth decade of life.54 Nonidiopathic BPPV has
been associated with head trauma, insult to the labyrinth,
surgical stapedectomy, chronic suppurative otitis media,
and degeneration of the inner ear.52,53,55
Two pathophysiological theories have been proposed
to explain the etiology of BPPV: cupulolithiasis and
Peripheral Lesions
• Often intermittent
• Severe
• Always present
• Unidirectional
• Never vertical
• Often present
• Never present
canalithiasis.53 The theory of cupulolithiasis proposes
that sedimentous material, possibly macular otoconia, is
released into the endolymphatic fluid in the SCCs. This
release of sedimentous material is hypothesized to result
from trauma or degenerative changes. When the head is
upright, this material will settle on the SCC cupula. Fixed
deposits on the cupula increase the density of this struc-
ture, making the cupula, which previously had the same
density as the surrounding endolymphatic fluid, now sen-
sitive to gravity and, therefore, head position. The theory
of cupulolithiasis is based on dissection studies in which
cupular deposits appear to be relatively common, but a
correlation with clinical symptomatology is lacking.53
The canalithiasis theory proposes that BBPV is the
result of free-floating endolymphatic densities in the
SCCs.53 Changes in head position are hypothesized to
produce movement of these particles, creating a current
in the SCCs; the resultant hydrodynamic drag could then
displace the cupula, stimulating the SCC hair cells. The
canalithiasis theory provides a better explanation for
the latency of vertigo observed in BPPV than does the
cupulolithiasis theory. One could assume that it takes
a few seconds for the endolymphatic densities to over-
come the inertia of the endolymphatic fluid in the SCC
before they are able to create sufficient hydrodynamic
drag to move the cupula. Fatigability or habituation of the
vertigo response with repeated provocative head move-
ment could be explained by dissolution of the clumped
endolymphatic material. Free-floating particulate matter
has been observed in SCC endolymphatic fluid during
surgery.53
Canalithiasis and cupulolithiasis may well represent
2 stages of the same pathological process. All etiological
factors for BPPV may result in endolymphatic densities,
which may be free floating or adhered to the cupula.53
Infections (eg, acute labyrinthitis and chronic suppura-
tive otitis media) result in white blood cells, phagocytes,
and endothelial fragments floating in the endolymphatic
fluid. Head trauma or stapedectomy may result in red
blood cells in the endolymphatic fluid, and age-related
degeneration may release cellular debris and macular
otoconia.53
The name BPPV implies that this type of vertigo is po-
sitional in nature. However, it may be more correct to call
BPPV a positioning-type vertigo. In posterior SCC BPPV,
vertiginous symptoms occur when a patient transfers
quickly into a supine position, especially when the head
is turned to the affected side, extending the head on the
neck.52 Symptom onset occurs within 1 to 5 seconds upon
a change in position.52,53 Symptom duration is brief (30 to
60 seconds); hence, it is a positioning-type vertigo rather
than a positional-type vertigo as occurs in vertebrobasilar
insufficiency (VBI). A horizontal-rotary nystagmus is the
hallmark of BPPV originating in the posterior SCC.52,55
Excitation of neurons innervating the ipsilateral supe-
rior oblique muscle and the contralateral inferior rectus
muscle is responsible for the horizontal-rotary direction.52
Symptoms of dysequilibrium and nausea may also occur,

with a rare occurrence of vomiting.52,55 Most commonly
the posterior SCC is involved in BPPV.52,55 However, BPPV
may also involve the horizontal SCC.56 Rolling the head in
the plane of the horizontal SCC while in a supine position
usually induces the horizontal SCC variant of BPPV. Other
provocations include flexion and extension of the head
or shifting from supine to upright.56 An accompanying
monograph has discussed BPPV in more detail.
Ménière disease
Ménière disease is characterized by paroxysmal ver-
tigo lasting minutes to days accompanied by tinnitus,
fluctuating low-frequency hearing loss, and a sensation of
fullness in the ear.41,43 Sensorineural hearing loss (a hear-
ing loss caused by lesions in the cochlea or the cochlear
nerve43) is progressive over multiple episodes, whereas
the vertigo tends to become less severe.43 Before the first
acute attack, patients frequently note an insidious onset of
tinnitus, hearing loss, and the sensation of fullness in the
ear.43 Subsequent attacks typically occur suddenly with
incapacitating vertigo, roaring unilateral tinnitus, and
ipsilateral hearing loss.41 Attacks are often associated with
nausea and vomiting.41,43 Age of onset is usually between
the ages of 20 and 50, and men are more often affected
than women.43 Up to 20% of patients have a family history
of Ménière disease.41 During an acute episode, spontane-
ous horizontal or rotary nystagmus may be present, which
may change direction.43 The underlying cause is thought
to be an increase in the volume of the endolymphatic
fluid in the membranous labyrinth.43 This endolymphatic
hydrops results in excessive amounts of endolymphatic
fluid, which displaces the inner ear structures with resul-
tant signs and symptoms.41
Acute peripheral vestibulopathy
Sudden onset vertigo, nausea, and vomiting lasting up
to 2 weeks characterize acute peripheral vestibulopathy.
This diagnosis includes diagnoses of acute labyrinthitis
and vestibular neuronitis. Simon et al43 noted that these
2 diagnoses are based on unverifiable inferences regard-
ing pathophysiology and location of disease. Eaton and
Roland41 mentioned acute labyrinthitis as a separate
diagnosis characterized by acute onset of severe vertigo,
nausea, vomiting, and diaphoresis lasting 1 to 5 days with
subsequent resolution of complaints over a period of 2
to 3 weeks. A viral origin is likely. Approximately 50% of
patients have an associated upper respiratory infection.41
Simon et al43 noted that acute vestibular neuropathy is
not accompanied by hearing loss. The disease may be
recurrent and some degree of vestibulopathy may be
permanent.43 Differential diagnosis from central disorders
characterized by acute vertigo is imperative.43
Otosclerosis
The pathophysiology mechanism behind otosclerosis
is immobility of the stapes. The stapes normally transmits
sound-induced vibration of the tympanic membrane to
the inner ear. Otosclerosis is characterized by conductive
hearing loss (a hearing loss resulting from disorders in the
external or middle ear),43 but sensorineural hearing loss
and vertigo also occur. Vertigo is recurrent and episodic,
with or without positional vertigo, but may also be more
constant. Nystagmus can be spontaneous or positional.
Hearing loss has an age of onset before 30, and a positive
family history is common.43
Head trauma
We discussed head trauma in the etiology of BPPV.
Head trauma may result in labyrinthine damage and
subsequent vertigo. Undiagnosed skull fractures (petrosal
bone) may damage the vestibulocochlear nerve with
resultant vertigo and hearing loss. Otorrhea (discharge of
cerebrospinal fluid from the ear) may be present.43
Cerebellopontine angle tumor
A benign acoustic neuroma, a tumor of the Schwann
cells covering the vestibular portion of the vestibulo-
cochlear nerve in the internal auditory canal, and me-
ningiomas of the cerebellopontine angle can produce
insidious unilateral sensorineural hearing loss.43,57 Ver-
tigo, tinnitus, and a sensation of fullness in the ear are
less common. Due to their anatomic relationship to the
vestibulocochlear nerve, the trigeminal (cranial nerve V)
and facial (cranial nerve VII) nerves are often affected.
Patients may complain of headache, facial pain, or facial
weakness.43 Vertigo develops in 20% to 30% of patients,
but a nonspecific unsteadiness is more common.43 Age of
onset is usually between 30 and 60. Acoustic neuromas
are more common in neurofibromatosis patients. Café-
au-lait spots on the skin and axillary or inguinal freckles
may be external indicators to suspect neurofibromatosis
1 or Von Recklinghausen disease.43
Toxic vestibulopathies
Ingested alcohol differentially distributes between
the cupula and the endolymphatic fluid. It initially dif-
fuses preferentially into the cupula, decreasing its density
relative to that of the endolymphatic fluid, thus rendering
the peripheral vestibular apparatus unusually sensitive
to gravity. With time, alcohol also diffuses the endolym-
phatic fluid. As blood levels decrease, alcohol leaves the
cupula before leaving the endolymphatic fluid again,
causing temporary differences in sensitivity to gravity. Al-
cohol-induced vertigo, therefore, consists of 2 symptom-
atic phases separated by 1 to 2 hours. The whole episode
lasts up to 12 hours. Vertigo and nystagmus are evident in
the lateral recumbent position and are accentuated when
the eyes are closed.43
Aminoglycosides are antibiotics that can cause both
vestibular and auditory symptoms.43,57 Streptomycin,
gentamicin, and tobramycin are likely to cause vestibular
toxicity by destroying hair cells in the membranous laby-
rinth. The use of amikacin, kanamycin, and tobramycin
is associated with hearing loss. Vertigo, nausea, vomit-
ing, and a spontaneous nystagmus may have an acute
onset.43

Salicylates (aspirin and derivatives) can damage the
vestibular and cochlear end organ resulting in vertigo, tin-
nitus, and sensorineural hearing loss. Headache, nausea,
vomiting, thirst, hyperventilation, and sometimes confu-
sion may all indicate chronic salicylate overdosage.43
Quinine and quinidine can cause tinnitus, hearing loss,
vertigo, vision deficits (including disorders of color vision),
nausea, vomiting, abdominal pain, hot and flushed skin,
and diaphoresis. Fever, encephalopathy, coma, and death
can occur in severe cases. Symptoms can be the result of
overdosage or may result from a single dose.43
The chemotherapeutic drug Cis-platinum causes oto-
toxicity in about 50% of patients, with resultant reversible
tinnitus, hearing loss, and vestibular dysfunction.43
Acoustic neuropathy
Basilar meningitis from a bacterial, syphilitic, or
tuberculous infection or from sarcoidosis can lead to
compression of the vestibulocochlear (acoustic) nerve.
Hypothyroidism, diabetes mellitus, and Paget disease can
also affect the vestibulocochlear nerve. Vertigo can occur,
but hearing loss is more common. Other cranial nerves
may also be affected.43
Perilymphatic fistula
A perilymphatic fistula is a rare cause of vertigo. An
opening develops between the middle and inner ear (oval
or round window rupture). Head injury, barotrauma due
to diving or flying, or a very forceful Valsalva maneuver are
thought to induce the fistula.41 With rapid loss of perilym-
phatic fluid, severe vertigo and hearing loss may develop.
Low-volume leaks may only produce episodic vertigo or
dysequilibrium and hearing loss may be absent.41
Autoimmune disease of the inner ear
This diagnosis is associated with fluctuating deafness
and recurrent vertigo. Other autoimmune diseases (eg,
rheumatoid arthritis, Crohn disease, or polyarteritis) are
often concurrently present.57
Central Vestibular Disorders
We discussed above the differences between vertigo
of central and peripheral origin (Table 1). Some central
vestibular disorders may occur without vertigo. All cer-
ebellar disorders produce gait ataxia, inviting a misdiag-
nosis of the dizziness subtype of dysequilibrium (Table
2). Central vestibular disorders can also be the result of
ischemic processes. We will discuss vascular causes of
central vestibular dysfunction (vertebrobasilar ischemia
and infarction) under presyncope.
Drug intoxication
Many drug intoxication syndromes produce global
cerebellar dysfunction. Agents include43,57:
• Alcohol
• Sedative hypnotics: barbiturates, benzodiazepines,
meprobamate, ethchlorvynol, methaqualone
• Anticonvulsants: phenytoin
Table 2. Signs and Symptoms of Cerebellar Disorders*
Location of Cerebellar Signs Diagnoses
Involvement

Midline • Nystagmus • Tumor

• Head and trunk oscillation (titubation) • Multiple sclerosis
• Gait ataxia
Superior vermis • Gait ataxia • Wernicke encephalopathy
• Alcoholic cerebellar degeneration
• Tumor
• Multiple sclerosis

Cerebellar hemisphere • Nystagmus • Infarction

• Ipsilateral gaze paralysis • Hemorrhage
• Dysarthria • Tumor
• Ipsilateral hypotonia • Multiple sclerosis
• Ipsilateral limb ataxia
• Gait ataxia
• Falling to the side of the lesion

Global cerebellar • Nystagmus • Drug intoxication

• Bilateral gaze paralysis • Hypothyroidism
• Dysarthria • Hereditary cerebellar degeneration
• Bilateral hypotonia • Paraneoplastic cerebellar degeneration
• Bilateral limb ataxia • Wilson disease
• Gait ataxia • (Para) infectious encephalomyelitis
• Creutzfeldt-Jakob disease
• Multiple sclerosis

* Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

• Hallucinogens: phencyclidine in the cerebellum. The cerebellum may be infected by

• Street drugs: heroin
• Mercuric and organophosphoric compounds
Drug intoxication often also produces a confused state.
Alcohol and sedatives tend to produce somnolence, and
hallucinogens tend to cause agitation. The importance of
taking a good history including medication or drug use
is evident.
Wernicke encephalopathy
This acute disorder is comprised of the diagnostic triad
of ataxia, ophthalmoplegia (lateral rectus palsy), and con-
fusion. It is caused by thiamine (vitamin B1) deficiency
and is common in alcoholics but may also be caused
by general malnutrition. Ataxia affects the arm in 10%
of patients; the legs are involved in 20%. A horizontal
or combined horizontal-vertical nystagmus is classically
present.43
bacteriae in Haemophilus Influenzae meningitis and
Legionnaires disease.43 Some diseases are hypothesized
to have an autoimmune origin. Acute cerebellar ataxia
of childhood usually follows a viral infection or inocula-
tion. Acute disseminated encephalomyelitis and a variant
of Guillain-Barré syndrome also fall in this category.43
Multiple sclerosis
Vertigo is rarely the first symptom of multiple scle-
rosis but is common during the course of the disease.
It may have an acute onset and can be positional. Gait
ataxia is the presenting complaint in 10% to 15% of
patients. Nystagmus is also a common sign in multiple
sclerosis. A history of remitting and relapsing neurologic
dysfunctions affecting multiple sites in the central neu-
rologic system may be indicative of multiple sclerosis in
undiagnosed patients.43

Inflammatory disorders Alcoholic cerebellar degeneration

Viral cerebellar infections can occur in patients with
St Louis encephalitis, AIDS dementia complex, and me-
ningoencephalitis associated with varicella, mumps, po-
liomyelitis, infectious mononucleosis, and lymphocytic
choriomeningitis. Bacterial infection of the cerebellum
is rare; only 10% to 20% of brain abscesses are located
Alcoholic cerebellar degeneration usually occurs
in patients with a history of 10 or more years of binge
drinking. It usually has its onset between the ages of
40 and 60 and is more common in men. The onset is
insidious and progression is gradual. As in Wernicke en-
cephalopathy, this syndrome affects mainly the superior


cerebellar vermis. Gait ataxia is the most common find-
ing; nystagmus is a less frequent finding. Distal sensory
deficits in the feet and absent ankle reflexes from diabetic
polyneuropathy and signs of malnutrition may clue the
clinician in to the diagnosis.43
Phenytoin-induced cerebellar degeneration
Phenytoin is an anti-epileptic medication. Long-term
treatment with phenytoin may produce a global cerebel-
lar degeneration.43
Hypothyroidism
Hypothyroidism produces a global cerebellar dysfunc-
tion. The cerebellar syndrome associated with hypothy-
roidism is usually subacute or chronically progressive in
its onset. It is most common in middle-aged or elderly
women. Gait ataxia is the prominent finding; nystagmus
and dysarthria are less common. Other neurologic disor-
ders associated with hypothyroidism include sensorineu-
ral hearing loss, carpal tunnel syndrome, neuropathy, and
myopathy; these signs and symptoms may raise suspicion
of hypothyroidism in undiagnosed patients.43
Paraneoplastic cerebellar degeneration
The pathophysiological mechanism in paraneoplastic
cerebellar degeneration appears to involve antibodies to
tumor cell antigens cross-reacting with cerebellar Purkinje
cells. Patients with lung cancer, ovarian cancer, Hodgkin
disease, and breast cancer are most at risk of developing
this type of global cerebellar degeneration. Onset can be
before or after the diagnosis of cancer; progression oc-
curs over the course of months. Gait and limb ataxia and
dysarthria occur in most cases; nystagmus is rare.43
Hereditary spinocerebellar degenerations
There are 7 autosomal dominant spinocerebellar
ataxias characterized by adult-onset, slowly progressive
cerebellar ataxia that affects gait early and severely. Fried-
reich ataxia is an autosomal recessive spinocerebellar
disease with an onset in childhood. Progressive gait ataxia
is the first symptom, followed by ataxia of all limbs within
2 years. Decreased tendon reflexes in the legs, dysarthria,
impairments of proprioceptive and vibration sense, and
weakness in the legs are common, as are nystagmus,
vertigo, and hearing loss.43
Ataxia-telangiectasia
This syndrome is an autosomal recessive disorder with
an onset before age 4 and global cerebellar involvement
producing nystagmus, dysarthria, and gait, limb, and trunk
ataxia. Loss of vibration and position sense in the legs
further adds to gait ataxia. Vascular lesions are present on
the skin and the eyes, especially on the ears, nose, face,
and antecubital and popliteal fossae.43
Wilson disease
Wilson disease is a disorder of the copper metabolism
with copper deposition in multiple body tissues. A rusty-

