Vestibular function evaluation &

diagnosis
Han Young Hoon, M.D.
Department of Otorhinolaryngology, Head & Neck Surgery, MNUSC
Basic Anatomy & physiology
• The physiologic range of head movements in SCC : 0.1 to 15 Hz
: in this range SCC integrate acceleration signal into a velocity signal.
• Resting firing rate in each afferent of SCC and Otolith organs
:10~100 spikes/second
• Activity in the vestibular nerve is the major source of sensory input to
the vestibular nuclei, with almost 30,000 afferents projecting from each
labyrinth to the brainstem in humans
• The limits of stability are defined by a horizontal ellipse measuring
approximately 12.5 degrees from front to back.
• The lateral dimension of limits of stability depends on the subject’s
height relative to spacing between the feet. For a person 70 inches tall
with feet placed 4 inches apart, the lateral dimension of the “limits of
stability” ellipse is approximately 16 degrees from left to right.
Definitions of vestibular Sx.
( by International Classification of Vestibular Disorders)
• Vertigo - sensation of self (internal) or environmental (external)
movement when such movement is not occurring, for example,
spinning, rocking, swaying, tilting, bobbing, sliding, or bouncing.
• Dizziness - sensation of disturbed or impaired spatial orientation
without a sensation of self or environment movement
• Unsteadiness - sensation of being unstable-independent of position
without a directional preference.

Bisdorff A. Von Brevem M, Lempert T, et al. Classiiication of vestibular

symptoms: towards an international classification of vestibular disorders. J
Vestib Res 2009;19(1-2):1-13
Definitions of vestibular Sx.
(by textbook Bailey’s H&N surgery, otolaryngology, 2013)
1. Vertigo
• a false sense of motion within the patient's environment
• is usually described as a spinning, whirling, tumbling or even
rhythmic rocking feeling
• valuable indicators of peripheral inner ear or nerve
dysfunction
2. Disequilibrium
• difficulty maneuvering within their physical environment
often without experiencing an illusion of motion
3. light-headedness
• both a wide range of sensations (such as "wooziness,
giddiness, feeling faint, or as if one is about to pass out") and
of etiologies (including migraine, vascular, metabolic, drug-
induced, endocrine, or primary psychogenic causes)
Definitions of vestibular Sx.
Dizziness : all of disturbed sense of relationship to space
including abnormal rotatory, linear move sense.

Kerber KA, Meurer WJ, West BT, et al. Dizziness presentations in U.S.
emergency departments, 1995–2004. Acad Emerg Med. 2008;15(8):744–750
Vertigo
• Vertigo
: an illusion of spinning movement of subjective or objective
1. True Vertigo
• must be nystagmus with spinning sense in opened eyes
• vestibular system origin
• mostly is induced by ENT origin, pre-vestibular nuclei
region
2. False Vertigo
• rotatory sense of one’s head only in closed eyes
• not true vertigo, r/o psychological Dx.
Vertigo
• Vertigo
3. Central Vertigo
• vertigo due to a disease originating from the CNS
• Cause
: hemorrhage or ischemia to the cerebellum, vestibular
nuclei, and their connections within the brainstem
: CNS tumor, infection, trauma, multiple sclerosis
 Most of Sx. is gradually developed  acute Sx. rare
Differential Diagnosis of Vertigo
Peripheral lesion (vertigo) M/C, no CNS Sx.
Vestibular nuclei’s lesion Combined peripheral and CNS Sx.
Central lesion (vertigo) rare, no hearing Sx.

• Acute Vestibular Syndrome

• localizing lesion to the vertebra-basillar circulation including
vestibular nuclei
• Vertigo(+), Nystagmus(+)
• N/V, head motion intolerance, unsteady gait
 Distribution of Diziness Patients
% ER1 Otology2 Dizzy Clinic4 Neuro-Otology3 Neurology6