brown ring around the cornea is indicative of this disease
and may indicate the origin of the cerebellar symptoms
that are associated with this disorder.43
Creutzfeldt-Jakob disease
This disease is characterized by dementia, cerebellar
signs in 60% of patients, and gait ataxia in 10%. The
ataxia is usually accompanied in 50% of patients thus
affected with nystagmus, dysarthria, and trunk and limb
ataxia. The disease involves progressive dementia, (extra)
pyramidal dysfunction, and myoclonus, with death within
a year of onset.43
Posterior fossa tumors
Cerebellar tumors frequently present with headache
due to increased intracranial pressure or with ataxia.
Nausea, vomiting, vertigo, and cranial nerve palsies are
also common. Most common in adults are secondary
tumors metastasized from primary tumors in the breast or
lung. Primary tumors are more frequent in children and
include astrocytomas and medullablastomas. Headache
and vomiting are frequently presenting symptoms; ataxia
and visual dysfunction are also a common first symptom
with medullablastomas in children.43
Posterior fossa malformations
Congenital anomalies may cause vestibular or cer-
ebellar symptoms in adulthood.43,57 Type I Arnold-Chiari
malformation involves downward displacement of the
cerebellar tonsils through the foramen magnum, caus-
ing symptoms of cerebellar involvement and brainstem
compression. Ataxia in this malformation affects gait and
is bilateral. Hydrocephalus may cause headache and
vomiting. Brainstem compression can be associated with
vertigo, nystagmus, and cranial nerve palsies.43 Other
symptoms demonstrated in patients with compression at
the level of the foramen magnum include suboccipital
pain or neck pain described as a tight collar (65%), often
exacerbated by neck movement; pain in the hand (59%)
or arm (55%), especially burning along the ulnar border of
the contralateral arm in unilateral lesions; pain in the leg
(26%) and face (7%); weak arm (40%) or leg (30%); hand
clumsiness (27%); bladder dysfunction (22%); dysphagia
(13%); dysarthria (3%); and paresthesia along the spine
with trunk and neck flexion (L’ Hermitte sign) (3%). Signs
of foramen magnum compression include hyperreflexia
and limb weakness (70%); a positive Babinski sign (60%);
paraplegia with arms affected more than legs; wasting
of the hand muscles (13%); disproportionate weakness
of the sternocleidomastoid and trapezius as a result of
compression of the spinal accessory nerve (30%); disso-
ciated sensory loss, papilledema (7%); Horner syndrome
(4%); and hiccups (2%). In patients with unilateral
compression, paralysis may present in a clock-face way
with ipsilateral arm, then leg, then contralateral leg, and
finally contralateral arm weakness. Intracranial extension
of the compressive lesion may result in a down-beating
nystagmus (25%) and cruciate hemiplegia (ipsilateral lower
limb and contralateral upper limb weakness caused by a
lesion at the motor decussation in the medulla).58
Familial paroxysmal ataxia
This hereditary recurrent ataxia is associated with
nystagmus and dysarthria. Other symptoms may include
vertigo, tinnitus, diplopia, oscillopsia, facial palsy, head-
ache, and fever. Attacks last from 15 minutes to several
hours and may be triggered by physical exercise, caffeine,
alcohol, or sudden movements.57
PRESYNCOPE
As discussed earlier, presyncope is a sensation of an
impending faint or loss of consciousness that is not associ-
ated with an illusion of movement. Presyncope results from
conditions that compromise the brain’s supply of blood,
oxygen, or glucose. This can compromise the function
of the cerebral hemispheres or the brainstem. Different
conditions can cause either a pancerebral hypoperfusion
or a selective hypoperfusion of the brainstem.43
Pancerebral Hypoperfusion
Causes for presyncope due to pancerebral hypoperfu-
sion can be classified into 4 categories43:
• Vasovagal presyncope
• Cardiovascular presyncope
• Cerebrovascular presyncope: migraine, benign parox-
ysmal vertigo of childhood, Takayasu disease, carotid
sinus syncope
• Miscellaneous causes of presyncope: orthostatic hy-
potension, hyperventilation syncope, cough syncope,
micturition syncope, glossopharyngeal neuralgia
Insufficient supply of glucose and subsequent com-
promised pancerebral function can also result in presyn-
cope.
Vasovagal presyncope
With a vasovagal presyncope, parasympathetic hy-
peractivity causes a decrease in cardiac output with a
subsequent decrease in cerebral blood flow.41 Precipitat-
ing factors include emotional stimulation, pain, the sight
of blood, fatigue, medical instrumentation, blood loss,
or prolonged motionless standing. Vasovagal presyncope
occurs in all age groups and affects men and women
equally. Short prodromes (10 seconds to a few minutes)
will precede syncope and include lightheadedness, nau-
sea, pallor, salivation, blurred vision, and tachycardia.41,43
Vasovagal presyncope mainly occurs with the patient in a
sitting or standing position; it is rare with a patient in the
recumbent position.43
Cardiovascular presyncope
A cardiovascular syncope should be suspected when
syncope occurs with the patient in a recumbent position,
during or after physical activity, or in a patient with a
known medical history of heart disease. Table 3 provides
an overview of cardiac causes of syncope. Associated
symptoms may include chest pain or discomfort, neck or
10
arm pain and discomfort, palpitation, dyspnea, fatigue,
cough, cyanosis, edema, and claudication.59
Migraine
Migraine is generally characterized by headache that
is usually unilateral and of a pulsatile quality. Nausea,
photophobia, phonophobia, vomiting, and lassitude are
frequently associated with migraine. Migraine can occur
without or with an aura. Visual or other neurological au-
ras occur in 10% of patients. The International Headache
Society has provided diagnostic criteria for both types
of migraine (Table 4).60 Also, in about 10% of patients,
migraine may be associated with presyncope. Syncope
will occur during the migraine attack, often when the
patent quickly rises to a standing position, suggesting a
component of orthostatic hypotension. A family history
of migraine is usually present. Migraine is more common
in women with an onset early in life.43
Table 3. Causes of Cardiovascular Syncope*
Cardiac arrest
Cardiac inflow obstruction
• Left atrial myxoma or thrombus
• Tight mitral stenosis
• Constrictive pericarditis
• Cardiac tamponade
• Restrictive cardiomyopathies
• Tension pneumothorax
Cardiac outflow obstruction
• Aortic stenosis
• Pulmonary stenosis
• Hypertrophic obstructive cardiomyopathy
Dissecting aortic aneurysm
Severe pulmonary-vascular disease
• Pulmonary hypertension
• Acute pulmonary embolus
Cardiac dysrhythmias
• Tachyarrhythmias: paroxysmal atrial
tachycardia, atrial filter, atrial fibrillation,
accelerated junctional tachycardia,
ventricular tachycardia, ventricular
fibrillation
• Bradyarrhythmias: sinus bradycardia, sinus
arrest, second or third degree heart block,
implanted pacemaker failure
• Mitral valve prolapse
• Prolonged Q-T interval syndromes
• Sick sinus syndrome
• Drug toxicity: digitalis, quinidine,
procainamide, propranolol, phenothiazines,
tricyclic antidepressants, potassium
*Reprinted with permission from Huijbregts P,
Vidal P.6 Copyright 2004, Journal of Manual and
Manipulative Therapy.
Table 4. Diagnostic Criteria for Migraine Without and With Aura60
Migraine Without Aura
A. At least 5 attacks fulfilling criteria B and D
B. Headache attacks lasting 4 to 72 hours (untreated or
unsuccessfully treated)
C. Headache has at least 2 of the following
characteristics: unilateral location, pulsating quality,
moderate or severe pain intensity, aggravation by or
causing avoidance of routine physical activity
D. During headache, at least 1 of the following: nausea
or vomiting, photophobia, phonophobia
E. Not attributed to another disorder
Benign paroxysmal vertigo of childhood
This condition is a childhood periodic syndrome that
is a common precursor of migraine in later life, and it is,
therefore, because of proposed shared pathophysiology,
classified with migraine as a form of cerebrovascular
presyncope.60 Benign paroxysmal vertigo of childhood
is characterized by brief, recurrent attacks of vertigo
that occur without warning and resolve spontaneously
in otherwise healthy children. It is often associated with
nystagmus and vomiting. Unilateral throbbing headache
occurs at times. The International Headache Society has
provided diagnostic criteria (Table 5).60
Takayasu disease
Takayasu disease is most common in women of Asian
descent. Presyncope can occur after exercise, standing,
or head movement and is associated with impaired vision
and confusion. The disease is also known as pulseless
disease because brachial artery pulsations are absent or
decreased.43
Carotid sinus syndrome
Carotid sinus syndrome is relatively rare. It occurs in
men twice as frequently as in women. Patients are usually
over the age of 60. Propranolol, digitalis, and methyldopa
seem to predispose patients to this syndrome. Pressure on
the carotid sinus due to a tight collar or local neck tumor
will cause vagal stimulation leading to bradycardia and
subsequent syncope.43
Orthostatic hypotension
Orthostatic hypotension may occur in teenagers, but
it is most common in the sixth and seventh decades of
Table 5. Diagnostic Criteria for Benign Paroxysmal Vertigo of Childhood60
A. At least 5 attacks fulfilling criterion B
B. Multiple attacks of severe vertigo, occurring without warning and resolving spontaneously after minutes to
hours
C. Normal neurologic examination and audiometric and vestibular function between attacks
D. Normal electro-encephalogram
11
Migraine With Aura
A. At least 2 attacks fulfilling criteria B
B. Migraine aura with criteria with regard
to symptoms and time of occurrence and
duration specific to 6 subforms
C. Headache may or may not satisfy criteria
B, C, and D from “migraine without aura”
column; typical aura without headache not
associated with headache
D. Not attributed to another disorder
life. It occurs more often in men than in women. Syncope
and presyncope happen when rapidly rising to a standing
position, standing motionless for prolonged periods, and
standing after prolonged recumbency. The pathophysiol-
ogy of orthostatic hypotension usually involves reduced
blood volume or autonomic nervous system dysfunc-
tion.41,43 Table 6 lists causes of orthostatic hypotension.
Hyperventilation
Hypocapnia is the pathophysiological cause for pre-
syncope in patients with hyperventilation. It induces ce-
rebral vasoconstriction resulting in central nervous system
hypoperfusion. Patients are usually women between the
ages of 20 and 40. Other symptoms include lightheaded-
ness, shortness of breath, perioral numbness and pares-
thesia, and muscular twitching. Hyperventilation-induced
presyncope commonly occurs when supine and can be
brought on by asking the patient to hyperventilate.43
Cough-related syncope
Cough syncope is immediately preceded by coughing,
which need not be prolonged. It occurs mainly in middle-
aged men with a history of chronic obstructive pulmonary
disease. There are no prodromal symptoms. Syncope (and
presyncope) may be caused by an increase in intracranial
pressure due to coughing with resultant cerebral hypoper-
fusion. Cough-induced presyncope may occur when the
patient is supine and may be reproduced by asking the
patient to cough.43
Micturition syncope
Micturition-induced presyncope occurs almost exclu-
sively in men; episodes occur mainly at night and they oc-
Table 6. Causes of Orthostatic Hypotension* esophageal lesions (diffuse esophageal spasm, achalasia,
Hypovolemia or hemorrhage hiatal hernia, diverticula, and stricture).61
Addison disease
Drug-induced hypotension Hypoglycemia
• Antidepressants Presyncopal dizziness may also be the result of a
• Antihypertensives hypoglycemic reaction. Asking the patient whether the
• Bromocriptine dizziness occurs mainly when he or she has not eaten
• Diuretics may clue in the clinician to hypoglycemia as a cause
• Levodopa for dizziness. Polyuria (excessive urination), polydipsia
• Monoamine oxidase (MOA) inhibitors (excessive thirst), polyphagia (excessive hunger), weight
• Nitroglycerin loss, and fatigue may be diagnostic indicators for patients
• Phenothiazines with undiagnosed diabetes.62
Polyneuropathies
• Myeloid neuropathy Brainstem Hypoperfusion
• Diabetic neuropathy Selective hypoperfusion of the brainstem is the result
• Guillain-Barré syndrome of compromise or disease processes in the vertebrobasilar
• Porphyric neuropathy system.
• Vincristine neuropathy
Other neurologic disorders Vertebrobasilar insufficiency
• Idiopathic orthostatic hypotension Vertebrobasilar insufficiency is characterized by diz-
• Multiple sclerosis ziness symptoms associated with focal neurologic abnor-
• Parkinsonism malities of sudden onset and brief duration (seconds to
• Posterior fossa tumor minutes) that relate to the specific areas supplied by the
• Shy-Drager syndrome vertebrobasilar vessels.44,53,63 Terrett64 provided us with
• Spinal cord injury with paraplegia a useful mnemonic for signs and symptoms associated
• Surgical sympathectomy with VBI (Table 7). Van der Velde53 suggested classifying
• Syringomyelia dizziness caused by VBI as a positional-type dizziness
• Syringobulbia to distinguish it from the positioning-type dizziness pro-
• Tabes dorsales (syphilis) duced by BPPV and cervicogenic dizziness. Dizziness,
• Wernicke encephalopathy and other symptoms, will increase in patients with VBI
Cardiovascular disorders when maintaining the head in the provocative position
Prolonged bed rest or immobilization in contrast to the latter 2 pathologies where symptoms
are provoked by positioning but adapt when the head is
*Reprinted with permission from Huijbregts P, maintained in the provocative position. Table 8 provides
Vidal P.6 Copyright 2004, Journal of Manual and characteristics helpful for the differential diagnosis of
Manipulative Therapy. these 3 conditions.
Vertebrobasilar insufficiency may be caused by intrin-
sic or extrinsic mechanical disorders.63 Atherosclerosis,
cur before, during, or after micturition. Peripheral blood thromboembolic events, and arterial dissections are
pooling, vagus-induced bradycardia, and prolonged examples of intrinsic mechanical disorders.63-65 Anoma-
recumbency are likely responsible.43
Table 7. Five D’s and Three N’s*
Glossopharyngeal neuralgia
Syncope in glossopharyngeal neuralgia is the result of Dizziness
a glossopharyngeal-vagal reflex circuit causing transient Drop attacks
bradyarrhythmia that results in cerebral hypoperfusion. Diplopia
Ventricular asystole, sinus bradycardia, and atrioven-
Dysarthria
tricular block correlated with swallowing have all been
described. This syndrome is also known as deglutition Dysphagia
syncope, swallow syncope, or syncopal dysphagia.61 Ataxia of gait
Glossopharyngeal neuralgia is rare; symptoms include Nausea
paroxysmal pain in the tonsillar pillar or the external ear Numbness
canal during swallowing, talking, or coughing.43 Dizzi- Nystagmus
ness, lightheadedness, confusion, or fainting on swal-
lowing can also occur. Medications that increase atrio- *Reprinted with permission from Huijbregts P,
ventricular block (eg, digoxin, calcium channel blockers, Vidal P.6 Copyright 2004, Journal of Manual and
and beta-blockers) may increase symptoms. Many pa- Manipulative Therapy.
tients with glossopharyngeal neuralgia have identifiable

12
Table 8. Differential Diagnostic Characteristics of Cervicogenic Dizziness, Benign Paroxysmal Positional Vertigo, and
Vertebrobasilar Insufficiency8,53,64*
Vertigo Type Nystagmus Characteristics Associated Signs and Symptoms
Cervicogenic Positioning-type • No latency period • Nystagmus
Dizziness • Brief duration • Neck pain
• Fatigable with repeated motion • Suboccipital headaches
• Cervical motion
abnormality
Benign Paroxysmal Positioning-type • Short latency: 1 to 5 seconds • Nystagmus
Positional Vertigo • Brief duration: less than 30
seconds
• Fatigable with repeated motion

Vertebrobasilar Positional-type • Long latency: 55 ± 18 • Dizziness

Insufficiency seconds8 • Drop attacks
• Increasing symptomatology • Diplopia
with maintained head position • Dysarthria
• Not fatigable with repeated • Dysphagia
motion • Ataxia of gait
• Nausea
• Numbness
• Nystagmus

*Reprinted with permission from Huijbregts P, Vidal P.6 Copyright 2004, Journal of Manual and Manipulative Therapy.

lous soft tissue structures, such as bands of the deep
cervical fascia, or compression of the vertebral artery
between the longus colli and anterior scalene muscles
are examples of extrinsic mechanical disorders.63 Osteo-
phytes laterally projecting from the uncinate processes
and backward bending of the upper cervical spine in
the forward head posture may also cause mechanical
compression.65 Additionally, vertebral artery occlusion
may result following acute cervical spine trauma, caus-
ing fracture and dislocation.66
The nystagmus in patients with VBI may be vertical,
implicating the central vestibular structures affected by
this ischemic process.67 When syncope occurs, recovery
is frequently prolonged (30 to 60 minutes or longer).43
Patients may report symptoms following cervical ma-
nipulation, but symptoms have also been reported after
activities such as a shampoo treatment at the hair salon,
yoga exercises, painting a ceiling or wall, changing a
light bulb, turning the head when backing up the car,
giving birth, having surgery, hanging the wash, archery,
swimming, Tai Chi, sexual intercourse, and wrestling.64,68
Terrett64 provided a comprehensive overview of all
reported nonmanipulative causes of VBI. A position of
rotation or extension is frequently implicated in causing
VBI. However, even in a patient with mechanical disor-
ders of the vertebral artery, this position need not result
in symptoms due to compensation by the collateral
circulation, namely the opposite vertebral artery and
the carotid arteries.63 Symptoms of VBI are more likely
to occur when the collateral circulation is concurrently
compromised.63 The previous monograph has discussed
in more detail the role of the vertebral artery in producing
dizziness.
Vertebrobasilar infarction
Recurrent vertebrobasilar ischemic attacks lead to
stroke in 20% of patients.43 Stroke can develop acutely or
subacutely after arterial wall damage due to a combina-
tion of vasospasm, thrombus formation, thromboemboli-
zation, and the formation of a dissecting aneurysm.64 Due
to its association with cervical manipulation and other
nontraumatic causes, but also because of the contrain-
dication to further manipulative treatment and the need
for medical referral, knowledge of signs and symptoms
of a dissecting aneurysm is important. A sudden onset
of severe neck and occipital pain is the hallmark of dis-
section of the vertebral artery.69,70 Vertigo, unilateral facial
paresthesia, cerebellar signs, and visual field defects may
also be present.69 It is sobering to realize that the sudden
onset of neck and occipital pain may, in fact, be the com-
plaint for which a patient with arterial dissection seeks
physical therapy intervention.
Vertebrobasilar infarction will produce signs and
symptoms based on the area cut off from its vascular sup-
ply. Presyncopal dizziness in an acute cerebellar infarc-
tion is accompanied by unilateral sensorineural hearing
loss and nystagmus with occlusion of a branch from
either the basilar artery or the anterior inferior cerebellar
artery, called the internal auditory artery, which supplies
the vestibulocochlear nerve.43 Acute proximal vertebral
artery occlusion may result in Wallenberg syndrome,
combining presyncopal dizziness with vertigo, vomiting,

13
nausea, dysphagia, hoarseness, nystagmus, ipsilateral
Horner syndrome, sensation loss in the face, limb ataxia,
and loss of light touch and position sense in the limbs.
Cerebellar infarction due to occlusion of the anterior
inferior cerebellar artery, posterior inferior cerebellar ar-
tery, or superior cerebellar artery all result in ipsilateral
limb ataxia and hypotonia. Other symptoms and signs
include headache, nausea, vomiting, vertigo, nystagmus,
dysarthria, ocular or gaze palsies, facial weakness or
sensory loss, contralateral hemiparesis, and hemisensory
deficit.43
Basilar-type migraine
Basilar-type migraine is a subtype of migraine with
an aura that indicates involvement of the brainstem or
both hemispheres simultaneously. Average duration of
symptoms is 20 to 30 minutes and symptoms can be
relieved by sleep. The most common symptoms include
bilateral visual and sensory disturbances, changes in
consciousness and mood, and vertigo.71 As basilar artery
involvement is uncertain, the International Headache So-
ciety has suggested using the name basilar-type migraine
rather than basilar or basilar artery migraine. It is distinct
from vertebrobasilar migraine (discussed below) by its
absence of motor deficits. Basilar-type migraine most
commonly occurs in young adults. Many patients also
report migraine episodes with a more typical aura. The
International Headache Society has provided diagnostic
criteria for basilar-type migraine (Table 9).60 It is suggested
that in the presence of motor symptoms, patients should
be classified under sporadic or familial hemiplegic mi-
graine.60
Vertebrobasilar migraine
This pathology usually affects young women with
prolonged attacks (up to 72 hours) consisting of intense
vertigo, vomiting, dysarthria, and limb and perioral
paresthesia. Transient quadriplegia, fainting, confusion,
and stupor for a period of hours can occur during an
attack but are rare. A visual aura may occur preceding
the attack, and an attack may be followed by an occipi-
tal-region headache. A family history of migraine and a
correlation of attacks with the menstrual period are diag-
nostic indicators.57 This type of migraine is not part of the
International Headache Society classification, and due to
the duration of symptoms, it would not seem to fit any of
the diagnostic categories.60
Vestibular migraine
Dieterich and Brandt72 reported on 90 patients with
episodic vertigo for whom they were able to substantiate
a diagnosis of migraine. The disease was characterized
by rotational or translational vertigo lasting from a few
seconds to several hours or even days. Duration of a
few minutes or several hours was most common. Most
patients (78%) only noted vertigo; 16% also had auditory
symptoms. In 32% of patients there was no headache.
In the symptom-free intervals, 66% of patients showed
oculomotor abnormalities including dysfunction in verti-
cal or horizontal saccadic pursuit and gaze-evoked, po-
sitional, and spontaneous nystagmus. Initial presentation
could occur at any age. Prevalence in men was highest
in the fourth decade and in women from the third to the
fifth decade. Because of the duration of symptoms and
predominantly monosymptomatic aura, most patients
did not fit the International Headache Society criteria,
leading the authors to propose a diagnostic entity of
vestibular migraine. Lempert and Neuhauser73 have
suggested the name migraine-associated vertigo based
on the presence of signs and symptoms indicative of an
underlying causative migraine disorder.
Subclavian steal syndrome
This syndrome results from retrograde flow in the
vertebral artery and subsequent brainstem hypoperfusion
due to subclavian or innominate artery stenosis.43 In the
subclavian steal syndrome, blood passes from the verte-
bral artery into the distal subclavian artery with physical
activity of the ipsilateral arm.74 Symptoms include ver-
tigo, diplopia, limb paresis, arm fatigue, paresthesia, and
ataxia, all of which are more common than presyncope.43
Symptoms are brought on by arm exertion, not head or
neck movements, allowing for differential diagnosis with,
for example, VBI.74
DYSEQUILIBRIUM
As discussed earlier when we introduced the 4-cat-
egory diagnostic classification system for the diagnosis
of patients complaining of dizziness, dysequilibrium is a
sense of imbalance without associated vertigo.

Table 9. Diagnostic Criteria for Basilar-type Migraine60

A. At least 2 attacks fulfilling criteria B, C, and D

B. Aura consisting of at least 2 of the following fully reversible symptoms but no motor weakness: dysarthria, vertigo,
tinnitus, hypacusia, diplopia, visual symptoms simultaneously in both temporal and nasal fields of both eyes,
ataxia, decreased level of consciousness, simultaneous bilateral paresthesia
C. At least 1 of the following: at least 1 aura symptom develops gradually over ≥5 minutes, different aura symptoms
occur in succession over ≥5 minutes, or both; each aura symptom lasts ≥5 and ≤60 minutes
D. Headache fulfilling criteria B, C, and D from “migraine without aura” column (Table 4) that begins during the aura
or follows the aura within 60 minutes
E. Not attributed to another disorder

14
Visual Impairment
We already discussed the gaze-related palsies and
decreased gaze fixation related to vestibular, cerebellar,
and brainstem lesions. More germane changes, such as
decreased visual field, visual acuity, and depth percep-
tion, may also produce dysequilibrium and subsequent
complaints of dizziness.75
Somatosensory Impairment
Somatosensory deficits result from pathologies that
cause sensory ataxia. These pathologies can be classified
as polyneuropathies, myelopathies, or a combination
of both. Table 10 reviews causes of sensory ataxia. My-
elopathy and cervicogenic dizziness are most relevant to
orthopaedic physical therapy practice. Mal de debarque-
ment syndrome is another pathological entity that may
fall into this category. We discussed cervicogenic dizzi-
ness in detail in the beginning of this monograph.
Myelopathy
Table 10 also provides an overview of pathologies
associated with spinal cord compression. Cord compres-
sion can occur in the cervical, thoracic, and high lumbar
regions of the spine. With obvious variations in presen-
Table 10. Causes of Sensory Ataxia*
tation depending on the segmental level of spinal cord
compromise and the amount of compromise, spinal cord
compression may result in76-78:
• Variable upper limb, lower limb, neck, and trunk
pain
• Sensory impairment of the upper and lower limbs not
limited to a single dermatome
• Nonmyotomal arm or leg weakness
• Velocity-dependent limb hypertonia
• Upper motor neuron signs in the extremities: hyper-
reflexia, positive Babinski sign and Hoffman reflex,
gait ataxia, and spastic bladder
Atrophy of the intrinsic hand muscles is the result
of segmental necrosis of anterior horn cells in patients
with cervical myelopathy.76,78 Anterior horn cell necrosis
usually occurs at the level of compression. Myelopathic
hands result from compression of the C8-T1 nerve levels
at the C6-C7 spinal level because of the oblique course
of the cervical nerve roots. Cord compression can also
result from interactions with the musculoskeletal system.
This indicates a possible need for range-of-motion and
provocative (ie, spinal arthrogenic instability) testing; the
cervical spine has especially been implicated due to a
combination of degenerative stenosis, instability, and a
physiological narrowing of canal diameters in backward
bending.79

Polyneuropathy or Myelopathy Landsickness and mal de debarquement syndrome

• Friedreich ataxia Motion sickness is common and likely the result of a
• Neurosyphilis (tabes dorsalis) mismatch between visual, vestibular, and somatosensory
• Nitrous oxide afferent input during exposure to motion. Landsickness
• Vitamin B12 deficiency or post-motion vertigo refers to inappropriate sensations
• Vitamin E deficiency of movement after exposure to motion. An incidence
Polyneuropathy of landsickness of 73% has been reported in healthy
• Autosomal-dominant sensory ataxic crewmen of seagoing vessels. The duration of symptoms
neuropathy ranged from 1 minute to 2 days, with 88% of subjects
• Cis-platinum use noting symptoms for less than 6 hours.80
• Dejerine-Sottas disease Mal de debarquement syndrome is defined as land-
• Diabetes sickness lasting greater than 1 month.80 Information on
• Diphtheria mal de debarquement syndrome is limited, but it seems
• Hypothyroidism to occur predominantly in middle-aged women after a
• Immune-mediated neuropathies sea voyage or air or train travel. Symptoms are mostly
• Isoniazid constant but can be intermittent and include a rocking
• Paraneoplastic sensory neuronopathy or swaying sensation and imbalance. A sensation of tilt-
• Pyridoxine ing and ear symptoms including a sensation of fullness,
• Refsum disease tinnitus, hyperacusis, ear pain, and decreased hearing
• Taxol occur in about half of patients. Nausea and headache
Myelopathy are less common and vertigo is rare. Provoking factors
• Acute transverse myelitis include further motion exposure, anxiety and stress,
• AIDS (vacuolar myelopathy) rapid head movement, and positional changes. Symp-
• Multiple sclerosis toms of headache, tilting, and ear symptoms were nega-
• Tumor or cord compression tively related to the duration of mal de debarquement
• Vascular malformations syndrome (ie, were less frequent with longer duration).
Otolith dysfunction and a persistent adaptation of the
*Reprinted with permission from Huijbregts P, central nervous system to altered afferent input have
Vidal P.6 Copyright 2004, Journal of Manual and been suggested in the etiology of mal de debarquement
Manipulative Therapy. syndrome.80 Limited evidence exists of a moderate effect
of physical therapy consisting of vestibular habituation

15
and postural control exercises.81 A link with Ménière
disease, psychological abnormalities, and migraine has
not been established.80
Musculoskeletal Impairment
The musculoskeletal system is the effector organ of
the balance control systems. Decreased muscle strength
and endurance, decreased joint range of motion and sta-
bility, increased through-range resistance of joints, and
posture negatively affecting the location of the center
of gravity in relation to the base of support can all have
a negative effect on balance and may contribute to a
sense of dysequilibrium for which the patient will seek
our assistance. This provides the indication for a com-
prehensive evaluation of musculoskeletal impairment in
the differential diagnostic process of patients complain-
ing of dizziness.
Basal Ganglia Impairment
Parkinsonism is common, especially in older
adults.41,43 It occurs in all ethnic groups with an ap-
proximately equal distribution among men and women.
Clinical findings include tremor, rigidity, hypokinesia,
and gait and postural abnormalities.43 The characteristic
forward bent posture negatively affects the location of
the center of gravity in relation to the base of support.
The characteristic festinating gait with short, shuffling
steps that become successively more rapid can further
contribute to a sense of imbalance.41 Phenothiazines,
butyrophenones, metoclopramide, reserpine, and tet-
rabenazine are drugs associated with a reversible par-
kinsonian syndrome. Manganese dust, carbon disulfide,
and carbon dioxide poisoning can also result in Parkin-
sonism. Use of the illicit meperedine-analog Angel Dust
can also cause Parkinsonism.43 We earlier mentioned
parkinsonism as a cause for presyncopal dizziness due
to orthostatic hypotension (Table 6).
OTHER DIZZINESS
As discussed above, other dizziness is dizziness de-
scribed as a vague or floating sensation with the patient
having difficulty describing the sensation.31 Other diz-
ziness may be associated with anxiety and depression.
In fact, psychiatric disorders are considered the primary
cause of this subtype of dizziness, accounting for about
10% to 25% of all dizziness cases.31 Yardley et al82 found
a significantly higher rate of psychiatric disorders in
primary care patients who complained of dizziness as
compared to age-matched controls who did not com-
plain of dizziness. In older adults, anxiety, depression,
and adjustment reactions were factors contributing to
dizziness.83 Tilting of the environment also falls under
the other dizziness subtype.
Psychogenic Dizziness
We will discuss 2 types of psychiatric disorders fre-
quently associated with dizziness: panic disorder and
phobic postural vertigo.
16
Panic disorder
Panic disorder is a chronic illness characterized by so-
matic and psychological complaints (Table 11).50,84 This
disorder occurs in 1 of 75 persons worldwide and can
be either inherited (incomplete autosomal dominance)
or acquired.50 It accounts for 15% of all medical visits
and has been reported to average 10 different physician
evaluations before it is correctly diagnosed.50 Patients
with panic disorder are thus 7 more times likely to be
high users of health care.50 Work disability is also com-
mon in panic disorder.50 Additionally, panic disorder is
associated with significantly increased risk of suicide,
increased cardiovascular morbidity, and, if left untreated,
increased occurrence of stroke.85 Patients who suffer from
panic disorder usually have an abrupt onset of fear or
discomfort that peaks in approximately 10 minutes.50 It
is accompanied by at least 4 of the signs and symptoms
listed in Table 11. Correct diagnosis also requires that
panic attacks either recur unexpectedly every 2 weeks or
that a single attack be followed by at least 1 month of the
following symptoms50:
• Persistent concern about future attacks
• Worry that attacks will cause physical illness or insan-
ity
• Significant changes in behavior related to the attacks
Phobic postural vertigo
Phobic postural vertigo may be the second most com-
mon cause of patient complaints of dizziness after BPPV,
and it seems to be associated with somatization as well
Table 11. Diagnosis of Panic Disorder*
Signs and symptoms (diagnosis requires 4):
• Sweating
• Rapid heart rate, palpitations, pounding heart
• Tremor
• Shortness of breath
• Feeling of choking
• Chest pain
• Nausea or abdominal distress
• Dizziness
• Lightheadedness
• Feeling of unreality
• Fear of losing control
• Fear of dying
• Paresthesia
• Hot flashes
Associated signs and symptoms
• Anxiety
• Depression
• Insomnia
• Chronic fatigue
• Gastroesophageal reflux
*Reprinted with permission from Huijbregts P,
Vidal P.6 Copyright 2004, Journal of Manual and
Manipulative Therapy.
as compulsive, depressive, and anxiety disorders.86 The
diagnostic criteria for phobic postural vertigo consist of86:
• Vertigo and subjective complaints of dysequilibrium
in the absence of findings from neurologic or balance
examination
• Description of fluctuating dysequilibrium with stand-
ing or walking and paroxysmal fear of falling without
actual falls
• Description of feelings of anxiety and sympathetic
symptoms during or shortly after attacks or vertigo
without accompanying anxiety
• Provocation of dizziness in situations commonly
implicated in other phobic syndromes (eg, crossing
bridges, driving a vehicle, being in empty spaces or
among large numbers of people)
• Premorbid compulsive personality traits and depressive
characteristics
• Initial onset of symptoms related to vestibulopathy or
external stressors
Tilting of the Environment
Tilting of the environment is a rare form of dizziness at-
tributed to otolith dysfunction. The function of the otoliths
(utricle and saccule) is to provide sensory information on
linear motion and acceleration in the horizontal and verti-
cal directions, respectively. They also provide information
on static head tilt due to the presence of the otoconia.
Tilting of the environment is probably caused by an imbal-
ance of otolith signals due to unilateral vestibular loss and
is enhanced when rapid perturbations of posture make
somatosensory cues difficult to interpret.87 This asym-
metry in otolith input to the vestibular nuclei causes the
individual to sense a tilt of the environment to the side of
the involved inner ear.87,88 As the symptom is tilting of the
environment, and not spinning or rotating, this asymmetry
of otolith input is not classified under vertigo, despite it
being a vestibular disorder. Tilting of the environment
leading to a sudden fall has also been referred to as a drop
attack.89 Drop attacks associated with vestibular disorders
usually occur in the later stages of Ménière disease and
are called otolithic crises of Tumarkin.89,90 An increase in
endolymphatic pressure causes physical distention and
mechanical disruption of the otolith organs, causing a
sudden sense of tilting or falling.89 Otolithic crises of Tu-
markin occur without warning and are not associated with
vertigo, loss of consciousness, numbness, or paralysis.89
We previously discussed drop attacks associated with VBI
(Table 7).
The symptom of tilting of the environment may be
rare due to central compensation and substitution from
the visual and somatosensory systems.91 Additionally, roll
tilt illusion and linear acceleration perception deficit due
to unilateral vestibular loss are generally experienced
only within the first few hours or up to 1 week following
onset.91
Tilting of the environment is another form of dizziness
that tends to challenge the diagnostic classification system
introduced in this monograph. Ischemia or infarction in
17
the vertebrobasilar system and its branches unilaterally
affecting the vestibular nuclei, the medial longitudinal
fascicle, other nuclei involved in the vestibular mecha-
nism, or the thalamus can also result in a patient report-
ing a subjective tilt of the visual vertical axis in a frontal
plane.92
PHYSICAL THERAPY VERSUS MEDICAL DIFFERENTIAL
DIAGNOSIS
We discussed above a 4-category diagnostic clas-
sification system to facilitate the differential diagnosis
of patients with a complaint of dizziness. It should be
obvious that many of the pathologies discussed above
require medical evaluation and management rather than,
or in addition to, physical therapy evaluation and man-
agement. Also, many tests and measures that are needed
for a full differential diagnostic work-up of patients pre-
senting with dizziness are clearly outside of the physical
therapy scope of practice. It is the role of the physician
to play the lead role in this comprehensive medical dif-
ferential diagnostic process.
However, there is mounting evidence that conserva-
tive measures as provided by the physical therapist may
be beneficial for a select subset of patients with dizzi-
ness. Repositioning maneuvers may decrease symptoms
in patients with BPPV involving the posterior, horizontal,
and anterior SCCs.93-97 Manual physical therapy inter-
ventions may positively affect cervicogenic dizziness.35
Musculoskeletal impairments, such as decreased muscle
strength and endurance, joint stability and mobility, and
posture, which are implicated in patients with the dys-
equilibrium subtype of dizziness, are dysfunctions tra-
ditionally addressed by physical therapists.6 Habituation
exercises have proven beneficial for patients with acute
unilateral vestibular loss, and adaptation and balance ex-
ercises have produced positive outcomes in patients with
chronic bilateral vestibular deficits.95 Limited evidence
also exists of a moderate effect of vestibular habituation
and postural control exercises in patients with mal de de-
barquement syndrome.81 For the latter 3 patient groups,
physical therapy management is preceded by a medical
differential diagnostic work-up. An isolated otolith dys-
function may theoretically also be amenable to conserva-
tive management, but as no clinical tests exist to identify
this dysfunction, we cannot make any evidence-based
recommendations at this time. Table 12 provides signs
and symptoms indicative of the pathologies amenable to
sole physical therapy management.
The greatest danger for patients complaining of dizzi-
ness (and for the therapist managing such patients) is that
the therapist may fail to recognize signs and symptoms
that are indicative of a pathology requiring urgent medi-
cal or surgical management but that resemble pathology
amenable to sole physical therapy management.93 A
delayed medical diagnosis and delayed subsequent ap-
propriate medical or surgical management may prove
harmful in these cases.93 Therefore, the foremost goal
of physical therapy differential diagnosis for previously
Table 12. Signs and Symptoms Indicative of Pathologies Amenable to Sole Physical Therapy Management*
Benign • Intermittent, severe positioning-type dizziness
Paroxysmal • Precipitated by positioning, movement, or other stimuli (see below)
Positional • Short latency: 1 to 5 seconds
Vertigo (BPPV) • Brief duration: less than 30 seconds
• Fatigable with repeated motion
• Associated signs and symptoms: nystagmus, nausea, and at times vomiting
• Occurs in people over age 40 with peak incidence of onset in the sixth decade
• Rare in people under 20
• Medical history of head trauma, labyrinthine infection, surgical stapedectomy, chronic
suppurative otitis media, and degenerative changes to the inner ear may indicate nonidiopathic
BPPV
Posterior • Patients complain of dizziness when they quickly transfer to a supine position, especially when
Semicircular the head is turned to the affected side
Canal BPPV • Positive response of vertigo and apogeotropic torsional nystagmus on ipsilateral Hallpike-Dix
maneuver
Anterior • Patients also complain of dizziness when they quickly transfer to a supine position, especially
Semicircular when the head is turned to the affected side, but there is less specificity as to the direction of
Canal BPPV head rotation
• Bilateral positive response on Hallpike-Dix maneuver with vertigo and geotropic torsional
nystagmus on ipsilateral test
• Hallpike-Dix maneuver may also cause down-beating vertical nystagmus
• Positive response on straight head-hanging test
Horizontal • Dizziness is brought on when rolling over in supine but can also occur with flexion and
Semicircular extension of the head or when transferring from supine to upright
Canal BPPV • A bilaterally positive test with a purely horizontal nystagmus on Hallpike-Dix maneuver;
the nystagmus will be geotropic beating in the direction of the face turn or downside ear;
nystagmus will occur in both directions but is generally stronger when the head is turned
toward the affected side
• Positive roll test
• Positive walk-rotate-walk test to affected side
Cervicogenic • Intermittent positioning-type dizziness
Dizziness • Precipitated by head and neck movement
• No latency period: onset of symptoms is immediate upon assuming the provoking position
• Brief duration but may last minutes to hours
• Fatigable with repeated motion
• Associated signs and symptoms: nystagmus, neck pain, suboccipital headaches, sometimes
paresthesia in the trigeminal nerve distribution
• Possible lateral head tilt due to tightness of the sternocleidomastoid or upper trapezius
• Possible forward head posture
• Medical history of cervical spine trauma and degeneration
• Motion dysfunction in the upper cervical segments on active range-of-motion and passive
intervertebral motion testing
• Positive neck torsion test: nystagmus with reproduction of dizziness
Musculoskeletal • Subjective complaints of weakness, unsteadiness
Impairments • Insidious onset
• Postural deviations negatively affecting the location of the center of gravity in relation to the
base of support: trunk flexion, hip flexion, knee flexion, and ankle plantarflexion contractures
• Decreased trunk extension, hip extension, knee extension, and ankle dorsiflexion on range-of-
motion testing
• Loss of strength and endurance in antigravity muscles
• Impaired joint position sense lower extremity
*Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history
and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and
Manipulative Therapy.

18
undiagnosed patients complaining of dizziness should be
to distinguish between 2 groups of patients:
• Patients that may respond to conservative interven-
tions within the physical therapy scope of practice,
specifically patients with BPPV, cervicogenic dizzi-
ness, and musculoskeletal impairments leading to
dysequilibrium
• Patients that require referral for medical differential
diagnosis and medical or surgical comanagement
Below we will provide a template for the history
(Tables 13 and 14) and physical examination (Table 15)
relevant to the physical therapy differential diagnosis of
previously undiagnosed patients with a main complaint
of dizziness. Consistent with the foremost goal of this
physical therapy differential diagnostic process as iden-
tified above, we have provided in the text and tables
indications for when to refer the patient for medical or
surgical evaluation. In keeping with the evidence-based
practice paradigm, we have attempted to provide, where
available, data on reliability and validity of history items
and physical tests by way of a Medline search over the
period 1995 to April 2006 of English-language articles
with a title containing search terms relevant to these tests
and items. The complete list of search terms is available
upon request from the authors. In addition, we performed
a hand search of articles in our personal libraries. Our
recommendations for referral throughout the text are
based to the maximum extent possible on psychometric
properties of the tests and measures. However, data on
diagnostic accuracy of the history items and physical
tests are often absent, contradictory, or insufficient for
confident diagnostic decision making.
Table 13. Patient Self-report Intake Questionnaire*
Patient Name_________________________________________ Age__________ Gender M/F
MEDICAL HISTORY
Have you in the past been diagnosed with or do you currently have (check all that apply):
m Head trauma
m Neck trauma
m Inner or middle ear infection
m Middle ear surgery
m Inner ear degeneration
m Recent upper respiratory infection
m Recent bacterial infection
m Syphilis
m Tuberculosis
m Rheumatoid arthritis
m Crohn disease
m Polyarteritis (autoimmune disease affecting
the arteries)
m AIDS
m Recent chicken pox
m Recent mumps
m Recent poliomyelitis
m Mononucleosis (Epstein-Barr, mono)
19
The therapist should also be guided by an analysis
of the risk of harm to the patient should the therapist
decide not to refer. At times, it is better to refer the
patient and have the patient found normal than to not
refer and do potential harm. Considering the patholo-
gies possibly responsible for complaints of dizziness,
the potential for harm is real and present when working
with this population. Clearly documenting the reason
for a medical or surgical referral based on the infor-
mation presented in this article will clarify the need
for referral and allow for better communication with
our medical colleagues. Any uncertainty regarding the
proper diagnosis should result in referral. But even if
the signs and symptoms appear to fit with a diagnosis
amenable to sole physical therapy management, the
patient’s failure to respond to seemingly appropriate
conservative measures also indicates the need for a
medical second opinion.95
In summary, the decision to refer the patient for a
medical or surgical evaluation is based on our findings,
the interpretation of such findings in light of data on
diagnostic accuracy of history items and physical tests,
an analysis of the risk of harm to the patient, and the
response to seemingly appropriate intervention.
HISTORY
Our literature search located no studies that dis-
cussed the reliability or validity of history items. History
taking with patients complaining of dizziness is com-
plex. Table 13 provides a suggested patient self-report
intake questionnaire and Table 14 contains a template
for a structured interview.
m Recent viral infection
m Recent inoculation
m Multiple sclerosis
m Lung cancer
m Ovarian cancer
m Hodgkin disease (lymphatic cancer)
m Breast cancer
m Heart disease
m Chronic obstructive lung disease
m Atherosclerosis (hardening arteries)
m Thromboembolic disease (blood clots)
m Neck degeneration
m Recurrent episodes of vertebrobasilar ischemia
(limited blood supply to the brain)
m Visual impairments
m Migraine or migraine-related disorders
m Joint replacement in the leg
m Other orthopaedic surgical procedure
Table 13. Continued.

Have you recently:

m Been in contact with rodents (mice, guinea pigs, hamsters) m Gone flying
m Gone diving m Coughed, sneezed, or strained forcefully
m Gone for a long train ride m Lifted very heavy items
m Had your neck manipulated m Gone on a boat trip

Has a member of your family ever been diagnosed with or does a family member currently have
(check all that apply):
m Familial paroxysmal ataxia m Coronary artery disease
m Ménière disease m Peripheral vascular disease
m Otosclerosis m Spinocerebellar ataxia
m Migraine m Friedreich ataxia
m Vertebrobasilar migraine m Ataxia-telangiectasia

Have you used or are you currently using (check all that apply):
m Alcohol m Gentamicin m Phenytoin
m Amikacin m Heroin m Potassium
m Angel dust m Isoniazid m Procainamide
m Antidepressants m Kanamycin m Propranolol
m Antihypertensives m Levodopa m Pyridoxine
m Aspirin m Meprobamate m Quinidine
m Barbiturates m Methaqualone m Quinine
m Benzodiazepines m Methyldopa m Reserpine
m Bromocriptine m Metoclopramide m Streptomycin
m Butyrophenones m Monoamine oxidase (MOA) inhibitors m Taxol
m Cis-platinum m Nitroglycerin m Tetrabenazine
m Digitalis m Phencyclidine m Tobramycin
m Diuretics m Phenothiazines m Tricyclic antidepressants
m Ethchlorvynol

How many different medications are you using in total on a daily basis? ____________
Are you taking the medication as prescribed? Y/N

*Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history
and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and
Manipulative Therapy.

Symptoms indicating presyncopal and other dizziness may indicate

Symptom description
A description of dizziness symptoms may be help-
ful for initial classification into 1 of the 4 dizziness
subtypes of vertigo, presyncope, dysequilibrium, and
other dizziness. Vertigo is often described as a spinning
or rotating sensation, a sensation of self-movement or of
the environment moving, whereas patients with presyn-
copal dizziness complain of lightheadedness, a sense of
impending fainting, or tiredness. Patients with dysequi-
librium may complain of unsteadiness and weakness.
Patients who fall into the subtype of other dizziness may
report anxiety, depression, or fatigue. However, patients
commonly have difficulty describing their symptoms.
The above classification system is also challenged when
an individual complains of symptoms fitting more than
1 subtype, as may be the case in older adults with mul-
tisystem impairment.51 However, symptom description
the need for referral.
Vertigo
An illusion of rotary movement implicates the SCC.67
Rotary vertigo is a symptom in most peripheral ves-
tibulopathies. An illusion of linear movement, arguably
not true vertigo, indicates a lesion involving the otolith
organs but can also occur in patients with a perilym-
phatic fistula.67 Vertigo as a result of peripheral lesions
is often severe, intermittent in nature, and of a shorter
duration than vertigo due to a central lesion. A central
lesion often produces constant but less severe vertigo.43
Vertigo is a symptom in patients with BPPV, Ménière
disease, acute peripheral vestibulopathy, otosclerosis,
toxic vestibulopathies, and autoimmune disease of the
inner ear.43,57 It is less common in patients with cerebel-
lopontine angle tumors or acoustic neuropathy.43 Vertigo

20
Table 14. Patient History Form*†

Patient Name__________________________________________________________ Date______________________

Symptom description ______________________________________________________________________________

_________________________________________________________________________________________________
m Vertigo m Dysequilibrium
m Presyncopal dizziness m Other dizziness

Symptom onset m Sudden m Insidious________________________________________________________________

_________________________________________________________________________________________________
Precipitating factors m Constant m Intermittent m Episodic______________________________________________
_________________________________________________________________________________________________
m Transfer sitting to supine position m Prolonged standing
m Rolling over in supine m While recumbent and motionless
m Head flexion and extension m Wearing tight collar
m Transfer supine to sitting position m Hyperventilation
m Any head movement m Coughing
m Caffeine m Urination
m Exercise m Rapid rising from sitting
m Alcohol m Prolonged neck extension-rotation
m Emotional stimuli m Menstrual period
m Pain m Arm activity
m Fatigue m Anxiety
m Fear

Prodromal symptoms Y/N Duration__________________________________________________________________

m Lightheadedness m Tachycardia
m Pallor m Visual aura
m Salivation m Other neurological aura
m Blurred vision

Symptom latency Y/N Duration_____________________________________________________________________

Symptom duration m 30-60 sec____________________________________________________________________
Symptom fatigability Y/N__________________________________________________________________________
Associated symptoms
m Ataxia_____________________________________________________________________________________
m Hearing loss: m Sudden onset m Fluctuating m Progressive m Left m Right m Both____________________
m Tinnitus: m Left m Right m Both _____________________________________________________________
m Sensation of fullness in the ear: m Left m Right m Both____________________________________________
m Nausea____________________________________________________________________________________
m Vomiting___________________________________________________________________________________
m Dysarthria__________________________________________________________________________________
m Pain_______________________________________________________________________________________
m Headache in combination with neck pain m Tonsillar pillar or external ear pain with swallowing,
m Unilateral and pulsating headache talking, or coughing
m Sudden onset neck and occipital pain m Abdominal pain
m Chest, neck, and arm pain
m Sensory abnormalities_______________________________________________________________________
m Perioral numbness and paresthesia m Quadrilateral paresthesia
m Unilateral facial paresthesia m Trigeminal distribution paresthesia
m Strength___________________________________________________________________________________
m Facial weakness m Transient quadriplegia
m General fatigue m Arm fatigue-paralysis
m Chronic fatigue m Generalized arm and leg weakness

21
Table 14. Continued.

m Visual abnormalities___________________________________________________________________________
m Loss of color vision m Blurry vision
m Visual field deficits m Diplopia with head movement
m Constant diplopia m Photophobia
m Tilt illusion
m Mental and psychological status_________________________________________________________________
m Decreased cognition m Stupor
m Acute confusion m Anxiety
m Memory deficits m Depression
m Other________________________________________________________________________________________
m Diaphoresis m Coughing
m Hot flushed skin m Cyanosis
m Myoclonus m Edema legs
m Muscular twitching m Claudication
m Spastic bladder m Feeling of choking
m Discharge from the ear m Feeling of unreality
m Thirst m Fear of losing control
m Polyuria m Fear of dying
m Polyphagia m Insomnia
m Unexplained weight loss m Gastroesophageal reflux
m Palpitations m Drop attacks
m Shortness of breath m Remitting-relapsing neurological dysfunction

Current history_____________________________________________________________________________________
__________________________________________________________________________________________________
__________________________________________________________________________________________________
__________________________________________________________________________________________________
Diagnostic tests____________________________________________________________________________________
__________________________________________________________________________________________________
Occupation________________________________________________________________________________________
Leisure time________________________________________________________________________________________
Social history N/A __________________________________________________________________________________
General health Unexplained weight loss +/- Night pain +/- Consistent pattern of night pain +/- Loss of appetite +/-
Other_____________________________________________________________________________________________

*Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history
and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and
Manipulative Therapy.
†
Reason for referral indicated in italics.