Otologic 24.0 41.4 64.7 34 45

Neurological 1.7 4.8 8.1 23 22.6

Medical 32.0 1.8 0 5

Psychogenic 21.1 9.0 18.8

Unknown 18.9
42.3 (both) 13.3 21 13.6
or Unlocalized 5.5, 40%5

number studied 121 2222 812 102 7205

Diagnoses in dizzy patients
1. Madlon-Kay, 1985. Unlocalized category included vasovagal, psychogenic, unknown.
2. Nedzelski, Barber, McIlmoyl, 1985. Unlocalized category included head injury.
3. Drachman and Hart, 1972. Unlocalized category included hyperventilation, psychogenic,
"excessive awareness of normal sensation", unknown.
4. Bath et al, 2000. 5. Guilemany, 2004
6. Dtsch Arztebl Int. 2008 Mar;105(10):173-80. doi: 10.3238/arztebl.2008.0173. Epub 2008 Mar 7
History taking & physical
examination of Dizziness
Patient
Evaluation of Dizziness Patients
Purpose of Dizziness Pts. evaluation
to rule out significant cardiovascular and neurological
disorders, quiet symptoms
1. To determine True Vertigo(spinning) or not
2. To determine Peripheral vertigo or central vertigo
to diagnose & management
1. To identify acute or chronic vertigo
2. To identify the specific cause and disease
3. To identify to need admission or not
4. To select proper medications and rehabilitation tools
Evaluation of Dizziness Patients
Acute patients
Extensive laboratory testing is generally unnecessary
since the presenting symptoms and office examination will
primarily guide initial management decisions
Chronic patients : intermittent or persistent symptoms for
greater than 2 months
Selection of appropriate laboratory tests is neccessary
3 goals
The reason why natural central compensation has not
taken place in a significant manner to reduce Sx.
Refined diagnosis
Establish the treatment program
History taking in dizziness patients
The most important tool in pts evaluation is history taking
Just after the first history taking 75 ~ 90% patient is diagnosed
before physical examinations and laboratory tests
Reasons
1. Most disease processes that cause dizziness have a
particular symptom pattern
2. Diseases of the inner ear and eighth cranial nave cause
distinctly different sensations than CNS, systemic,
musculoskeletal, or psychogenic processes
3. Most patients are not experiencing an acute sensation of
dizziness at the time of examination
4. the CNS has a remarkable way of compensating
between episodes such that clinical examinations and
laboratory findings are only seen during acute episodes
or in cases of significant damage.
Algorithm for the differential diagnosis for dizziness, based on information from the patient’s history
History taking in dizziness patients
1) Description of Sx.
: presyncope, lightheadedness, disequilibrium, vertigo
2) Aggravator & Induction factor of Sx.
: association with head position, lying down, getting up quickly
3) Onset : slowly Vs acute attack, memorable Vs spontaneous
4) Frequency : episodic(eventually) - /mm, /hrs, /days, /wks, or
continuous
5) Duration : last < ss, 1m, mm, hrs, days,
History taking in dizziness patients
6) Associated Ear Sx. : tinnitus, ear fullness, otorrhea,
fluctuation in hearing
7) Associated eye Sx. : diplopia, vision/visual field change
8) Associated general Sx.
: nausea, vomiting
: headache (interaction with vertigo/dizziness)
: weakness, LOC
: facial pain, paresthesia, paralysis, dysphagia
9) History of ear infection, perforation, head injury, ear surgery
10) History of drug
 History taking in dizziness patients
11) History of generalized disease
: DM, neurologic disorders, arteriosclerosis, HBP, thyroid disease
: syphilis(STD), anemia, malignancy, heart or lung Ds, allergy
12) Family history : headache, DM, Syndrome
13) Social history
: Job - office/field, day/night, <10hr/>10hr
: smoking – cigarette ? ea/day*year
: drinking – alcohol ? g/day* time/wks*year
: Stress amount scale
: exercise amount scale
 History taking in dizziness patients
Components of the Interview
What is the character of the dizzy
sensation?
What is the dizziness pattern?
What is the time course of dizzy
episodes?
Was there an event associated with
dizziness onset?
What associated symptoms
accompany the dizzy episodes?
Key Historical Features
Vertigo, disequilibrium, or light-headedness
Continuous or episodic
Seconds, minutes, hours, days, or longer
Head/inner ear trauma, barotrauma, upper respiratory
infection, ear infection, systemic illness or infection,
ototoxic medication
Hearing loss, tinnitus (continuous vs. pulsatile), aural
fullness, conductive hyperacusis, diplacusis,
dysacusis, autophony, oscillopsia, otorrhea, otalgia,
headache, facial or limb weakness, dysphagia,
dysphasia, visual changes, photophobia, phonophobia,
loss of consciousness, seizure
 History taking in dizziness patients
Components of the Interview Key Historical Features
What exacerbates the dizziness? Rapid head movement, particular head positions,
increased pressure(Hennebert sign), sounds (Tullio
phenomenon). hyperventilation, strong
environmental stimuli (bright lights, odors, etc.),
food triggers
What medications (past and present) Antibiotics, antineoplastic, analgesics, sedatives,
could be involved? antihypertensives, neuro leptics, antidepressants
What is the patient's past medical Migraine, endocrine (e.g., diabetes), rheumatologic,
history? cancer, cardiovascular, systemic infections
What is the patient's past surgical Focusing on otologic or brain surgery
history?
What is the family history? Migraine, endocrine (e.g., diabetes), rheumatologic,
cancer, cardiovascular, systemic infections, genetic
mutations
Differential diagnosis in history taking
• By duration (time course) of vertigo
Duration of vertigo Diagnosis possible