may only be episodic in patients with a perilymphatic
fistula in case of a low-volume leak but can be severe
in patients with a large fistula.41 Vertigo also occurs in
the diseases causing brainstem hypoperfusion (eg, VBI,
vertebrobasilar infarction, basilar-type migraine, verte-
brobasilar migraine, vestibular migraine, and subclavian
steal syndrome).43,57,60,64,69,71,72 Any complaint of vertigo
other than intermittent, severe, rotary, short-lasting ver-
tigo likely indicates a need for referral.
Ataxia
Ataxia is a dyscoordination or clumsiness of movement
not associated with muscular weakness.43 It is a symptom
in patients with cerebellar tumors and subclavian steal
syndrome.43 Ataxia may affect gait in patients with hy-
pothyroidism, paraneoplastic cerebellar degeneration,
ataxia-telangiectasia, Arnold-Chiari malformation, VBI,
and myelopathy.43,64,76-78 Gait ataxia is the presenting
symptom in all patients with hereditary spinocerebellar
degenerations. It is also the most common finding in
patients with alcoholic cerebellar degeneration and the
presenting complaint in 10% to 15% of patients with
multiple sclerosis. Trunk ataxia is a symptom in patients
with ataxia-telangiectasia and Creutzfeldt-Jakob disease;
these 2 diseases also produce limb ataxia, as does para-
neoplastic cerebellar degeneration.43 In addition, 10%
of patients with Wernicke encephalopathy present with
ataxia of the arms while 20% present with ataxia affect-

22
Table 15. Patient Physical Examination Form*†‡

Patient Name___________________________________________________________ Date___________________

OBSERVATION
Skin m Red spider veins on ears and cheeks m Dry skin m Brittle hair m Lemon-yellow discoloration skin
m Papilledema m Clubbing fingernails m Trophic changes skin m Peripheral edema
Posture m Increased kyphoscoliosis m Craniocervical junction abnormalities m Lateral head tilt
m Forward head posture
Eyes m Pigmented corneal rings m Red spider veins corner of the eyes m Vertical misalignment L high
m Vertical misalignment R high m Horizontal misalignment m Horner syndrome
m Corrective lateral head tilt when covering one eye in case of vertical misalignment
Other________________________________________________________________________________________

VITAL SIGNS
Blood pressure m Arm systolic difference (≥45 mm Hg) +/-_______________________________________
Heart rate m Palpitations +/-______________________________________________________________
Sit-to-stand test m Blood pressure (decrease ≥20 mm Hg) +/- m Heart rate (increase ≥20 bpm) +/-
m Lightheadedness____________________________________________________________
Auscultation m Carotid bruit +/- m Cardiac abnormalities +/-____________________________________

GAIT ASSESSMENT____________________________________________________________________________
_____________________________________________________________________________________________
m Wide-based gait m Steppage gait
m Titubation m Improved gait with assistive device
m Unilateral deviation when walking a straight line m Difficulty with concurrent head rotation
m Unable to walk tandem gait m Wildly lurching without loss of balance

VESTIBULOSPINAL EXAMINATION
Single-leg stance m L ______sec m R ____sec_______________________________________________
Romberg m Eyes open________________________ m Eyes closed ______________________
Sharpened Romberg m Eyes open________________________ m Eyes closed ______________________
CTSIB m Level, eyes open___________________ m Level, eyes closed_________________
m Foam, eyes open___________________ m Foam, eyes closed_________________
Fukuda step test m Rotate >30° +/- m Rotate L/R m Forward displacement >50 cm +/-

CRANIAL NERVE EXAMINATION_______________________________________________________________

Cranial nerve Test L/R

I. Olfactory Identify different odors + -
II. Optic Test visual fields (confrontation method) + -
III. Oculomotor Upward, downward, and medial gaze + -
IV. Trochlear Downward and lateral gaze + -
V. Trigeminal Corneal reflex, face sensation, clench teeth + -
VI. Abducens Lateral gaze + -
VII. Facial Close eyes tight, smile, whistle, puff cheeks + -
VIII. Vestibulocochlear Hear watch ticking, hearing tests, balance tests + -
IX. Glossopharyngeal Gag reflex, ability to swallow + -
X. Vagus Gag reflex, ability to swallow, say “ahhh” + -
XI. Accessory Resisted shoulder shrug + -
XII. Hypoglossal Tongue protrusion (observe for deviation) + -

23
Table 15. Continued.

OCULOMOTOR EXAMINATION
Spontaneous nystagmus central gaze +/-________________________________________________________
m Jerk m Skew
m Pendular m Alternating m Periodic m Irregular
m Horizontal m L m R m Suppressed with visual fixation m Yes m No
m Vertical m Up-beating m Down-beating m Suppressed by convergence
m Torsional m Increased by fixation
Spontaneous nystagmus eccentric gaze +/-________________________________________________
m Increased with looking towards fast phase m Provoked on lateral or upward gaze
m Horizontal nystagmus m Small, unsustained eye movements at end range
Saccadic eye movements +/-______________________________________________________________
m Hypometria m Saccades during fixation on target
m Hypermetria m Oscillating horizontal saccades with gaze shift
m Horizontal saccades with vertical test
Smooth pursuit testing +/-________________________________________________________________

HEARING EXAMINATION
Weber test m Midline m L m R
Rinne test m Bone conduction > air conduction m Bone conduction ≤ air conduction

ACTIVE RANGE-OF-MOTION EXAMINATION Asterixis +/- Myoclonus +/- Chorea +/-______________________

_________________________________________________________________________________________________
_________________________________________________________________________________________________

LIMB ATAXIA EXAMINATION

Finger-to-nose test m Intention tremor L+/R+/- m Overshooting L+/R+/-
Finger-to-finger-test m Horizontal overshooting L+/R+/- m Vertical overshooting L+/R+/-
Heel-to-shin test m Intention tremor L+/R+/- m Overshooting L+/R+/-
Toe-to-finger test m Intention tremor L+/R+/- m Overshooting L+/R+/-
Dysdiadochokinesia m Finger tapping +/- m Pronation-supination +/- m Toe tapping +/-
Barre test L+/R+/-________________________________________________________________________________

PASSIVE RANGE-OF-MOTION EXAMINATION Hypotonia +/- Rigidity +/- Spasticity +/- Clonus +/-
_______________________________________________________________________________________________
_______________________________________________________________________________________________
Stability tests____________________________________________________________________________________
PPIVM/PAIVM__________________________________________________________________________________

STRENGTH EXAMINATION ______________________________________________________________________

_______________________________________________________________________________________________
_______________________________________________________________________________________________

REFLEX EXAMINATION Hoffman reflex L+/R+/- Babinski sign L+/R+/- DTR______________________________

_______________________________________________________________________________________________

SENSATION TESTS______________________________________________________________________________
m Joint position sense__________________________________________________________________________
m Vibration sense_____________________________________________________________________________

VERTEBROBASILAR EXAMINATION
De Kleyn-Nieuwenhuyse test L+/R+/-______________________________________________________
m Latency 0 _____sec m >60 sec m Vertical down-beating nystagmus
m Duration 0 ____ sec m Nonaccommodating m Other nystagmus
m Fatigable Y/N m Geotropic
m Horizontal nystagmus m Apogeotropic
m Torsional nystagmus

24
Table 15. Continued.

Sustained cervical rotation test L+/R+/-___________________________________________________________

m Latency 0 _____sec m >60 sec m Vertical down-beating nystagmus
m Duration 0 ____ sec m Nonaccommodating m Other nystagmus
m Fatigable Y/N m Geotropic
m Horizontal nystagmus m Apogeotropic
m Torsional nystagmus
Hautant test m Midrange +/- m Extension-rotation L+/R+/- m Latency with + extension-rotation position Y/N

VESTIBULO-OCULAR EXAMINATION
Dynamic visual acuity Decrease by ≥2 lines on Snellen chart +/-____________________________________
Autorotation test Inability to continue for 60 sec +/- <100 oscillations in 60 sec +/-____________________
Doll’s head test Catch-up saccades toward fixation target +/-________________________________________
Head-shaking nystagmus test +/ - m Nystagmus toward side of lesion m Nystagmus away from side of lesion
m Nonhorizontal nystagmus
Head thrust test +/- m Corrective saccade on head moving right m Corrective saccade on head moving left

BPPV EXAMINATION
Hallpike-Dix L+/R+/-___________________________________________________________________________
m Positive bilateral m L < R m L > R m Torsional nystagmus
m Latency 0 _____sec m >60 sec m Vertical down-beating nystagmus
m Duration 0 ____ sec m Nonaccommodating m Other nystagmus
m Fatigable Y/N m Geotropic
m Horizontal nystagmus m Apogeotropic
Straight head-hanging test +/-___________________________________________________________________
m Latency m _____sec m >60 sec m Torsional nystagmus
m Duration m ____ sec m Nonaccommodating m Vertical down-beating nystagmus
m Fatigable Y/N m Other nystagmus
m Horizontal nystagmus
Roll test +/-_________________________________________________________________________________
m L<R m Torsional nystagmus
m L>R m Vertical down-beating nystagmus
m Latency 0 _____sec m Other nystagmus
m Duration 0 ____ sec m Geotropic
m Fatigable Y/N m Apogeotropic
m Horizontal nystagmus
Walk-rotate-walk test L+/R+/-_________________________________________________________________

CERVICOGENIC DIZZINESS EXAMINATION

Neck torsion test L+/R+/-________________________________________________________________
m Latency m Immediate m_____sec m Torsional nystagmus
m Duration m ____ sec m Vertical down-beating nystagmus
m Fatigable Y/N m Other nystagmus
m Horizontal nystagmus

BREATHING-RELATED TESTS
Hyperventilation test m Dizziness +/- m Nystagmus +/- m Minimal latency +/- Latency _____sec
Valsalva test m Dizziness +/- m Nystagmus +/- m Minimal latency +/- Latency _____sec
Cough test m Dizziness +/-

*Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history
and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and
Manipulative Therapy.
†
Reason for referral indicated in italics.
‡
CTSIB indicates Clinical Test of Sensory Integration of Balance; PPIVM, passive physiological intervertebral motion;
PAIVM, passive accessory intervertebral motion; and BPPV, benign paroxysmal positional vertigo.

25
ing the legs.43 A patient report of ataxia confirmed by
physical tests indicates a need for referral.
Hearing loss
A sudden onset of unilateral deafness may be due
to labyrinthine artery infarction, possibly indicating an
infarction in the vertebrobasilar system.42 A rapid loss of
perilymphatic fluid due to a perilymphatic fistula will
produce hearing loss, but hearing may be normal in the
case of a low-volume leak.41 Ménière disease produces a
fluctuating low-frequency hearing loss, which is progres-
sive over multiple episodes.43,98 Autoimmune disease of
the inner ear also produces a fluctuating hearing loss.57
Progressive unilateral hearing loss is also a typical pre-
sentation of patients with acoustic neuromas.99 Hearing
loss is also a symptom in patients with acute labyrinthi-
tis, quinine or quinidine toxicity, salicylate overdosage,
Friedreich ataxia, otosclerosis, vestibulocochlear nerve
compression due to bacterial, syphilitic, or tuberculous
infection or due to sarcoidosis, Paget disease, diabetes
mellitus, hypothyroidism, and in 50% of patients treated
with the chemotherapeutic drug Cis-platinum.43,98 Any
previously undiagnosed complaint of hearing loss, espe-
cially when confirmed by physical tests, indicates a need
for referral.
Tinnitus
Tinnitus may occur in patients with Ménière disease
as does a feeling of fullness of the ear.41,43,98 Tinnitus
also occurs in patients with Cis-platinum and salicy-
late toxicity and in patients with familial paroxysmal
ataxia.43,57 Tinnitus can also be more benign, resulting
from increased tone in the tensor tympani muscle due to
trigeminal hyperactivity associated with an upper cervi-
cal injury.100 A complaint of tinnitus combined with aural
fullness, a positive medication history, or a family history
positive for familial paroxysmal ataxia indicates a need
for referral.
Nausea
Nausea is common in patients with BPPV, Ménière
disease, acute peripheral vestibulopathy, salicylate
overdosage, quinine or quinidine overdosage, cerebel-
lar tumors, Arnold-Chiari malformation, migraine, or
VBI.41,43,52,64 It can also be indicative of panic disorder.50,84
A positive family history for Ménière disease or a positive
medication history in combination with nausea indicates
a likely need for referral.
Vomiting
Vomiting may be a symptom for patients with Mé-
nière disease, acute peripheral vestibulopathy, salicylate
overdosage, quinine or quinidine overdosage, cerebellar
tumors, Arnold-Chiari malformation, and vertebrobasilar
migraine.41,43,57 The occurrence of vomiting in patients
with BPPV is rare.52,55 Vomiting, headache, ataxia, and
visual dysfunction are often the presenting symptoms
in children with primary cerebellar tumors and a clear
26
indication for referral.43 A complaint of vomiting with
dizziness may indicate a need to refer in adults and
constitutes a clear reason for referral in children.
Dysarthria
Dysarthria can be a symptom in patients with hy-
pothyroidism, paraneoplastic cerebellar degeneration,
Friedreich ataxia, ataxia-telangiectasia, Creutzfeldt-Jakob
disease, familial paroxysmal ataxia, VBI, Arnold-Chiari
malformation, and vertebrobasilar migraine.43,57,58,64 A
complaint of dysarthria indicates the need for referral.
Pain
Headache is a symptom in patients with cerebel-
lopontine angle and cerebellar tumors, salicylate over-
dosage, Arnold-Chiari malformation, familial paroxys-
mal ataxia, and cervicogenic dizziness.17,43,57 In fact,
a correlation between neck pain and dizziness is one
of the diagnostic criteria for cervicogenic dizziness.17
Suboccipital and neck pain described as a tight collar
and aggravated by neck movements and burning pain
along the ulnar arm may indicate posterior fossa mal-
formation with compression at the foramen magnum.58
A unilateral pulsatile headache may be indicative of
migraine.43,60 A sudden-onset neck and occipital pain is
the hallmark symptom of vertebral artery dissection.69,70
Occipital headache is a symptom of vertebrobasilar mi-
graine.57 Chest, neck, and arm pain or discomfort may
be symptoms implicating a cardiovascular etiology for
patients complaining of presyncopal dizziness.59 Chest
pain may also occur in patients with panic disorder.50,84
Paroxysmal pain in the tonsillar pillar or external ear
with swallowing, talking, or coughing implicates glos-
sopharyngeal neuralgia as a cause for presyncopal
dizziness.43,98 Variable patterns of arm, leg, and trunk
pain can be a symptom in patients with myelopathy.76-78
Abdominal pain may occur due to quinine or quinidine
toxicity.43 In the context of evaluating patients with diz-
ziness, any pain pattern other than those indicative of
cervicogenic dizziness-related neck pain and musculo-
skeletal pain possibly associated with musculoskeletal
impairments causing dysequilibrium indicates a need
for referral.
Sensory abnormalities
Perioral numbness and paresthesia are symptoms in
patients with hyperventilation but also occur in patients
with VBI.43,64 Limb paresthesia is also a symptom for pa-
tients with vertebrobasilar migraine.57 Bilateral or quad-
rilateral limb paresthesia, either constant or reproduced
or aggravated by neck movements, may indicate VBI.4
Arm paresthesia is common in patients with subclavian
steal syndrome.43 Nondermatomal sensory impairments
are indicative of myelopathy.76-78 Paresthesia along the
spine that occurs with neck and trunk flexion may indi-
cate a compressive lesion at the foramen magnum.58 Pe-
ripheral neuropathy in the lower extremities commonly
occurs in persons with diabetes, resulting in impaired
somatosensory function.101 Paresthesia in the trigeminal
nerve distribution may occur with cervicogenic dizzi-
ness, indicating involvement of the trigemino-cervical
nucleus.63 Trigeminal distribution (facial) and nonder-
matomal patterns of paresthesia indicate the need for
careful evaluation and possible referral.
Strength and endurance
Facial weakness is a symptom in patients with cer-
ebellopontine angle tumor and familial paroxysmal
ataxia.43,57 General fatigue occurs in patients with dia-
betes or cardiovascular etiologies for presyncopal dizzi-
ness complaints.59,62 Chronic fatigue is also a symptom
of panic disorder.50,84 Transient quadriplegia is a rare
symptom in patients with vertebrobasilar migraine.57
Ipsilateral arm fatigue or even paresis is indicative of
subclavian steal syndrome.43 Nonmyotomal weakness in
the legs and arms may indicate myelopathy; generally,
complaints of weakness may focus the clinician on a
musculoskeletal impairment as causative or contributory
to the patient’s complaint of dizziness or dysequilibrium.
Any weakness not directly related to a discrete musculo-
skeletal problem indicates a need for referral.
Visual abnormalities
Quinine and quinidine toxicity may cause vision
deficits, including the loss of color vision.43 Visual
dysfunction is often one of the presenting symptoms in
children with primary cerebellar tumors.43 Visual field
deficits may indicate vertebrobasilar infarction.69 Blurred
vision may be a prodromal symptom for vasovagal
syncope.41,43 Visual instability with head movement or
oscillopsia suggests an impaired vestibulo-ocular reflex
and is indicative of vestibular system involvement.102 A
tilt illusion or deviation of the subjective visual vertical
axis may indicate otolith dysfunction; however, it can
also be caused by ischemia or infarction in the vertebro-
basilar system and its branches, unilaterally affecting the
vestibular nuclei, the medial longitudinal fascicle, and
other nuclei involved in the vestibular mechanism, or
the thalamus.92 Nonvestibular disorders can also cause a
tilt illusion; third and fourth cranial nerve palsies may be
responsible for monocular tilts of the subjective visual
vertical.103 In general, nonvestibular causes for a tilt of
the subjective visual vertical result in minor and unpre-
dictable changes as compared to vestibular disorders.103
Otolith dysfunction or pathological processes in the oto-
lith-ocular reflex pathways involving central processes
can result in patients complaining of vertical diplopia or
sometimes diplopia, where one image is tilted in relation
to another.67 Diplopia is also a symptom in patients with
paroxysmal familial ataxia, VBI, and subclavian steal
syndrome.43,57,64 Visual auras can precede vertebrobasi-
lar migraine; 10% of patients with migraine experience
a visual or other neurological aura.43,57 Photophobia is
another symptom in patients with migraine.43 Any report
of visual abnormality, with the possible exception of
oscillopsia, indicates a need for referral.
27
Mental and psychological status
Changes in mental and psychological status may be
noted by the patient or by people close to the patient.
Dementia is a state in which there is a significant loss
of intellectual capacity and cognitive functioning, lead-
ing to impairment in social or occupational functioning
or both.104 Wilson disease, Creutzfeldt-Jakob disease,
hypothyroidism, paraneoplastic syndromes, and some
spinocerebellar degenerations may cause dementia in
association with ataxia. Dementia with sensory ataxia
may indicate neurosyphilis or vitamin B12 deficiency.
An acute confusional state with ataxia may occur with
alcohol, sedative, salicylate, or hallucinogen intoxica-
tion, or in patients with Wernicke encephalopathy.
Korsakoff anamnestic syndrome and cerebellar ataxia
are associated with chronic alcohol abuse. Lassitude
is common in patients with migraine.43 Confusion and
stupor can result from vertebrobasilar migraine.57 Anxiety
and depression may be indicative of dizziness due to
panic disorder.50,84 In one study, depression and panic
disorder were present in 50% of patients with initially
organic vestibular hypofunction 3 to 5 years after onset,
leading Tusa105 to suggest that psychological disturbances
that develop due to vestibular disorders may become the
primary cause of dizziness, replacing the initial organic
cause. Eckhardt-Henn et al86 reported that 15.8% of 190
patients complaining of dizziness fell into this category
of psychosomatic dizziness. Standardized measures with
established reliability and validity, such as the Mini-Men-
tal State Examination106 and the Beck Depression Inven-
tory107 may facilitate communication with a physician
when referring a patient for further medical evaluation.
Any noted mental or psychological abnormality indicates
the need for referral.
Other symptoms
Diaphoresis is a symptom in patients with acute
labyrinthitis, quinine or quinidine toxicity, and panic dis-
order.41,43,50,84 Patients with quinine or quinidine toxicity
may indicate hot and flushed skin.43 Fever is a symptom
of familial paroxysmal ataxia.57 Myoclonus may occur
in patients with Creutzfeldt-Jakob disease; hyperventila-
tion is associated with muscular twitching.43 A spastic
bladder can be caused by myelopathy.76-78 Patients with
undiagnosed skull fractures may note discharge from the
ear.43 Extrapyramidal signs and symptoms may occur in
Creutzfeldt-Jakob disease.43 Carpal tunnel syndrome,
myelopathy, and neuropathy may raise suspicion of
hypothyroidism in undiagnosed patients.43 The clinician
may suspect multiple sclerosis with a history of remitting
and relapsing dysfunctions in multiple locations in the
nervous system.43 Salicylate toxicity and diabetes melli-
tus may cause excessive thirst.43,62 The clinician may also
suspect undiagnosed diabetes in cases of polyuria, poly-
phagia, and unexplained weight loss.62 Palpitation and
shortness of breath are symptoms in both patients with
cardiovascular disease and panic disorder.50,59,84 Patients
with cardiovascular disease may also note coughing,
cyanosis, edema in the legs, and claudication,59 whereas
patients with panic disorder may complain of a feeling
of choking, a feeling of unreality, fear of losing control
or dying, insomnia, and gastroesophageal reflux.50,84
Unremitting hiccups may indicate a posterior fossa mal-
formation.58
Pettman4 noted that drop attacks, defined as buckling
of the legs in response to neck movements without loss
of consciousness, may indicate VBI. Due to the ischemic
etiology of VBI, the authors would expect true vertebro-
basilar compromise due to neck movement to have a slow
onset that is progressive with sustained neck position and
that causes presyncopal dizziness or actually results in
loss of consciousness. In the authors’ clinical experience,
a drop attack may occur with neck motion in patients
with traumatic, degenerative, or disease-related upper
cervical instability. Although the resultant shear forces
certainly would seem to have the potential of mechani-
cally compromising the vertebral artery, the typical drop
attack seems more likely related to cord compromise
in this region. With a patient report indicative of drop
attacks, we also need to consider a vestibular etiology
as discussed above. Vestibular drop attacks or otolithic
crises of Tumarkin occur without warning and are not as-
sociated with vertigo, loss of consciousness, numbness,
or paralysis.89 A patient report of any of the symptoms
above indicates the need for referral.
Symptom behavior
Symptom onset
The initial episode of Ménière disease has an
insidious onset, with the patient first noticing tinnitus,
hearing loss, and a sensation of fullness in the ear.43 Most
symptoms in patients with central vestibular disorders
are the result of slowly progressive pathologies and
thus have an insidious onset. The onset of symptoms in
patients complaining of dysequilibrium is also generally
insidious. The onset of dizziness and other symptoms is
sudden in patients with acute peripheral vestibulopathy,
aminoglycoside toxicity, labyrinthine damage due to
head trauma, and large perilymphatic fistulae, and in pa-
tients suffering subsequent attacks of Ménière disease.41,43
Presyncopal dizziness usually is sudden in onset when
precipitating activities are performed. Landsickness and
mal de debarquement syndrome are often brought on by
sea, air, or train travel.80 An abrupt onset is also charac-
teristic of patients with symptoms due to panic disorder.50
An insidious onset of vertiginous dizziness and an abrupt
onset of presyncopal or other dizziness indicate a need
for referral.
Precipitating factors
Dizziness is often constant in patients with central and
bilateral peripheral vestibular lesions.43,67 Other forms of
dizziness are intermittent and precipitated by positioning,
movement, or other stimuli. Patients with posterior SCC
BPPV complain of dizziness when they quickly transfer
to a supine position, especially when the head is turned
28
to the affected side.52 This also occurs in patients where
the anterior SCC is involved, but there is less specific-
ity as to the direction of head rotation.108 Dizziness is
brought on in patients with horizontal SCC BPPV when
rolling over in supine, but it can also occur with flexion
and extension of the head or when transferring from
supine to upright.56 Head movement may also provoke
symptoms in patients with cervicogenic dizziness.17
Dizziness in patients with otosclerosis may be po-
sitional but can also be constant.43 Attacks of familial
paroxysmal ataxia can be triggered by exercise, caffeine,
alcohol, or sudden movements.57 A vasovagal presyn-
cope can be brought on by emotional stimuli, pain, the
sight of blood, fatigue, medical instruments, blood loss,
or prolonged motionless standing,41,43 and it usually oc-
curs when the patient is in a sitting or standing position;
only very rarely is the patient recumbent.43,98 A patient
complaining of presyncopal dizziness while recumbent
or after physical exercise should be screened for a car-
diovascular etiology.43 Carotid sinus syndrome has been
related to wearing collars that are too tight or may be
due to local tumors in the neck pressing on the carotid
sinus.43,98 In patients with Takayasu disease, exercise,
standing, or head movements may bring on dizziness.43
Hyperventilation and coughing may bring on hyperven-
tilation and cough presyncope, respectively.43 Dizziness
due to micturition syncope may occur before, during, or
after micturition.43 Orthostatic hypotension-related diz-
ziness occurs when rapidly rising from a sitting position,
when standing up after prolonged recumbency, or after
prolonged motionless standing.41,43 A position of cervical
extension and rotation is often implicated as a trigger
for VBI.63 Neck manipulation has been associated with
cervical artery dissection (adjusted odds ratio 3.8; 95%
confidence interval 1.3-11).5 Vertebrobasilar migraine
occurs frequently during the menstrual period.57 Subcla-
vian steal syndrome produces symptoms with physical
activity of the ipsilateral arm.74 Stress, hyperventilation,
and anxiety can all produce the symptoms of dizziness
associated with panic disorder.50,84 Situations commonly
associated with other phobic syndromes (eg, large
crowds, open spaces, driving, or crossing a bridge) can
precipitate an attack of phobic postural vertigo.86 Dizzi-
ness described as tilting of the environment is aggravated
by rapid postural changes.87 Constant vertiginous dizzi-
ness or dizziness brought on by factors other than neck
or head movement indicate a likely need for referral.
Prodromal symptoms
Some pathology is characterized by prodromal symp-
toms, which occur after encountering the precipitating
stimulus but before the symptoms of dizziness. Prodromes
lasting 10 seconds to a few minutes and consisting of
lightheadedness, pallor, salivation, blurred vision, and
tachycardia often precede a vasovagal syncope.41,43 A
visual aura may precede migraine, basilar-type migraine,
and vertebrobasilar migraine;57,71 10% of patients with
migraine report a visual or other neurological aura.43
Any report of prodromal symptoms indicates a need for
referral.
Symptom latency
Symptom latency refers to the time lapsed between
exposure to the precipitating stimulus and the onset of
symptoms. Symptoms in patients with BPPV occur after
a latency period of 1 to 5 seconds.52,53 The latency pe-
riod in patients with VBI is long; Oostendorp8 reported a
latency period of 55 ± 18 seconds after assuming the De
Kleyn-Nieuwenhuyse test position. One could assume
that patients with subclavian steal syndrome also have
a longer latency period; sufficient ischemia needs to
develop before symptoms occur. Depending on the eti-
ology, a vertebrobasilar infarction may be rapidly or very
slowly progressive.64 Onset of symptoms is immediate in
patients with cervicogenic dizziness upon assuming the
provoking position.53 A prolonged latency period (more
than 60 seconds) indicates a likely need for referral.
Symptom duration
As noted before, dizziness symptoms in patients with
central vestibulopathies are generally less severe but
constant and prolonged; symptoms with peripheral ves-
tibulopathies are often severe but intermittent.43 Symp-
toms in patients with BPPV generally last less than 30
seconds but may occur for up to 60 seconds.53 Vertigo
may last from minutes to days in patients with Ménière
disease.41,43,98 In patients with acute peripheral vestibu-
lopathy, vertigo may be constant for up to 2 weeks.43
Symptoms in patients with familial paroxysmal ataxia
last from 15 minutes to several hours.57 The average
symptom duration for patients with basilar-type migraine
is 20 to 30 minutes.71 Symptoms last for up to 72 hours
in patients with vertebrobasilar migraine.57 On average,
vertigo and auditory symptoms last from a few minutes
to several hours in patients with vestibular migraine.72
Symptoms in patients with VBI and subclavian steal syn-
drome are progressive and nonaccommodating until the
precipitating postures or activities are discontinued.53,74
One could assume that, based on the pathophysiology,
the other types of presyncopal dizziness will behave
similarly. The duration of symptoms in patients with
cervicogenic dizziness is usually brief after assuming
the provoking position, although symptoms have been
reported as lasting minutes to hours.17,53 Dizziness and
other symptoms in patients with panic disorder have an
abrupt onset and peak in about 10 minutes.50 Symptom
duration of longer than 60 seconds and nonaccommo-
dating forms of dizziness indicate the need for referral.
Symptom frequency
Dizziness associated with precipitating factors is,
of course, recurrent in nature depending on exposure
to those factors, as discussed above. Dizziness and
other symptoms are episodic in patients with Ménière
disease, otosclerosis, perilymphatic fistulae with low-
volume leaks, migraine, vertebrobasilar migraine, panic
29
disorder, and phobic postural vertigo.41,43,50,86,98 We have
already discussed the constant symptoms in patients with
central vestibular lesions.6,43 Episodic bouts of dizziness
indicate a likely need for referral.
Symptom fatigability
Fatigability of symptoms refers to the decrease in symp-
toms of vertigo and nystagmus with repeated position-
ing.108 It is characteristic for cervicogenic dizziness and
BPPV.53 Nonfatigable dizziness indicates a likely need for
referral, even though few patients will willingly provoke
dizziness repeatedly to find out about this characteristic.
Pertinent Past and Present Medical History
Patient demographics
Ataxia-telangiectasia has its onset before the age of 4.43
Friedreich ataxia also starts in childhood.43 Migraine and
vertebrobasilar migraine also usually have their onset early
in life.43,57 Prevalence of vestibular migraine is highest in
the fourth decade in men and from the third to the fifth
decade in women; initial presentation can occur at any
age.72 Cervical artery dissection is most prevalent in sub-
jects below the age of 45.5 Takayasu disease affects mainly
women between the ages of 15 and 30.109 Panic disorder
often first occurs in young adulthood.50 Hyperventilation
most commonly affects patients between ages 20 and 40.43
The age of onset in Ménière disease is usually between
20 and 50.43 Hearing loss associated with otosclerosis
generally starts before age 30.43 Cerebellopontine angle
tumors have an age of onset between 30 and 60.43 The
age of onset for alcoholic cerebellar degeneration is 40
to 60.43 Cough syncope is most prevalent in middle-aged
men.43 Hypothyroidism is most common in middle-aged
or elderly women.43 Benign paroxysmal positional vertigo
generally occurs in people over age 40, and it rarely
occurs in people under 20; however, peak incidence of
onset for BPPV is in the sixth decade of life.54 Orthostatic
hypotension is most common in people in the sixth and
seventh decades.41,43 Parkinsonism is most prevalent in
older adults.41,43 Vasovagal syncope as a cause of dizzi-
ness can occur in all age groups.41,43 Onset of dizziness
and ataxia in childhood is a strong indicator for referral.
Men are more often affected by Ménière disease, al-
coholic cerebellar degeneration, orthostatic hypotension,
carotid sinus syndrome, and cough syncope.41,43 Women
are more often affected by hypothyroidism, migraine,
vertebrobasilar migraine, and hyperventilation-induced
presyncope.43,57 Mal de debarquement syndrome is most
prevalent in middle-aged women.80 Takayasu disease
affects only women, while micturition syncope occurs
almost exclusively in men.43 Takayasu disease only affects
women of Asian descent. Parkinsonism affects all ethnic
groups equally.43
Medical history
Past and concurrent medical history may provide di-
agnostic or screening clues in patients with complaints of
dizziness. A medical history of head trauma, labyrinthine
infection, surgical stapedectomy, chronic suppurative
otitis media, and degenerative changes to the inner ear
may indicate nonidiopathic BPPV.52,53,55 An upper-respi-
ratory infection precedes acute peripheral vestibulopathy
in 50% of patients.41 Acoustic neuromas are more com-
mon in patients with neurofibromatosis.43 Vestibuloco-
chlear nerve compression can be the result of bacterial,
syphilitic, and tuberculous infection or sarcoidosis.41
Barotrauma due to diving or flying, a forceful Valsalva
maneuver, or head trauma can produce a perilymphatic
fistula.41,98 Head trauma can also cause occult skull
fractures; a petrosal bone fracture can cause vertigo and
hearing loss.43 Autoimmune diseases such as rheumatoid
arthritis, Crohn disease, and polyarteritis are often con-
currently present in patients with autoimmune disease
of the inner ear.57 Varicella, AIDS, mumps, poliomyelitis,
infectious mononucleosis, and lymphocytic choriomen-
ingitis (a virus borne by rodents) can all provide the
viral agent responsible for viral cerebellar infections.43
Acute cerebellar ataxia of childhood is often preceded
by a viral infection or inoculation.43 Vertigo is a common
symptom in patients with multiple sclerosis, albeit not
often the presenting symptom.43 Epilepsy in the medical
history should prompt questions about phenytoin; long-
term treatment with phenytoin may produce cerebellar
degeneration.43 Patients with lung cancer, ovarian can-
cer, Hodgkin disease, and breast cancer are at risk for
paraneoplastic cerebellar degeneration.43 Breast and lung
cancer are also apt to metastasize to the posterior fossa in
adults.43 A medical history positive for heart disease could
imply a cardiovascular origin for presyncopal dizziness
complaints.59 Chronic obstructive pulmonary disease is
frequent in patients with cough-related presyncopal diz-
ziness.43 Atherosclerosis, thromboembolic disease, and
cervical spine trauma and degeneration have been sug-
gested to predispose patients to VBI.55,65,66 However, Ru-
binstein et al5 noted no correlation for cervical artery dis-
section and atherosclerosis risk factors, such as cigarette
smoking, oral contraceptive use, diabetes, hypertension.
They noted this might have been related to comparison
in their systematic review with studies on patients with
ischemic stroke not related to arterial dissection. A medi-
cal history of migraine did show a strong association with
cervical artery dissection (adjusted odds ratio 3.6; 95%
confidence interval 1.5-8.6).5 Atherosclerosis can also
lead to subclavian steal syndrome.11 Recurrent episodes
of VBI predispose patients to vertebrobasilar infarction.43
Cervical spine trauma and degeneration may also be the
basis for cervicogenic dizziness.16,17 A recent optometry
or ophthalmology report may reveal the visual impair-
ments associated with complaints of dysequilibrium.75
A recent lower extremity joint replacement or other
orthopaedic surgery may be the cause for dysequilibrium
in the elderly patient. A history of migraine or migraine-
related disorders has been associated with vestibular
dysfunction.110,111 In fact, vertigo is 3 times more com-
mon in patients with migraine, and there is a 30% to
50% prevalence of migraine in patients with vertigo.112
30
With the exception of neck trauma and degeneration
and recent lower extremity joint replacement or other
orthopaedic procedures, a positive medical history in the
absence of signs and symptoms indicative of the 3 con-
ditions amenable to sole physical therapy management
discussed above may indicate the need for referral.
Family history
Familial paroxysmal ataxia is a hereditary recurrent
form of ataxia.57 Also, 20% of patients with Ménière
disease have a positive family history.41 Patients with
otosclerosis, migraine, and vertebrobasilar migraine also
commonly have a positive family history.43,57 Coronary
artery disease and peripheral vascular disease with a
possible role in producing presyncopal dizziness have a
strong family history.113 Some of the spinocerebellar atax-
ias are hereditary autosomal dominant diseases, while
Friedreich ataxia and ataxia-telangiectasia are autosomal
recessive diseases.43 A positive family history linked to
relevant pathognomonic signs and symptoms constitutes
a reason for referral.
Medication history
Table 16 lists prescription, over-the-counter, and
recreational drugs associated with the various subtypes
of dizziness, allowing the therapist to establish whether
symptom description matches the possibly causative
medication use reported. A strong relationship has been
established between the number of medications taken
(more than 5) and dizziness symptoms.51 Careful ques-
tioning may implicate such overmedication as a cause
of dizziness. Noncompliance with medication may
also be an issue (eg, the failure to take antidepressants
in a patient with panic disorder). Additionally, the use
of a particular medication may signal to the therapist
a medical condition that the patient failed to report. A
positive medication history with symptoms indicative of
a relevant dizziness subtype (Table 16), polypharmacy,
and noncompliance with prescribed medication may all
constitute reason for referral.
PHYSICAL EXAMINATION
Physical examination with the aim of differential di-
agnosis in patients complaining of dizziness requires a
multitude of tests. Table 15 provides a suggested format
for the physical examination. The proposed order of
examination in this format is intended to safeguard previ-
ously undiagnosed patients from unnecessary and poten-
tially harmful physical tests by establishing the need for
referral and obviating the need for further testing in case
of a positive response to an earlier physical test.
Observation
Skin
Children with ataxia-telangiectasia have tiny, red spi-
der veins on the ears and cheeks. Dry skin with brittle hair
may indicate hypothyroidism. Vitamin B12 deficiency can
cause a lemon-yellow skin discoloration. Papilledema
Table 16. Medications Associated With Subtypes of Dizziness*
Vertigo Presyncope Dysequilibrium Other Dizziness
Alcohol Digitalis Phenothiazines Alcohol
Aminoglycoside antibiotics Quinidine Butyrophenones Aminoglycoside antibiot-
• Streptomycin Procainamide Metoclopramide ics
• Gentamicin Propranolol Reserpine • Streptomycin
• Tobramycin Phenothiazines Tetrabenazine • Gentamicin
• Amikacin Tricyclic antidepressants Angel dust • Tobramycin
• Kanamycin Potassium Cis-platinum • Amikacin
Salicylates Methyldopa Isoniazid • Kanamycin
Quinine and quinidine Antidepressants Pyridoxine Salicylates
Cis-platinum Antihypertensives Taxol Quinine and quinidine
Sedative hypnotics Bromocriptine Cis-platinum
• Barbiturates Diuretics
• Benzodiazepines Levodopa
• Meprobamate Monoamine oxidase (MOA)
• Ethchlorvynol inhibitors
• Methaqualone Nitroglycerin
Anticonvulsants Phenothiazines
• Phenytoin
Hallucinogens
• Phencyclidine
Street drugs
• Heroin
Mercuric and
organophosphoric
compounds

*Reprinted with permission from Vidal P, Huijbregts P. Dizziness in orthopaedic physical therapy practice: history
and physical examination. J Man Manipulative Ther. 2005;13:222–251. Copyright 2005, Journal of Manual and
Manipulative Therapy.

due to increased intracranial pressure occurring together
with dysequilibrium is indicative of an intracranial mass
lesion, usually in the posterior fossa.43,58 Clubbing of the
fingernails, cyanosis of lips, trophic changes of the skin,
and peripheral edema could suggest a cardiovascular
disorder.104,113 All abnormalities above in combination
with relevant symptoms noted in the history may indicate
the need for referral.
Posture
Postural deviations negatively affecting the location of
the center of gravity in relation to the base of support may
result in patients complaining of the dysequilibrium type
of dizziness. These deviations also prompt further muscu-
loskeletal examination to determine cause and potential
management strategies. Postural deviations may also
indicate possible pathology. Friedreich ataxia typically
causes an increased kyphoscoliosis. Neurosyphilis fre-
quently leads to hypertrophic or hypermobile joints with
subsequent effects on posture. Craniocervical junction
abnormalities can occur with Arnold-Chiari malforma-
tion.43 A lateral head tilt might indicate an otolith prob-
lem (tilting of the environment) or just tightness of the
sternocleidomastoid or upper trapezius commonly seen
in cervicogenic dizziness,17,29 but it may also be caused
by ischemia or infarction in the vertebrobasilar system.92
A forward head posture, with the head backward bent on
the upper cervical spine, may cause external mechani-
cal compression of the vertebral artery, thus potentially
producing symptoms of VBI,63 but it may also lead to
hypomobility of soft tissue and joint structures especially
in the upper cervical spine, an area implicated in cervi-
cogenic dizziness. We should interpret findings from a
visual posture assessment with caution: Fedorak et al114
noted fair mean intrarater reliability (κ = 0.50) and poor
mean interrater reliability (κ = 0.16) for visual posture
evaluation using a 3-point rating scale. Craniocervical
junction abnormalities and lateral head tilt may indicate
the need for referral.
Eyes
Pigmented corneal Kayser-Fleischer rings are due to
copper deposition in the cornea in patients with Wilson
disease.43 Children with ataxia-telangiectasia also have
spider veins in the corners of the eyes. Vertical and
horizontal misalignments of the eyes may be caused
by cranial nerve palsies. A skew deviation is a vertical
misalignment of the eyes that is not the result of ocular

31
muscle palsy.67 Skew deviation is best detected by alter-
nately covering the eyes; patients with skew deviation
make a vertical corrective movement in the sense of a
lateral head tilt when switching the cover from the unaf-
fected to the affected side. Skew deviation, head tilt, and
ocular counter-rolling constitute the ocular tilt reaction.67
Unilateral lesions of the vestibular nucleus, the medial
longitudinal fascicle, and other vestibular centers due to
vertebrobasilar infarction can produce a full ocular tilt re-
action.92 A unilateral thalamus lesion or a benign otolith
dysfunction can produce a partial ocular tilt reaction.92 In
patients with peripheral or vestibular nucleus lesions, the
lower eye indicates the side of the lesion; lesions above
the level of the vestibular nucleus present with the higher
eye on the side of the lesion.67 Horner syndrome occurs
in some patients with foramen magnum compressive le-
sions.58 Any of these abnormalities indicates a need for
referral.
Vital Signs
Blood pressure
In patients with subclavian steal syndrome, a differ-
ence in blood pressure between the affected and unaf-
fected arm is virtually always present. On average, systolic
blood pressure is 45 mm Hg lower in the arm supplied
by the stenotic blood vessel.43 Symptoms indicative of
subclavian steal syndrome in combination with at least
45 mm Hg lower systolic blood pressure in the symp-
tomatic arm is a reason for referral. Hypertension and
hypotension can contribute to dizziness symptoms.104
Monitoring the patient’s blood pressure response when
transferring from a lying to a standing position is used as
a diagnostic test for orthostatic hypotension. A drop in
systolic blood pressure of at least 30 mm Hg or a drop
of 10 mm Hg in diastolic blood pressure is indicative of
orthostatic hypotension.43 Eaton and Roland41 considered
a drop of 20 mm Hg in systolic or 10 mm Hg in diastolic
blood pressure 2 minutes after standing indicative of
orthostatic hypotension, but they also warned that blood
pressure readings in elderly patients might not precisely
meet those criteria. Witting and Gallagher115 established
normative values; in 176 healthy subjects, systolic blood
pressure decreased by 1.2 ± 9.8 mm Hg after 1 minute
of standing preceded by 5 minutes of sitting. A drop in
systolic blood pressure of at least 20 mm Hg had a speci-
ficity of 0.97 for detecting orthostatic hypotension.115
Combined with a complaint of presyncopal dizziness,
this finding warrants referral.
Heart rate
Palpation of pulses may be useful in detecting a cardio-
vascular disorder. Palpitations, the presence of an irregular
heartbeat, may indicate a disturbance in the heart’s abil-
ity to normally conduct electrical impulses104 and may be
benign or quite dangerous. Palpitations lasting for hours
or irregular heartbeats accompanied by pain, shortness of
breath, or lightheadedness require referral to a physician
for medical evaluation.104 Similarly, tachycardia (greater
32
than 100 beats per minute) and bradycardia (less than 60
beats per minute) may indicate relatively benign condi-
tions, such as mitral valve prolapse and athlete’s heart
but may also occur in more serious conditions such as
coronary artery disease and aneurysm.104,113 Monitoring
pulse rate during a sit-to-stand test may also be helpful
for diagnosing orthostatic hypotension. Witting and Gal-
lagher115 established a normative value of a pulse rate
increase of 5.3 ± 6.6 beats per minute in normal subjects
and suggested an increase of at least 20 beats per minute
as a positive test for orthostatic hypotension based on a
sensitivity of 0.98. Combined with a complaint of presyn-
copal dizziness, this finding warrants referral.
Auscultation
Auscultation tests can provide information on a pos-
sible cardiovascular disorder responsible for a patient
complaint of presyncopal dizziness. Lok et al116 found
poor accuracy and interrater agreement for identification
of some cardiac auscultation parameters. Listening for
carotid bruits has been suggested as a screening tool for
the likelihood of a vertebrobasilar incident with cervical
manipulation.64 We earlier discussed the role of collateral
(carotid) circulation in the occurrence of VBI. Terrett64
noted that the validity of carotid bruits in the diagnosis
of carotid stenosis or prediction of a vertebrobasilar inci-
dent is questionable. Negative auscultation results would
seem to provide the therapist with a false sense of doing a
relevant vertebrobasilar screening.64 In contrast, Magyar
et al117 reported 56% sensitivity and 91% specificity for
detection of a 70% to 99% carotid stenosis when com-
pared with color duplex ultrasound. They also reported
a positive predictive value of 27% of a bruit found and
a 97% negative predictive value for a normal ausculta-
tion. They concluded that carotid auscultation is a useful
screening procedure for carotid occlusion or stenosis. In
light of the possible contradictory interpretation of these
values for diagnostic test accuracy for auscultation of
carotid bruits and the poor values for accuracy of cardiac
auscultation, positive auscultation findings indicate the
need for cautious continued examination.
Gait Assessment
Patients with cerebellar ataxia have a wide-based
staggering gait, sometimes with titubation (staggering or
stumbling gait) or oscillation of head and trunk.43 Uni-
lateral cerebellar lesions result in a deviation toward the
side of the lesion when the patient attempts to walk in a
straight line. Patients with cerebellar ataxia are unable to
walk in a tandem gait. In patients with sensory ataxia, gait
is also wide based. Impaired proprioception may cause
steppage gait. The patient lifts the feet excessively high
off the ground and slaps them down rather heavily. Us-
ing a cane or a railing often dramatically improves gait.43
Difficulty walking with concurrent rotation of the head in
the horizontal plane may indicate a peripheral vestibular
deficit. Gait unsteadiness may also be a complaint in
patients with psychiatric or factitious disorders. Simon
et al43 noted that wildly reeling or lurching movements
from which the patient is able to recover without loss
of balance may be indicative of conversion disorder or
malingering. Recovery of balance from self-imposed
extreme positions and movements, in fact, demonstrates
well-developed balance function. Gait assessment can
also be done quantitatively with measures such as the
Tinetti Balance Scale and the Berg Balance Scale, both
with established predictive validity with regard to fall
risk. The former has been reported to identify 7 out
10 fallers with 70% sensitivity and 52% specificity,118
whereas the latter was able to correctly identify fallers
from nonfallers with 91% sensitivity and 82% specific-
ity.119 A score on either measure indicative of a low fall
risk despite a complaint of dizziness and dysequilibrium
may indicate kinesiophobia or movement-related fear,
which can be classified under other dizziness and may
indicate the need for referral. Titubation, oscillation of
head and trunk, unilateral deviation when attempting to
walk in a straight line, and wild reeling or lurching mo-
tions without loss of balance are less likely indicators of
musculoskeletal impairments and, therefore, indicators
for referral.
Vestibulospinal Examination
The vestibulospinal reflex stabilizes the body dur-
ing head movement; thus, it is responsible for postural
control. The vestibulospinal tests, in general, have poor
or untested diagnostic accuracy but can serve to guide
further examination by indicating the presence of pos-
tural instability and by implicating the vestibular versus
somatosensory system. In isolation, these tests do not
affect a decision to refer or treat.
Single-leg stance
Single-leg stance, with eyes open or closed, can be
used to screen for decreased postural control. In the
acute stage of vestibular loss, a patient will be unable to
perform this test; however, patients who have a compen-
sated vestibular loss may test normal.120 This screening
test is not specific to vestibular loss, as patients with
other balance disorders may have difficulty perform-
ing single-leg stance.120 A normal single-leg stance test
(especially with eyes closed) precludes further vestibu-
lospinal testing.
Romberg and sharpened Romberg
The Romberg test (Figure 1A) challenges balance by
decreasing the base of support. Patients with sensory or
vestibular dysfunction may be able to stand in a Romberg
stance, but closing the eyes takes away the visual cues
used to maintain balance, causing them to fall (ie, have
a positive Romberg sign).43 Patients with a vestibular le-
sion tend to fall in the direction of the lesion.43 Patients
with cerebellar ataxia are unable to use visual cues to
compensate and are unable to maintain their balance
in a Romberg stance whether their eyes are open or
closed.43 A normal performance on the Romberg test for
33
a young adult is 30 seconds, and a low normal score
is 6 seconds.121 The Romberg test has predictive validity
with regard to recurrent falls over a 6-month period in
patients with Parkinson disease (sensitivity was 65% and
specificity greater than 90%).122
A sharpened Romberg test (Figure 1B) involves stand-
ing with a decreased base of support as compared to
the Romberg test. The ataxic patient will prefer to stand
with a wider base of support and will show reluctance
when asked to stand with the feet close together. Patients
with sensory ataxia are usually able to stand with the
feet close together, as are some patients with vestibular
lesions. These patients will compensate for the loss of
somatosensory and labyrinthine input, respectively, with
an increased reliance on visual input.
A B
Figure 1. (A) Romberg test and (B) sharpened Romberg
test.
Modified Clinical Test of Sensory Integration of Balance
The modified Clinical Test of Sensory Integration of
Balance assesses the contribution of the visual, vestibu-
lar, and somatosensory systems to postural control. The
test has 4 components: the patient standing on a level
surface with the eyes open (Figure 2A), on a level sur-
face with eyes closed (Figure 2B), on foam with the eyes
open (Figure 2C), and on foam with eyes closed (Figure
2D). Initially, a patient will have available all sensory
systems to maintain balance. The eyes-closed condition
will eliminate visual contribution, putting increased
demand on the somatosensory and vestibular systems.
Standing on a foam surface with eyes closed alters the
somatosensory input and eliminates visual input; thus,
the patient has to rely mostly on vestibular input. Patients
with vestibulopathy will have difficulty maintaining an
upright posture.120 Platform posturography is a computer-
ized version of this test with greater than 90% specificity
but very low sensitivity for the diagnosis of patients with
peripheral vestibular deficits. Posturography in combina-
tion with other vestibular function tests has been shown
to increase sensitivity to 61% to 89%.123
 A B
C D
Figures 2A to D. Modified Clinical Test of Sensory Inte-
gration of Balance.
Fukuda step test
The Fukuda step test (Figure 3) assesses stability
during self-initiated movement by asking the patient to
march 50 or 100 steps in place with the arms raised in
front to 90° and with the eyes closed. A patient with a
unilateral vestibular lesion will tend to rotate greater than
30° toward the involved side.120 Forward displacement of
more than 50 centimeters is also considered positive.124
These unilateral lesions include infarctions in the distri-
bution of the anterior and posterior inferior cerebellar
arteries.92 Bonanni and Newton125 found higher reliability
for the 50-step than the 100-step protocol. Herdman and
Whitney120 noted that there are many false positives and
negatives. Fell124 noted that the Fukuda step test is not a
test specific to vestibular lesions.
Cranial Nerve Examination
Cranial nerve palsies may be present with central
vestibular disorders and some peripheral vestibular dis-
orders. A cranial nerve examination may also serve as
a nonprovocative test for suspected ischemic conditions
34
Figure 3. Fukuda step test.
affecting the brainstem. Obviously, the vestibulocochlear
nerve can be involved in patients complaining of dizzi-
ness as well as the anatomically closely related trigeminal
and facial nerves.43 Optic neuropathy can be the result
of multiple sclerosis, neurosyphilis, and vitamin B12 defi-
ciency. A depressed corneal reflex or a facial nerve palsy
on the same side as the ataxia can result from a cerebello-
pontine angle tumor. Lower brainstem disease can cause
tongue or palate weakness, hoarseness, and dysphagia.30
Some pathologies cause dizziness in combination with
hearing loss. Table 15 contains a sample cranial nerve
examination.126 Visual field confrontation testing (cranial
nerve II) had low sensitivity but high specificity (97%)
and positive predictive value (96%) when compared to
automated perimetry,127 indicating that a confrontation-
method visual field test may only have diagnostic value
if positive. We found no further data on reliability and
validity of the cranial nerve examination. Abnormal find-
ings on the cranial nerve examination constitute a reason
for referral.
Oculomotor Examination
To some extent, observation and the cranial nerve
examination already test oculomotor function. They also
allow clinicians to note static abnormalities (strabismus)
and ensure full range of movement for each eye before
doing the oculomotor tests. No data on reliability and
validity of the oculomotor examination were found.
Observation for spontaneous nystagmus
Nystagmus can be defined as repetitive, back-and-
forth, involuntary eye movements initiated by slow
drifts away from the visual target.128 It can be classified
as a pendular nystagmus, consisting of slow sinusoidal
oscillations, or as a jerk nystagmus, characterized by an
alternating slow drift and a quick corrective phase. In the
latter type, a slow phase takes the eye away and a quick
corrective phase brings it back to the target.128
The clinician first observes for spontaneous nystagmus
by asking the patient to fix on a stationary target at a dis-
tance of more than 2 meters.128 A spontaneous nystagmus
may imply an acute peripheral vestibular lesion and, in
this case, occurs due to an imbalance in the tonic firing
rate of the vestibular neurons.129 The spontaneous nystag-
mus following a lesion of the peripheral vestibular system
is a jerk nystagmus with the quick phase indicating the
unaffected side. In fact, the detectable eye movement
during spontaneous nystagmus is the quick phase toward
the unaffected ear.128,130 In the acute phase, patients will
have difficulty reading and watching television. After
the acute episode, a patient can suppress the nystagmus
with visual fixation, making it difficult for the examiner
to observe eye movements.129 A spontaneous nystagmus
may also occur in the symptom-free interval in patients
with vestibular migraine.72 Preventing visual fixation by
using Frenzel glasses facilitates observation of a spon-
taneous nystagmus. These glasses prevent light from
activating the smooth pursuit system, which can cancel
out the imbalance of the tonic firing rate produced by a
peripheral vestibular lesion.130 A purely vertical (upbeat
or downbeat) or torsional spontaneous nystagmus is
indicative of a central vestibular lesion.67,128 Nystagmus
due to a central lesion usually cannot be suppressed with
visual fixation.128,131 A positional down-beating vertical
nystagmus occurs particularly in posterior fossa lesions
with Arnold-Chiari malformation as its most common
cause.132,133 It may also indicate an intracranial exten-
sion of this or another compressive lesion at the foramen
magnum.58 Nystagmus with one eye beating down and
the other up (skew nystagmus) has only been reported
in patients with Arnold-Chiari malformation.133 A few
minutes of observation are required to identify periodic
alternating nystagmus, a horizontal jerk nystagmus that
changes direction about every 2 minutes and that is
indicative of midline cerebellar lesions.128 Spontaneous
nystagmus may also be congenital. This variant is gener-
ally horizontal, may alternate directions but not at regular
intervals, increases with attention, fixation, and anxiety,
and decreases with convergence.128 Pendular nystagmus
occurs most commonly in patients with multiple sclerosis
and brainstem stroke.128 The presence of a pendular, a
vertical or torsional jerk, skew, or a periodic alternating
horizontal jerk spontaneous nystagmus indicates the need
for referral. In fact, any spontaneous nystagmus requires
35
referral with the exception of the congenital variant noted
above.
The clinician then observes for spontaneous nystagmus
in eccentric positions.128 Deviation of the eye in the direc-
tion of the quick phase will increase the frequency and
velocity of the nystagmus (Alexander’s law) in patients
with a unilateral peripheral vestibular lesion, and it may
still produce a positional nystagmus in accommodated
patients.67 A gaze-evoked nystagmus may also occur
in the symptom-free interval in patients with vestibular
migraine.72 Detection of gaze-evoked nystagmus on lat-
eral or upward gaze suggests a central lesion.120 In fact, a
gaze-evoked horizontal nystagmus implies lesions in the
cerebellar flocculus and the medial vestibular nucleus-
nucleus prepositus hypoglossus complex, but it can also
be the effect of medications, such as hypnotics, sedatives,
and anxiolytics or alcohol intoxication.67,128 Gaze-evoked
nystagmus may also be the result of extra-ocular muscle
weakness as in myasthenia gravis.128 Unsustained eye
movements of low frequency and amplitude are indicative
of end-point nystagmus, a nonpathological variant in nor-
mal subjects.128 The presence of gaze-evoked nystagmus
(with the exception of end-point nystagmus) indicates the
need for referral.
Saccadic eye movements
Having the patient look back and forth between 2
targets tests saccadic eye movements. Abnormalities of
horizontal or vertical saccadic eye movements may occur
in the symptom-free interval in patients with vestibular
migraine.72 Overshooting of the target (saccade overshoot
dysmetria) may be observed in cerebellar disorders, such
as Friedreich ataxia.134 Undershooting of the target, or hy-
pometria, can occur in patients with Parkinson disease.134
Vertical saccadic eye movements in patients with Wal-
lenberg syndrome as a result of vertebrobasilar infarction
may result in eye lateropulsion requiring a corrective
horizontal saccade.67 Uncalled-for saccades during gaze
fixation on one of the targets can occur in patients with
viral cerebellar infection, paraneoplastic syndrome, and
Friedreich ataxia.67 Macrosaccadic oscillations, which
are horizontal saccades occurring in waxing and waning
bursts with 200-millisecond saccadic intervals induced by
a gaze shift, are indicative of midline cerebellar disease,
spinocerebellar degenerations, and pontine lesions.128
Although saccadic eye movement abnormalities using
electro-oculography have been reported in patients with
dizziness due to chronic WAD,21,25,26 they are not likely
to be noted in the clinical examination described here.
Abnormalities identified during saccadic eye movement
tests indicate the need for referral.
Smooth pursuit testing
Having the patient follow a slowly moving target (ie, no
faster than 20° per second) tests smooth pursuit. A marked
deficit in smooth pursuit is indicative of a degenerative
cerebellar process.67 Small bilateral saccades in the same
direction in both eyes during smooth pursuit testing are
indicative of spinocerebellar lesions, especially Friedreich
ataxia.128 Smooth pursuit testing may also be positive in pa-
tients with a severe acute peripheral vestibular lesion due
to superposition of an intense spontaneous nystagmus.67
Although smooth pursuit eye movement abnormalities
using electro-oculography have been reported in patients
with dizziness due to chronic WAD,21,26 they are not likely
to be noted in the clinical examination described here.
Abnormal findings on smooth pursuit testing indicate the
need for referral.
Hearing Examination
The cranial nerve examination may indicate hearing
loss. A conductive hearing loss results from disorders in
the external or middle ear; lesions in the cochlea or the
cochlear nerve43 cause a sensorineural hearing loss. A
sensorineural loss is a symptom of salicylate overdose.43
Ménière disease produces a sensorineural loss that is pro-
gressive over multiple episodes.43,98 Progressive unilateral
sensorineural hearing loss is also a typical presentation of
patients with acoustic neuromas.92 Otosclerosis can pro-
duce both a conductive and a sensorineural hearing loss.43
It is the authors’ experience that many elderly patients
complaining of dizziness present with an undiagnosed
but unrelated conductive hearing loss. Even without as-
sociated symptoms, this constitutes a reason for referral
to an audiologist. The presence of symptoms implicating
hearing loss as part of a pathology causing complaints of
dizziness indicates the definite need for medical referral.
Weber test
With the Weber test,43 the therapist places a tuning fork
[256 or 512 hertz (Hz)] on the top of the patient’s skull.
With unilateral sensorineural hearing loss, the patient will
perceive the sound as coming from the normal ear. With
a conductive disorder, the patient perceives the sound
as coming from the abnormal ear. Midline is the normal
response for this test.124 A non-midline response indicates
the need for referral.
Rinne test
The Rinne test43 allows the therapist to distinguish
between a sensorineural and a conductive deficit in the
affected ear. Normally, air conduction of the sound of a
vibrating tuning fork (256 or 512 Hz) is perceived as loud-
er than bone conduction. Holding the tuning fork next to
the external auditory canal produces a louder sound than
placing the base of the tuning fork on the mastoid bone in
patients with normal hearing. The same is true in patients
with sensorineural hearing loss. However, in patients with
conductive deficits, bone conduction will appear louder
than air conduction on the affected side. Burkey et al135
reported that the sensitivity of the Rinne test was sufficient
to be used as part of a screening protocol in the hands of
an experienced examiner and when interpreting equivo-
cal results as indicative of a conductive loss. The finding
of bone greater than air conduction indicates the need for
referral.
36
Active Range-of-motion Tests
Musculoskeletal impairments (ie, decreased muscle
strength and endurance, joint stability and mobility, and
posture) are implicated in patients with the dysequilib-
rium subtype of dizziness and may be amenable to sole
physical therapy management. Range-of-motion limita-
tions, specifically trunk, hip, and knee flexion and ankle
plantarflexion contractures, will adversely influence the
location of the center of gravity in relation to the base of
support. Active range-of-motion testing should, therefore,
concentrate on assessing trunk, hip, and knee extension
and ankle dorsiflexion. Assessing neck motions allows
the clinician to observe possible adverse responses in
the sense of ischemic reactions during patient-controlled
AROM. It also serves to see if patients will be able to
assume the test positions needed in further tests. Cervical
AROM tests may also reveal upper cervical hypomobility
implicated in cervicogenic dizziness.32,33
Active range-of-motion tests also provide indica-
tions on strength and coordination deficits in the form
of ataxia or abnormal involuntary motions. Asterixis is
an episodic cessation of muscular activity in patients
with hepatic encephalopathy, hepatocerebral degenera-
tion, and other metabolic encephalopathies.43 Episodic
cessation of extensor muscle activity occurs when the
patient holds the arms outstretched with wrists and
fingers extended causing the hands to fall into flexion
followed by a return to the extended position.43 Myoc-
lonus is a rapid, twitch-like muscle contraction. It can
result from the same conditions causing asterixis or with
Creutzfeldt-Jakob disease.43 Chorea can occur in patients
with Wilson disease, acquired hepatocerebral degenera-
tion, and ataxia-telangiectasia.43 Chorea is characterized
by rapid, irregular muscle jerks, occurring unpredictably
and involuntarily in different body parts.43 An ischemic
response during cervical AROM testing or the presence
of abnormal involuntary motions during AROM testing of
the limbs indicates the need for referral.
Limb Ataxia Tests
These tests serve to confirm possible limb ataxia ob-
served during AROM testing. During the finger-to-nose
test, the quality of arm motion is observed as the patient
moves the index finger to the tip of the nose or the chin.
Closing the eyes eliminates visual substitution. Mild cere-
bellar ataxia results in an intention tremor near the begin-
ning and end of the movement with possible overshooting
of the target.43 With the finger-to-finger test, the patient
attempts to touch his or her finger to the therapist’s finger.
Horizontal overshooting implicates a unilateral labyrin-
thine lesion; vertical overshooting occurs in patients with
midline lesions to the medulla oblongata or the bilateral
cerebellar flocculus.92 Having the supine patient track the
heel of the foot smoothly up and down the contralateral
shin tests for leg ataxia. Having the seated patient touch
the great toe to the examiner’s finger is another test for leg
ataxia.136 Dysdiadochokinesia is the inability to perform
rapidly alternating movements, and in adults it is usually
caused by multiple sclerosis; in children, it frequently
results from cerebellar tumors. Patients with other move-
ment disorders such as Parkinson disease also may have
difficulty with rapidly alternating movements, but this is
due to akinesia or rigidity rather than true dysdiadocho-
kinesia.137 Dysdiadochokinesia can be tested with rapid
alternating finger tapping, forearm pronation-supination,
and toe-tapping movements, for example.136,137 With
the Barre test, the standing or sitting patient holds the
hands outstretched with the forearms supinated and eyes
closed. Sinking of 1 arm with simultaneous pronation
may indicate a central neurological, likely cerebellar,
dysfunction.138
The finger-to-nose test has poor test-retest and inter-
rater reliability for dysmetria and tremor but excellent
reliability for time of execution.139 Swaine et al140,141
reported mean reliability coefficients of 0.77-0.82 for
time of execution of 5 repetitions of the finger-to-nose
test, indicating clinically sufficient test-retest reliability
in healthy adults and also established norms for healthy
subjects aged 15 to 34. Simon et al43 reported a posi-
tive heel-to-shin test in 80% of patients with alcoholic
cerebellar degeneration. We found no further data on
reliability and validity for these ataxia tests. Positive limb
ataxia tests (including seeming dysdiadochokinesia due
to akinesia or rigidity) indicate the need for referral.
Passive Range-of-motion Tests
Passive range-of-motion (PROM) testing includes
passive physiological motion, passive accessory motion,
and instability tests. In the spine, they include passive
physiological intervertebral motion (PPIVM), passive
accessory intervertebral motion (PAIVM), and segmental
stability tests. Upper cervical segmental motion abnor-
malities may be the cause for cervicogenic dizziness.
In the case of a hypomobility found on AROM testing,
PROM tests may determine cause and subsequent inter-
vention.
Instability tests of the upper cervical spine are espe-
cially relevant prior to tests involving regional passive
rotation of the neck or PPIVM and PAIVM testing. As
discussed above, inadvertent shear forces produced
during these tests due to ligamentous insufficiency may
damage the cord and vertebral arteries.4 The therapist
may want to postpone PPIVM and PAIVM tests to the
cervical spine until both the segmental stability tests and
the VBI tests have provided a negative response.
Intrarater reliability of PPIVM and PAIVM tests has
consistently been shown to be greater than interrater re-
liability, with the latter varying from generally poor to at
times perfect.142 Jull et al143 examined construct validity
and found 100% sensitivity and specificity when com-
paring cervical PPIVM and PAIVM testing with single
facet blocks. Cattryse et al144 found acceptable interrater
reliability only for the supine upper cervical flexion in-
stability test but not for the Sharp-Purser or atlas lateral
displacement test. A positive finding on upper cervical
segmental stability tests in combination with signs and
37
symptoms of cord or vertebral artery compromise indi-
cates the need for referral.
Passive range-of-motion tests can also detect muscle
tone abnormalities. Hypotonia is indicative of cerebellar
disorders with unilateral cerebellar disorders producing
ipsilateral limb hypotonia.43 Hypertonia or rigidity may oc-
cur in patients with cerebellar ataxia due to Wilson disease,
acquired hepatocerebral degeneration, Creutzfeldt-Jakob
disease, and some olivopontocerebellar degenerations.
Spasticity on PROM testing is common in patients with
multiple sclerosis, posterior fossa tumors, Arnold-Chiari
malformation, VBI or infarction, Friedreich ataxia and the
other hereditary ataxias, olivopontocerebellar degenera-
tion, Creutzfeldt-Jakob disease, neurosyphilis, and vitamin
B12 deficiency.43 Prochazka et al145 showed poor reliability
for a 5-point rating scale for rating rigidity in patients with
Parkinson disease. Tone abnormalities on PROM testing
indicate the need for referral in a previously undiagnosed
patient.
Strength Tests
The musculoskeletal system is the effector organ of the
balance control system. Sufficient strength and endurance
in the muscles involved in static and dynamic balance
is an obvious prerequisite for optimal balance. Loss of
strength and endurance in these muscles can be the cause
of patient complaints of dizziness and dysequilibrium.
The pattern of any weakness present may also provide
diagnostic indicators for the underlying dysfunction or
disease. Single or multiple muscle weakness can be the
result of disuse atrophy, especially in the elderly. Weak-
ness in a peripheral nerve distribution implies a peripheral
neuropathy. Monosegmental myotomal weakness can im-
plicate a nerve root problem. Multisegmental weakness
can implicate a process affecting the cauda equina or the
spinal cord. Distal neuropathic weakness can be the result
of disorders producing sensory ataxia (eg, polyneuropa-
thies). Multiple sclerosis, foramen magnum lesions, spinal
cord tumors, and vitamin B12 deficiency can cause para-
paresis.43 Paraparesis with the arms more affected than the
legs is typical of foramen magnum compressive lesions.
Compression of the spinal division of the accessory nerve
can cause weakness specific to the sternocleidomastoid
and trapezius in such lesions. Unilateral compression at
the foramen magnum results in clock-face paralysis, first
involving the ipsilateral arm, then the ipsilateral leg, then
the contralateral leg, and finally the contralateral arm.58
Intracranial extension of such a compressive lesion may
cause cruciate hemiplegia affecting the ipsilateral lower
and contralateral upper limb.58 Ataxic quadriparesis, hemi-
ataxia and contralateral hemiparesis, or ataxic hemiparesis
are all diagnostic indicators of a brainstem lesion.43
We discussed the possible role of deep cervical flexor
muscle dysfunction in the etiology and treatment of cervi-
cogenic dizziness. Grimmer146 described a useful clinical
test for determining the endurance of the deep cervical
flexors. The patient is supine without a pillow and is asked
to retract the neck and then lift the back of the head off the
plinth to a height of 2 centimeters. Endurance is measured
as the time from start of the test to the moment the chin
begins to thrust forward. Chin thrust can be determined
visually or by way of palpation. Grimmer146 reported high
test-retest reliability with an ICC of 0.92 in women and
0.93 in men.
Knepler and Bohannon147 and Bohannon and Cor-
rigan148 showed large interrater variability in the forces
used to establish manual muscle testing grades of 3+, 4-,
4+, and 5. Herbison et al149 recommended the use of a
handheld myometer over manual muscle testing to detect
strength changes. Jepsen et al150 established interrater κ-
values of 0.25 to 0.72 for upper extremity manual muscle
testing when using a dichotomous rating scale, and they
calculated an odds ratio of 2.5 to 7.7 for the presence
of symptoms in the case of reduced strength on manual
muscle testing, indicating that it may be an appropriate
screening test. In contrast, Bohannon151 calculated a
specificity of manual muscle testing of greater than 80%
and a sensitivity to detect between-side differences or
deficits relative to a grade of normal that did not exceed
75%; diagnostic accuracy was less than or equal to 78%,
leading Bohannon151 to doubt the value of manual muscle
testing as a screening tool. Multisegmental weakness,
including paraparesis, quadriparesis, and hemiparesis but
also progressive monosegmental paresis, indicates the
need for referral.
Reflex Tests
Cerebellar disorders cause hypoactive deep tendon re-
flexes with unilateral cerebellar disorders resulting in ipsi-
lateral hyporeflexia. Friedreich ataxia, neurosyphilis, and
polyneuropathies cause leg hyporeflexia. Hyperreflexia is
present in multiple sclerosis, vitamin B12 deficiency, focal
brainstem lesions, and some spinocerebellar and olivo-
pontocerebellar degenerations.43 A positive Babinski sign,
Hoffman reflex, and ankle clonus may occur in patients
with myelopathy, multiple sclerosis, vitamin B12 deficien-
cy, focal brainstem lesions, and some spinocerebellar and
olivopontocerebellar degenerations.6,67 Sung and Wang152
established 100% sensitivity for a positive Hoffman reflex
for detecting patients with cervical cord compression
confirmed on x-ray film or magnetic resonance imaging.
We found no additional data on reliability and validity of
reflex tests. Clearly, hypoactive or hyperactive deep ten-
don reflexes may indicate a need for referral; the presence
of pathological reflexes is a definite reason for referral.
Sensation Tests
Sensation testing may include tests for light touch per-
ception, sharp and dull discrimination, vibration sense,
and propriocepsis.27 Sensation testing may reveal deficits
in the distribution pattern of single or multiple peripheral
nerves, a nerve root, or a multisegmental pattern, provid-
ing diagnostic clues for underlying cause or contributing
factors to the patient’s complaint of dizziness. Joint posi-
tion sense can be tested by asking the patient to detect
the presence and the direction of a passive movement in
38
the joints.43,51 Simon et al43 suggested beginning this type
of testing distally and moving proximally to establish the
upper level of deficit in each joint. Placing a joint in a
position and having the patient reproduce this position
with the contralateral joint can also be used as a test for
abnormality of joint position sense;43 the patient’s eyes
are closed during joint position testing to prevent visual
compensation. Joint position sense in the legs is always
impaired in patients with sensory ataxia; the arms may be
affected depending on the type and extent of pathology
responsible. Placing a 128 Hz tuning fork over a bony
prominence may serve as a test of vibration sense. Suc-
cessively more proximal sites can determine the upper
level of deficit in limbs or even trunk. Sensory ataxia is
often combined with a decrease in vibratory sensation.43
Using a 3-point rating scale, Jepsen et al153 reported
median interrater κ-values of 0.69 for sensitivity to light
touch, 0.48 for sensitivity to pin prick, and 0.58 for sen-
sitivity to vibration using a 256 Hz tuning fork. Peters et
al154 showed limited interrater reliability for a quantita-
tive method of assessing vibration sense implying even
less reliability for the tuning fork method. Jepsen et al155
reported a sensitivity of 0.73, a specificity of 0.86, a
positive predictive value of 0.93, and a negative predic-
tive value of 0.90 for a combination of manual muscle
tests, sensation tests (light touch, pain, vibration), and
sensitivity of nerve trunks to mechanical pressure when
compared to patient report of pain, strength deficits, or
paresthesia indicating the screening value of this test
regimen. Okuda et al156 reported a positive correlation
between the degree of knee joint position sense deficits
and functional disability scores and electrophysiological
findings in patients with compressive myelopathy. It is
the authors’ experience that elderly patients frequently
present with undiagnosed decreased proprioceptive acu-
ity and vibration sense in the feet and ankles, which may
contribute to dysequilibrium-type dizziness. Multiseg-
mental deficits may indicate the need for referral.
Vertebrobasilar Insufficiency Tests
De Kleyn-Nieuwenhuyse test
Terrett64 noted that the original test description had
postulated decreased or even absent vertebral artery
blood flow based on cadaver perfusion studies in differ-
ent head and neck positions. A long latency, progressive
symptoms when held in the sustained test position of
cervical extension and rotation, and a lack of habituation
with repeated testing are indicative of VBI and not of cer-
vicogenic dizziness or BPPV.53 Oostendorp8 reported a
latency of 55 ± 18 seconds in these patients with positive
findings on variations of the De Kleyn-Nieuwenhuyse test
(Figure 4). He also reported a recovery time of 120 ± 40
seconds.8 A positive test may include symptoms of ver-
tigo, nausea, diplopia, and dysphagia. Positive signs may
include nystagmus and dysarthria,64 which may be noted
by having the patient talk during the test hold. Pettman4
noted horizontal nystagmus but the authors have noted
vertical and rotary nystagmus in symptomatic subjects.

Figure 4. De Kleyn-Nieuwenhuyse test.
This test has been extensively studied with equivocal
results. Some authors reported significant decreases in
blood flow,157,158 whereas others reported no changes.159,160
Support for this test becomes even more problematic with
case reports noting false negative results161,162 and case
series noting 75% to 100% false positive results.160,163
Cote et al164 reported 0% sensitivity for detection of in-
creased impedance to blood flow, 0% positive predictive
value, and 63% to 97% negative predictive value. This
test (and the cervical rotation test) is obviously a ques-
tionable screening procedure for VBI. Vidal165 questioned
its routine use, concluding that vertebral artery tests
are not clinically useful screening tools for VBI. Rather,
he suggested relying upon history suggestive of VBI,
medical history (especially when indicative of ischemic
processes, such as coronary artery disease, transient isch-
emic attacks, or cerebrovascular accidents), and other
relevant examination findings (eg, during cranial nerve
and AROM tests). Due to the potential for harm with this
test and its poor psychometric properties, it should not
be done in patients with a positive medical history or
a history strongly indicative of VBI.165 However, the test
may serve as a screening tool in patients not fitting these
categories. In those patients, a positive finding with clear
central neurological signs of nystagmus and dysarthria on
this test warrants referral.
Sustained cervical rotation test
Sustained supine cervical rotation may also test for
VBI. Symptom behavior can be expected to be similar
to the extension-rotation test with regard to latency,
nonaccommodation, and nonhabituation. However,
findings on sustained cervical rotation alone are equally
equivocal, with significant decreases in vertebral artery
flow157-159,166,167 or no effect on blood flow168 or blood
volume.169 Indications for this test and implications of a
clearly central neurological involvement are as described
for the extension-rotation test.
39
Hautant test
This test is used for differential diagnosis of vestibular,
cervicogenic, and ischemic dysfunction (Figures 5A and
B). However, it is also a test with multiple descriptions
in manual medical literature. Terrett64 described the test
with the patient seated, the arms outstretched, and the
forearms supinated. The therapist moves the patient’s
head in an extension-rotation position with the patient’s
eyes closed. Symptom reproduction and sinking of one
hand into pronation implicates the vertebrobasilar sys-
tem.64 Van der El138 described this test with the forearms
pronated. Deviation of one of the arms with the head
in midposition indicates vestibular dysfunction. A lateral
deviation of the contralateral arm in the opposite direc-
tion of the cervical extension-rotation implicates the
neck. Immediate arm motion suggests a somatosensory
dysfunction; a latency period indicates ischemic dysfunc-
tion.138 No data on reliability or validity were found. A
test indicating ischemic dysfunction suggests the need for
referral.
A B
Figures 5A and B. Hautant test.
Vestibulo-ocular Tests
These tests examine the vestibulo-ocular reflex circuit
by inducing movements at an angular velocity that does
not allow for compensation by the cervico-ocular reflex.
Dynamic visual acuity
After establishing baseline visual acuity with a Snel-
len chart, this test measures visual acuity with concurrent
head movement. The head is moved from side to side
at a frequency of 1 Hz while the patient reads the Snel-
len chart.108 A decrease by 2 lines is suspicious and by
3 or more is indicative of an abnormal vestibulo-ocular
reflex.27,108 This test is not suited for detecting unilateral
peripheral or central vestibular lesions but is indicated in
case of suspected bilateral vestibular loss.108,170 Herdman
et al95 reported poor reliability for this test.
Autorotation test
The autorotation test is performed with the patient
sitting with an upright posture, holding gaze on a station-
ary target, and performing small oscillations of the head
side to side and up and down.102 The patient is instructed
to move at 2 Hz (ie, 120 oscillations in 60 seconds). An
abnormal response includes the inability to continue
the test for 60 seconds due to dizziness, double vision,
or blurry vision due to oscillopsia, or fewer than 100
oscillations in 60 seconds, and may indicate peripheral
or central vestibular dysfunction.102 The autorotation test
is easier to perform in the clinical setting than high-
frequency range rotational chair testing, which requires A B
specialized and powerful systems. However, test-retest
reliability for the autorotation test is poor.171 Figures 6A and B. Head-thrust test.

Doll’s head test
The examiner faces the patient, who fixes the gaze
on the examiner’s nose. The examiner then oscillates
the patient’s head 30° side to side at 0.5 to 1 Hz. Eye
movements that are not smooth but interrupted by catch-
up saccades toward the fixation target indicate bilateral
vestibular lesions.108 We found no data on reliability and
validity.
Head-shaking nystagmus test
The examiner vigorously moves the patient’s head
back and forth horizontally for about 30 seconds with
the patient’s eyes closed. Upon opening the eyes, the
nystagmus will beat away from the side of a unilateral
peripheral vestibular lesion170 or toward the lesioned side
in patients with Ménière disease.172 When compared to
a caloric test, the head-shaking nystagmus test (with
Frenzel glasses) had 66% sensitivity and 77% specificity
for detecting canal paresis greater than 20%.173 Kamei
and Iizuka172 reported on the possible prognostic value
of a reversal of nystagmus direction toward the affected
ear to predict an imminent recurrence of Ménière dis-
ease. Wu et al174 reported head-shaking nystagmus when
the degree of horizontal canal paresis exceeded 25%.
Head-shaking nystagmus was also dependent on the
stage of vestibular compensation. Monophasic nystag-
mus occurred in patients with acute loss, while biphasic
nystagmus occurred with development of vestibular
compensation. Any result other than monophasic or
biphasic horizontal nystagmus was suggested to indicate
central abnormalities and, therefore, indicate a reason
for medical referral.
eye movement) to maintain gaze fixation on the nose.131
A corrective saccade following head thrust to the right
indicates the vestibular loss is on the right; corrective
saccades with head thrust to the left suggest an involved
left side.176 Schubert et al177 reported a sensitivity of 71%
and a specificity of 82% for the head-thrust test with the
head tilted down 30° in the diagnosis of patients with
unilateral vestibular loss and 84% sensitivity and 82%
specificity for bilateral loss.
Benign Paroxysmal Positional Vertigo Tests
These tests look for canalithiasis or cupulolithiasis in
all SCCs. A positive response on these tests in combination
with corroborating history findings and in the absence of
findings indicative of other pathology implies that sole
physical therapy management may be indicated.
Hallpike-Dix maneuver
This maneuver (Figures 7A and B) tests all SSCs.46 The
long-sitting patient turns the head 45° and is then assisted
into supine with the rotated head 30° below horizontal.
This position is maintained for at least 30 seconds. De-
layed-onset, torsional, horizontal, or (less commonly)
vertical nystagmus in combination with vertigo lasting
less than 60 (canalithiasis) or more than 60 seconds (cu-

Head-thrust test
The head-thrust test (Figures 6A and B) may also
detect an impaired vestibulo-ocular reflex.175 The patient
fixates the gaze on the therapist’s nose. The therapist
then moves the patient’s head in the horizontal plane in
a rapid passive manner with unpredictable timing and
direction (5° to 10° at 3000° to 4000° per second). A A B
patient with vestibular loss will have difficulty maintain-
ing gaze fixation, requiring a corrective saccade (fast Figures 7A and B. Hallpike-Dix maneuver.

40
pulolithiasis) that decreases with repeated testing consti-
tutes a positive finding.108,132,178 Relevant for differential
diagnosis with regard to which SCC is involved is the
type of nystagmus and whether the test is unilaterally or
bilaterally positive:
• An ipsilateral maneuver positions the posterior SCC
of the down-side ear in the plane of the pull of gravity.
Shifting of otoconia, whether free floating (canalithia-
sis) or adhered to the cupula (cupulolithiasis), deflects
the cupula and alters the posterior SCC neuronal
firing rate.178 This results in an apogeotropic (beating
away from the earth or down-side ear) torsional nys-
tagmus.178
• A bilateral positive test implicates either the anterior
or horizontal SCC.108,132 With anterior SCC BPPV, the
ipsilateral test provokes a geotropic (beating toward
the earth or the affected ear) torsional178 or a down-
beating vertical nystagmus.132
• A bilaterally positive test with a purely horizontal
geotropic (beating in the direction of the face turn or
down-side ear) nystagmus implicates the horizontal
SCC.108 Nystagmus will occur in both directions but
will generally be stronger with the head turned toward
the affected side.108
Positional nystagmus on this test has been shown
to identify patients with posterior SCC BPPV with 78%
sensitivity.179 Specificity as high as 88% has been re-
ported.30
Straight head-hanging test
In the straight head-hanging test, the patient is as-
sisted into lying back from long sitting with the head
extended but not rotated. This test may be more sensitive
for anterior SCC BPPV. An additional 20° of extension
as compared to the Hallpike-Dix maneuver causes the
ampullary segment of the anterior SCC to approach a
more vertical position.132 We found no data on reliability
and validity.
Roll test
The roll test detects horizontal SCC BPPV. The thera-
pist quickly log rolls the supine patient with the head 30°
flexed to one side, maintaining this position for at least
1 minute. Otoconia moving back and forth within the
SCC with left and right rotation will cause the positive
response of nystagmus and vertigo. Canalithiasis causes
fatiguing geotropic (toward the earth) nystagmus and
cupulolithiasis persistent apogeotropic (away from the
earth) nystagmus. More severe and longer lasting symp-
toms indicate the affected side.178 We found no data on
reliability and validity.
Walk-rotate-walk test
In this test for the horizontal SCC,180 the patient
walks straight ahead at the patient-selected maximum
tolerable speed in a room with ample space. The patient
then rotates 180° on the axis of the rotation-direction
foot, returning back in a continuous movement. The test
41
is performed to both sides. Staggering, side stepping,
making corrective movements of the body or hands,
discontinuing the rotation in one direction, or slowed
and difficult rotation indicate a positive test. A positive
response on rotation to the right implicates the right and
a positive response on rotation to the left implicates the
left SCC. The difference must persist over 3 repetitions.
Rahko and Kotti180 found 100% predictive validity for this
test in determining a positive response to a horizontal
SCC BPPV treatment. The 180° turn in this test versus the
90° turn in the roll test may allow for higher otoconia ac-
celeration and ampulla cell stimulation. Sensitivity was
acceptable; some patients with acute vestibular neuritis
tested positive on the walk-rotate-walk test.180
Cervicogenic Dizziness Testing
The neck torsion test (Figures 8A and B) is used to
detect cervicogenic dizziness.181,182 The head is held
stationary during neck and trunk rotation. An alternate
way of screening the cervical spine as the possible origin
of dizziness symptoms is to have the patient sit and flex
forward at the hips while simultaneously extending and
rotating the neck (Figure 9).183 As both tests keep the in-
ner ear stationary, the vestibular system is not stimulated.
Nystagmus and dizziness with this test are, therefore,
interpreted as cervicogenic. However, the therapist still
needs to differentiate between vascular or somatosensory
cervicogenic involvements.183 Diagnostic accuracy is
questionable; 50% of subjects without cervical pathology
tested positive for nystagmus,184 possibly a manifestation
of the cervico-ocular reflex.17 Fitz-Ritson2 found that
47% of patients with cervical trauma demonstrated sub-
jective symptoms of vertigo or postural instability during
the neck torsion test; 90% improved following therapy.
We found no additional data on reliability and validity.
A positive response on these tests in combination with
corroborating history findings in the absence of findings
indicative of other pathology implies that sole physical
therapy management may be indicated.
A B
Figures 8A and B. Neck torsion test.

Figure 9. Alternate neck torsion test.
Breathing-related Tests
Hyperventilation test
The hyperventilation test requires patients to vol-
untarily hyperventilate (ie, 30 breaths per minute for 3
minutes).109 It may be a useful and simple test for validat-
ing a diagnosis of panic disorder or dizziness related to
hyperventilation presyncope. In these patients, this test
will produce dizziness but no nystagmus.67 Patients with
demyelinating lesions of the vestibulocochlear nerve
due to an acoustic neuroma, compression by a small
blood vessel, or central demyelinating lesions (multiple
sclerosis) may show nystagmus on the hyperventilation
test.67 Hyperventilation may accentuate down-beating
nystagmus in patients with Arnold-Chiari malformation
and evoke a nystagmus toward the lesion in patients with
vestibular schwannomas.170 Nardi et al185,186 found that
the hyperventilation test produced significantly more
symptoms in patients with panic disorder than in patients
with obsessive-compulsive disorder or depression, or in
normals, and they noted that it might be an easy test to
validate panic disorder.186 Nakao et al187 reported 62%
sensitivity and 100% specificity for this test in the diagno-
sis of coronary spasm. The authors have noted clinically
that near-immediate reproduction of symptoms may indi-
42
cate psychogenic contribution to dizziness complaints.
A positive finding on these tests indicates the need for
referral.
Valsalva test
In patients with Arnold-Chiari malformation, perilym-
phatic fistulae, and other abnormalities of the ossicles
(eg, otosclerosis), oval window, and saccule, a Valsalva
maneuver may produce nystagmus. Changes of middle
ear pressure due to loud noises, application of positive
and negative pressure to the tympanic membrane (Hen-
nebert sign), and opening and closing the eustachian tube
may have a similar effect.67 The cough test is a variant on
the Valsalva test. Having the patient cough to increase
intrathoracic pressure may be useful in detecting dizzi-
ness due to cough presyncope.43 We found no data on
reliability and validity. Positive tests indicate the need for
referral.
HISTORY AND PHYSICAL EXAMINATION
About 50% of dizziness is vestibular and benign.30
More serious causes (eg, brain tumors and cerebrovas-
cular disorders) account for about 1% and 5% of cases,
respectively.30 Froehling et al188 studied diagnostic accu-
racy of symptoms and signs in distinguishing benign from
serious causes:
• Vertigo or vomiting combined with a positive Hall-
pike-Dix test demonstrated 85% positive predictive
value and a 7.6 positive likelihood ratio for a benign
cause
• A negative Hallpike-Dix maneuver and the absence
of vertigo or vomiting had a 68% negative predictive
value for peripheral vertigo
• Age of 69 or less, the absence of neurological deficits,
the presence of vertigo, or a combination of these
factors has a negative predictive value of 88% with a
negative likelihood ratio of 0.3 for a serious cause of
dizziness
• Age greater than 69, the presence of neurological defi-
cit, the absence of vertigo, or a combination of these
factors carries a positive predictive value of 40% and
a positive likelihood ratio of 1.5 for a serious cause of
dizziness
CASE STUDIES
Case Study 1
Subjective information
The patient, a 75-year-old white man, is a retired
Royal Canadian Navy fighter and helicopter pilot. Four
years prior to this first physical therapy evaluation, he
woke up severely perspiring in the middle of the night
with paresthesia around the left eye. The next morning
he noted severe and persistent dizziness, described as
disorientation. His primary care physician subsequently
referred the patient for a computerized tomography scan
of the head. This scan revealed a sinus infection that was
treated with antibiotics. The sinus infection was cured but
symptoms of dizziness persisted unabated. Referral to a
neurologist resulted in further testing. A magnetic reso-
nance imaging scan of the brain, an ultrasound examina-
tion of the carotid artery, a Holter monitor test, and lab
tests all came back negative. An ophthalmologist found
no abnormities implicating the visual system. A second
neurological opinion resulted in a diagnosis of probable
inner ear dysfunction with a suggested benign natural
history. No further intervention was suggested. Symptoms
indeed decreased some 2 years after the initial onset but
returned 1 year ago for another 6 months after swimming
and again 2 months ago after what was diagnosed by an
emergency room physician as an anxiety attack, perhaps
as an unusual side effect of taking the nonsteroidal anti-
inflammatory medication Meloxicam for right medial
compartment knee osteoarthritis.
The current complaint consists of episodes of constant
dysequilibrium that are preceded by a feeling of fullness
in the head. Symptoms remain at their worst intensity for
about 3 to 4 hours. The patient can report no precipitating
factors but has noted numbness around the left eye, some
difficulty swallowing, and chest palpitations accompany-
ing the feeling of unsteadiness. When severe, symptoms
also include nausea, general fatigue, impatience, and
irritability. Since this last onset, but not in previous epi-
sodes, the patient also reports a weakness in the legs that
fluctuates with other symptoms. The patient intake ques-
tionnaire (Table 13) revealed a positive personal medical
history of heart disease. Further questioning revealed a
coronary artery bypass graft surgery 9 years previous.
There were no further relevant check marks on the in-
take questionnaire. Current medications taken included
Simvastatin (hypercholesterolemia), aspirin (prevention
of cardiovascular events), Xalitan eye drops, and Rivotril
(anxiolytic). Anxiety had been suggested 3 years ago as
a possible cause for the prolonged complaints of dizzi-
ness. A history using the structured interview suggested
in Table 14 revealed no further relevant information.
Objective findings
The physical examination followed the proposed
examination template in Table 15. Postural observation
revealed a forward head posture. The sit-to-stand test for
orthostatic hypotension showed a normal blood pres-
sure and heart rate response. Cranial nerve, oculomotor,
hearing, and limb ataxia tests were all negative. Active
range-of-motion testing revealed decreased left rotation
and extension of the cervical spine. Passive range-of-
motion testing of the arms and legs showed no muscle
tone abnormalities. Upper cervical ligamentous stability
tests were normal, and the sustained rotation test of the
cervical spine produced no signs or symptoms indica-
tive of VBI. Segmental motion testing of the cervical and
thoracic spine revealed a decreased left C1-C2 rotation,
left C3-C6 extension, and C7-T5 bilateral rotation and
extension. The patient was unable to perform the cervical
deep flexor endurance test without forward chin thrust.
Pathological reflexes (Hoffman signs and Babinski reflex)
were bilaterally absent and deep tendon reflexes in the
43
arms and legs were bilaterally normal. Vibration sense
at bilateral ankles and big toes, tested with a 256 Hz
tuning fork, was equal and normal. The vestibulo-ocular
tests were all normal, with the exception of a horizontal
biphasic nystagmus initially beating right and then left
with the head-shaking nystagmus test. Tests for BPPV
were negative, with the exception of consistent stag-
gering and decreased speed of movement on the left
walk-rotate-walk test. The neck torsion test for detection
of cervicogenic dizziness was negative and so were the
Valsalva, cough, and hyperventilation tests.
Physical therapy diagnosis
The history and physical examination seemed to indi-
cate a physical therapy diagnosis of:
• Decreased or absent function of the left horizontal
SCC
• Decreased segmental mobility in the cervical and up-
per thoracic spine
• Decreased endurance of the deep cervical flexor
muscles
• Cervicogenic dizziness
• Lack of knowledge with regard to diagnosis and prog-
nosis of current complaint
The therapist was confident that previous medical ex-
aminations and the results of the current physical therapy
examination excluded a central vestibular or other central
neurologic, cardiovascular, and metabolic etiology for
the current complaint of dizziness. However, the report
of palpitations, nausea, generalized fatigue, irritability,
and impatience, as well as the prescription for anxiolytic
medication did not exclude a psychogenic contribution
to the current complaint of dizziness.6 Positive findings on
the left walk-rotate-walk test implicated the left horizontal
SCC.180 A biphasic horizontal nystagmus initially beating
right and then left with the head-shaking nystagmus test
implicated a central adaptation to a left horizontal SCC
hypofunction.174
The therapist entertained a working hypothesis of an
initial onset of the complaints due to compression of the
vestibulocochlear nerve in the internal auditory canal as a
result of an inflammatory or infectious process. This would
seem to explain the diaphoresis at initial onset and fit with
the diagnosed sinus infection. The paresthesia reported at
that time around the left eye and later the numbness may
have been a misinterpretation of motor deficits from the
facial nerve that might also have been compressed with
the vestibulocochlear nerve as they both travel through
the internal auditory canal.11 The horizontal canal paresis
had a benign course as other afferent information com-
pensated, most likely proprioceptive afferent information
from the cervical spine.
Although the neck torsion test was negative, the seg-
mental hypomobilities in the cervical spine and the de-
creased deep cervical flexor muscle function implicated
the cervical spine and resultant cervicogenic dizziness.
Fighter pilots are subjected to excessive acceleration and
deceleration and may be more prone to degenerative
changes in the cervical spine. A preexisting horizontal SCC
paresis and periodic aggravation of cervical dysfunctions
with resultant alterations in cervical proprioceptive input
to the central vestibular apparatus may have resulted in
decompensation of vestibular adaptive mechanisms and
the periodic described complaints of dizziness.
Guide to Physical Therapist Practice diagnosis
The diagnosis according to the Guide to Physical
Therapist Practice189 is:
• Practice pattern 4C: impaired muscle performance
• Practice pattern 4D: impaired joint mobility, motor
function, muscle performance, and range of motion
associated with connective tissue dysfunction
• Practice pattern 5D: impaired motor function and sen-
sory integrity associated with nonprogressive disorders
of the central nervous system acquired in adolescence
or adulthood
Physical therapy management and outcomes
Physical therapy management on the first visit con-
sisted of the examination described above followed by
patient education on examination findings, diagnosis,
prognosis, and proposed treatment plan. The goal of
this education was twofold: to get informed consent for
the suggested plan of care and to decrease any possible
causative anxiety regarding the current complaints. The
patient reported that the education had indeed put him
at ease and expressed his eagerness to participate in the
suggested plan of care.
Further treatment on the first visit included thrust trac-
tion manipulation to the upper thoracic restricted motion
segments, as thoracic thrust manipulation has not been
associated with the same risk of adverse effects as cervical
thrust manipulation and because preliminary evidence
exists for its immediate efficacy with regard to reported
mechanical neck pain.190 A cervical autorotation exercise
in the horizontal plane was used as a home exercise. The
patient was told to sit on a chair, focus on a fixed point,
and rotate the head 45° side to side for 30 to 60 seconds
5 times per day, just below the level of producing diz-
ziness. The intent of this exercise was to reintegrate the
cervical afferent input and allow for partial substitution of
the vestibulo-ocular reflex by the cervico-ocular reflex.
The second home exercise was an active upper thoracic
extension exercise to maintain post-thrust increase in
range of motion.
On the second visit, 1 week later, the patient reported a
decrease in the feeling of unsteadiness. However, AROM
testing and segmental motion tests of the cervical spine
still showed limitations as noted on the initial examina-
tion. Even though atherosclerosis and atherosclerotic
risk factors as present in this patient have not been im-
plicated as a risk factors for adverse effects with cervical
manipulation,5 after a risk-benefit analysis as part of an
informed consent procedure, the therapist and patient
decided not to use cervical thrust manipulation but rather
nonthrust techniques. Soft tissue techniques to the cervi-
44
cal spine, including effleurage, petrissage, and inhibitory
techniques, were followed up with grade IV-IV+ oscilla-
tory mobilization into left C1-C2 rotation and left C3-C6
extension. Upper thoracic traction thrust manipulation
was repeated because some segmental restrictions were
still noted at C7-T5. The home program was expanded to
include cervical autorotation techniques in standing first
with a normal stance and progressing as tolerated to a
narrow stance and heel-to-toe stance, stretching exercises
for the cervical and pectoral muscles, and left rotation of
the head and neck in flexion for self-mobilization of the
C1-C2 restriction noted.
On the third visit, 3 weeks after the initial examina-
tion, the patient reported only very minimal complaints
of unsteadiness. Cervical and thoracic active and seg-
mental motion were only minimally restricted. The walk-
rotate-walk test to the left resulted in staggering on only
1 trial out of 3. The cervical nonthrust and thoracic thrust
manipulations were repeated, as were the cervical soft
tissue techniques described above. The patient was in-
structed in a progression of deep cervical flexor muscle-
strengthening exercises with specific written instructions.
In an effort to ensure greater compliance, the home
program was cut down to just this strengthening exercise,
the autorotation exercise in heel-to-toe stance, and an
exercise that involved a left 180° rotation while walking
just below the rotational speed causing unsteadiness to
integrate visual, somatosensory, and remaining vestibu-
lar input in a motion with more relevance to functional
situations that in the past may have caused complaints.
The patient was discharged from physical therapy at this
time. A follow-up phone call 1 month later revealed only
minimal and occasional complaints of unsteadiness as
reported during the initial examination.
Case Study 2
Subjective information
The primary care physician referred this patient, a
45-year-old white woman, to physical therapy with a
diagnosis of acute cervical strain. The patient works as a
computer programmer, which requires her to sit in front
of a computer throughout the day. She is also an avid
recreational soccer player. Five days prior to referral to
physical therapy, the patient, in the midst of playing in
a soccer game, was struck on the right side of the back
of her head by a soccer ball. No loss of consciousness
occurred. After 2 days of self-management, which in-
cluded rest, ice, and over-the-counter anti-inflammatory
medication, the patient did not experience any decrease
in neck pain. The patient was subsequently examined by
her primary care physician and was prescribed Skelaxin
to help decrease muscle spasm and pain, and referred
to physical therapy with the diagnosis noted above.
Diagnostic tests including plain film radiographs of her
cervical spine were not ordered.
The patient’s chief complaint is of constant right-sided
cervical pain, but with variable intensity. Pain assessment
via a visual analog scale (0 = no pain, 10 = worst pain
imaginable) demonstrates the patient’s worst pain at 8 out
of 10 and best pain at 4 out of 10. Pain is worst at the end
of the workday and is aggravated by cervical flexion and
left rotation. Neck pain improves with Skelaxin (800 mil-
ligrams) and the application of a heating pad to the painful
area for 20 minutes. The patient denies any upper extrem-
ity or lower extremity symptoms, but she complains of a
recent onset of intermittent dizziness that began the day
after her physician examined her. The patient’s dizziness
symptom is described as spinning and lightheadedness,
most notably when rolling onto her right side and when
bending over to tie her shoes. She feels that the spinning
lasts about 30 seconds, but the lightheadedness may last
for a few hours. The lightheadedness seems to be worst at
the end of the workday when her neck pain is also at its
worst. The patient’s lightheadedness also seems to worsen
about 1 hour after taking the Skelaxin for her neck pain.
The patient denies other associated or prodomal symp-
toms. The patient’s medical intake questionnaire did not
reveal any past medical or surgical history. Skelaxin was
the only current medication.
Objective findings
Postural observation revealed a forward head posture,
rounded shoulders, and increased thoracic kyphosis.
Blood pressure and heart rate measurements were
normal in sitting and standing. The patient’s gait pat-
tern was normal except when performing concurrent
head rotation, which produced a decrease in cadence
and mild deviation to the right from a straight line. The
Romberg test was essentially unremarkable, producing
only a mild anterior to posterior sway with eyes closed.
Cranial nerve, oculomotor, and limb ataxia tests and
measures did not produce any significant findings. Visual
assessment of AROM revealed decreased left rotation,
left side bending, and flexion of the cervical spine. Pain
and lightheadedness were reproduced with all of these
motions at end range. A mild feeling of spinning was
produced with cervical flexion and right rotation. Upper
cervical stability tests were normal. The vertebral artery
test was not performed for reasons noted by Vidal.165
Passive mobility testing revealed restricted left rotation at
C1-C2, decreased forward nodding at Occ-C1 right, and
restricted bilateral rotation at C7-T3. Palpation revealed
a hypertonic right sternocleidomastoid muscle and pro-
duced mild lightheadedness. Decreased endurance was
detected in the cranial flexors during the cervical deep
flexor endurance test. Reflex testing was unremarkable.
The vestibular system examination was normal except
for a positive right Hallpike-Dix maneuver; this test pro-
duced a delayed onset of up-beating horizontal-rotary
nystagmus lasting less than 30 seconds. The roll test, left
and right, for horizontal canal BPPV failed to reproduce
nystagmus, but a sense of lightheadedness was experi-
enced with the left roll test. The neck torsion test did not
reproduce spinning but did reproduce a moderate sense
of lightheadedness with the trunk rotating right.
45
Physical therapy diagnosis
The history and physical examination seemed to indi-
cate a physical therapy diagnosis of:
• Decreased AROM of the cervical spine
• Decreased segmental mobility in the upper cervical
spine and upper thoracic spine
• Decreased endurance of the deep cervical flexor
muscles
• Cervicogenic dizziness
• Right posterior canal BPPV
• Potential medication-related side effect of Skelaxin
• Poor ergonomic and body mechanics awareness at
work
Based on the history and physical examination find-
ings, the therapist was confident that the patient’s neck
pain was musculoskeletal in origin and that the complaint
of dizziness was peripheral, not central, in origin. The
physical impairments detected in the cervical and tho-
racic spines combined with the finding that the patient’s
lightheadedness was worse when her neck pain was
worse, the absence of red flag items for vertebrobasilar
involvement (Table 7), an onset of neck pain related to
physical trauma, a reproduction of dizziness symptoms
with cervical AROM, and a positive neck torsion test led
to the most likely diagnosis of cervicogenic dizziness. Al-
though the diagnostic accuracy of the neck torsion test is
questionable, there was diagnostic concordance of both
the history and physical examination findings. A positive
right Hallpike-Dix maneuver with up-beating horizontal-
rotary nystagmus implicated nonidiopathic right poste-
rior canal BPPV, likely due to the head trauma described.
With a specificity for the Hallpike-Dix reported as high
as 88%,30 the therapist felt confident that this positive
test result ruled in the diagnosis of right posterior canal
BPPV. The therapist suspected that the muscle relaxant
(Skelaxin) contributed to the patient’s complaint of diz-
ziness, as the patient experienced an increased sense of
lightheadedness 1 hour after taking this medication. In
summary, the history and physical examination findings
indicated that cervicogenic dizziness and BPPV were
concurrently present, complicated by a potential side
effect of Skelaxin. Poor ergonomics and body mechan-
ics awareness were suspected given the results from the
visual posture assessment and reported occupational
demands.
The pain and lightheadedness reproduced with active
cervical motions and the neck torsion test was likely
from abnormal afferent somatosensory input stemming
from the upper cervical spine where irritated muscle
spindles and joint mechanoreceptors contributed to
altered postural control experienced by the patient as a
sense of lightheadedness.181 This was evident during the
gait assessment when concurrent head rotation caused
a decreased cadence and mild deviation from a straight
line. The findings on the right Hallpike-Dix maneuver
were consistent with canalithiasis, as there was a delayed
onset of symptoms lasting less than 60 seconds. Dizziness
has been reported as a potential medication-related side
effect of Skelaxin. Also, a potential result of overdosage
is low blood pressure.191 The normal blood pressure mea-
surements noted above led the therapist to suspect not an
overdosage but rather a medication-related side effect of
dizziness. Head trauma may affect central structures, such
as the brainstem, and thereby cause dizziness symptoms.
However, the history and physical examination were not
consistent with a central cause of dizziness. Poor ergo-
nomics and body mechanics awareness at work may have
further contributed to the patient’s pain and dizziness, as
abnormal stresses are applied on the cervical and thoracic
spines with the forward head, rounded shoulder posture.
Guide to Physical Therapist Practice diagnosis
The diagnosis according to the Guide to Physical
Therapist Practice189 is:
• Practice pattern 4B: impaired posture
• Practice pattern 4E: impaired joint mobility, motor
function, muscle performance, and range of motion
associated with localized inflammation
• Practice pattern 5D: impaired motor function and sen-
sory integrity associated with nonprogressive disorders
of the central nervous system acquired in adolescence
or adulthood
Physical therapy management and outcomes
Physical therapy management began following the
examination. The examination findings, diagnosis, prog-
nosis, and proposed plan of care were discussed with the
patient. A brief telephone conversation was held between
the therapist and the referring physician. The therapist
reviewed the examination findings with the referring
physician with particular focus on the patient’s complaint
of dizziness as the complaint of dizziness began after the
physician examination. In addition, the therapist inquired
about the current dosage (800 milligrams) of Skelaxin, as
the use of Skelaxin appeared to increase the patient com-
plaints of dizziness. The therapist and physician have a
close working relationship and they mutually agreed that
right BPPV was likely and the patient would most likely
benefit from canalith repositioning maneuvers. The physi-
cian also instructed the patient to decrease her dosage of
Skelaxin by half to 400 milligrams.
The patient agreed to the proposed plan of care, which
started with patient education regarding proper ergo-
nomic set-up at her workstation and body mechanics and
postural awareness. The intention of this education was
to facilitate minimizing external stresses that are applied
to the cervical spine and to promote healing of irritated
soft tissue structures. A moist heat pack was applied to
the cervical spine for 15 minutes followed by soft tissue
manipulation to the cervical spine, focusing on the right
sternocleidomastoid. Following this cervical intervention
intended to increase range of motion and tissue exten-
sibility and to decrease pain, a canalith repositioning
maneuver (right Epley maneuver) was performed to ad-
dress the right BPPV. A home exercise program was then
prescribed, including gentle self-stretching of the right
46
sternocleidomastoid (3 times for 15 seconds), pain-free
cervical range-of-motion exercises, and postural correc-
tion exercises (axial extension and scapular retraction).
The patient was instructed to perform these exercises 3
times per day. At the end of visit 1, retesting with the
Hallpike-Dix maneuver was negative for right BPPV.
On the second visit, 1 week later, the patient reported
that she had not experienced any vertiginous dizziness
since the first visit. She also reported decreased cervi-
cal pain (4 out of 10 at worst; 2 out of 10 at best) and
decreased lightheadedness. The patient also reported
that she no longer experienced increased lightheaded-
ness after taking the muscle relaxant. She also reported
having made changes to her workstation, which seemed
to help decrease her neck pain. Upon reexamination,
the Hallpike-Dix maneuver was negative for right BPPV.
However, active cervical rotation was still limited with
left rotation, left side bending, and flexion producing pain
and mild lightheadedness but no vertiginous dizziness.
The right sternocleidomastoid remained hypertonic, and
palpation of this muscle produced mild lightheadedness.
The therapist continued with soft tissue manipulation to
the right sternocleidomastoid followed by grade III-IV
forward-nodding mobilization to the right Occ-C1 ar-
ticulation and a muscle energy technique to improve left
rotation at C1-C2. Posterior-anterior grade III-IV mobili-
zations were also applied to C7-T3 bilaterally. Contract-
relax stretching of the right sternocleidomastoid followed
these articular manual therapy techniques. The patient
was instructed to continue her home exercise program as
prescribed during visit 1 but to increase the duration of
her right sternocleidomastoid stretch to 30 seconds.
The patient returned 3 days later and reported no
vertiginous dizziness and only mild lightheadedness: 0
at its best and 1 to 2 at its worst on a 0 to 10 numeric
rating scale used to measure intensity of dizziness com-
plaints. Similarly, she rated her neck pain as 0 at its best
and 1 to 2 on a 0 to 10 numeric pain rating scale; these
higher pain ratings were still experienced at the end of
the day. She reported that she was taking the Skelaxin
only as needed as compared to previously 3 times per
day. Active cervical range-of-motion tests revealed full
motion with a gentle stretching pain at end-range left side
bending. The AROM tests reproduced no lightheaded-
ness. Passive segmental mobility testing revealed normal
forward nodding at the right Occ-C1 joint and normal
left rotation at C1-C2. Mild restrictions were still noted
with bilateral rotation at the C7-T3 levels. Upper thoracic
traction thrust manipulation was applied to address these
remaining C7-T3 restrictions. Palpation still revealed
mild hypertonicity of the right sternocleidomastoid,
but this palpation no longer resulted in reproduction of
lightheadedness. Cervical deep flexor exercises using a
blood pressure cuff to provide feedback to the patient
with regard to effort were initiated to improve endurance
and followed the protocol as outlined by Jull et al.36,38
The patient’s home program was progressed to include
resistance bands for strengthening scapular retraction.
The patient was instructed to perform craniocervical flex-
ion exercises in supine 3 times per day for 10 repetitions
with a 10-second hold.
The patient returned 1 week later for visit 4. She re-
ported no complaints of dizziness and very minimal neck
pain (1 out of 10 at worst). Active cervical range of mo-
tion was full and pain-free. Passive segmental mobility of
the cervical and upper thoracic spine was unrestricted.
The right sternocleidomastoid demonstrated normal
tone. Improvement was observed in cervical deep flexor
endurance. The patient’s home exercise program was
reviewed for comprehension and proper performance.
As the patient had met all previously agreed upon long-
term goals, she agreed to discharge from physical therapy
intervention. A 1-month follow-up via a telephone call
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ACKNOWLEDGEMENTS
The authors would like to thank Maureen McKenna,
PT, MS, OCS, for her willingness to serve as a model, as
well as Paul Mensack, PTA, for their assistance with the
pictures included in this monograph. The material in this
monograph was based to a large extent on the articles
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NOTES

54
NOTES

55
 Orthopaedic Section Independent Study Course 17.3.3
Cervicogenic Dizziness and Differential Diagnosis of Dizziness
in the Orthopaedic Physical Therapy Setting
REVIEW QUESTIONS
1. The most common peripheral vestibular disorder is:
a. acoustic neuroma.
b. benign paroxysmal positional vertigo.
c. Ménière disease.
d. perilymphatic fistula.
2. Benign paroxysmal positional vertigo of the left pos-
terior canal due to adherent otoconia on the cupula
is characterized by:
a. down-beating torsional nystagmus lasting less
than 60 seconds.
b. down-beating torsional nystagmus lasting more
than 60 seconds.
c. up-beating torsional nystagmus lasting less than
60 seconds.
d. up-beating torsional nystagmus lasting more than
60 seconds.
3. What finding indicates a positive Weber test for
unilateral sensorineural hearing loss?
a. air conduction is louder than bone conduction.
b. bone conduction is louder than air conduction.
c. patient perceives sound coming from normal
ear.
d. patient perceives sound coming from abnormal
ear.
4. To differentiate dizziness originating from the pe-
ripheral vestibular system versus the upper cervical
spine, the therapist would compare active cervical
rotation with the:
a. Hallpike-Dix maneuver.
b. Fukuda step test.
c. head-thrust test.
d. neck torsion test.
5. The diagnosis of cervicogenic dizziness is compli-
cated by the fact that neck movements can affect
the:
a. cardiovascular system.
b. cervical musculoskeletal system.
c. vestibular and visual systems.
d. all of the above.
56
6. Which symptoms best describe an acute episode of
Ménière disease?
a. constant, severe vertigo with aural fullness and
severe tinnitus.
b. constant, severe vertigo without tinnitus but with
nausea and vomiting.
c. position-dependent, severe vertigo with tinnitus
and nausea.
d. position-dependent vertigo with mild tinnitus
and spontaneous nystagmus.
7. Disproportionate weakness in the sternocleido-
mastoid and trapezius muscles has been associated
with:
a. Arnold-Chiari malformation.
b. cervicogenic dizziness.
c. toxic vestibulopathy.
d. vertebrobasilar ischemia.
8. Which symptoms best describe basilar-type mi-
graine?
a. dysarthria, vertigo, ataxia, and bilateral paresthe-
sia.
b. hyperacusis, vertigo, unilateral visual symptoms,
and quadrilateral paresis.
c. vertigo, bilateral diplopia, ataxia, and ipsilateral
arm and leg paresis.
d. vertigo, stupor, tinnitus, and ipsilateral arm and
leg paresthesia.
9. Which diagnosis is associated with vertigo brought
on with arm exertion but not neck movements?
a. multiple sclerosis.
b. subclavian steal syndrome.
c. vertebrobasilar ischemia.
d. Wernicke encephalopathy.
10. A patient may report a sensation of tilting of the
environment as a the result of:
a. mal de debarquement syndrome.
b. unilateral otolith dysfunction.
c. vertebrobasilar infarction.
d. all of the above.
 1. b
2. d
3. c
4. d
5. d
6. a
7. a
8. a
9. b
10. d
ANSWERS