Vertigo lasting 15 Ideopathic endolymphatic hydrops (Ménière’s disease)

minutes to hours
Secondary endolymphatic Otic syphilis
hydrops
Cogan’s disease
Recurrent vestibulopathy
Delayed endolymphatic hydrops (after
profound HL, infection, trauma, etc)
Brainstem infarcts and cerebellar hemorrhages (Severe Sx + can’t stand)
Vertigo lasting 15 Transient ischemic attacks((TIA) involving the vertebrobasilar
minutes circulation and brainstem
Vertigo lasting seconds BPPV ( Benign Paroxysmal Positioning Vertigo)
Vertigo lasting days Vestibular neuritis
Vertigo of variable Inner ear fistula >1 Disease migrane
duration
Familial vestibulopathy Bilateral vestibular deficit
 Differential diagnosis in history taking
spontaneously vertigo attack for hrs ~ days, no audiologic Sx. and no
specific induction factor after URI  r/o Vestibular neuritis
vertigo attack for ss ~ 1m with head positioning  r/o BPPV (PSCC)
vertigo attack for ss ~ ms with lying down side  r/o BPVV(LSCC)
vertigo attack for 30m~hrs with ear fullness, fluctuating hearing loss,
tinnitus  r/o Meniere’s disease, r/o r/o posttraumatic delayed
endolymphatic hydrops
brief syncopal lightheadedness attack in upright  r/o postural
hypotension
Vertigo attack after middle ear surgery (tympanoplasty)  r/o
perilymphatic fistula of OW or RW or LSCC, r/o posttraumatic delayed
endolymphatic hydrops
Differential diagnosis in history taking
intermittent vertigo attack with history of COM  r/o fistula of
labyrinth
persistent vertigo with severe hearing loss  r/o labyrinthitis, r/o
delayed endolymphatic hydrops
mild dizzy but oscillopsia (up&down) even in static state  r/o both
side vestibulopathy
Acute vertigo attack in military service, scuba diving, hyperbaric
oxygen treatment, straining(childbirth, weight lift), flight  r/o
Post-traumatic vertigo with barotrauma
intermittent dizziness and temporal headache with N/V after ocular
pain, white-out, photophobia, phonophobia, or heightened sense of
smell  r/o migraine
Differential diagnosis in history taking
■ Acute attack of vertigo with otalgia, hearing loss, facial palsy,
blister of EAC  r/o Ramsay Hunt Syndrome (herpes zoster
oticus)
■ Vertigo attack with conductive autophony or hyper-acusis (such as
hearing one's own eye movements, one's own heartbeat, and/or the
impact of one's feet during walking or running in the affected ear)
 r/o dehiscence of Sup. SCC
■ Sound-induced vertigo (Tullio phenomenon) or pressure-induced
vertigo (Hennebert sign) with valsalva maneuvers, coughing, or
sneezing  r/o dehiscence of Sup. SCC
■ Vertigo attack after chemotherapy with cisplantin or
aminoglycoside antibiotics treatment or high dose NSAIDs r/o
Ototoxicity
Physical examination in dizziness Pts.
• General ENT examination on ear, nose, throat, and H&N
to r/o sinusitis, OME, nasal obstruction inducing dizziness
• Neuro-otologic examinations on
• sensory inputs ( vestibule, vision, Proprioception)
• central integration (general neurologic examination)
• motor outputs ( spontaneous & evoked eye movements,
VOR, VSR, VCR, posture, gait, cerebellar function )
 Physical examination in dizziness Pts.
■ Ear examination
: whether tympanic membrane intact
: whether hearing loss is
: whether OM is
: whether labyrinthine fistula is by pneumatization (fistula test )
: Weber test (512Hz) – CHL/SNHL lateralization
: Rinne test (512Hz, 1024Hz)
- in 512Hz, if BC better than AC, CHL>20dB
- in 1024Hz, if BC better than AC, CHL>25dB
Interpretation of Weber test & Rinne test
Ophthalmic examination in dizzy Pts.
■ Vision & oculomotor examination
: Visual acuity
: visual fixation (holds the image of a stationary object on the
fovea)
: Saccades (Bring images of objects of interest onto the fovea)
: Smooth pursuit (holds the image of a moving target on the
fovea)
: optokinetic reflex - holds images of the seen world steady on
the retina during sustained head rotations
: vergence (moves the eyes in opposite directions so that images
of a single object are placed simultaneously on both foveas)
Ophthalmic examination in dizzy Pts.
■ Ocular tilt reaction
: 3 Signs
(A) head tilt
(B) skew deviation
(C) ocular torsion
: reasons of skew deviation
- asymmetry in utricular projections
by cerebellum or brainstem damage
: The head tilt and ocular torsion
occur toward the hypotropic eye.
: occurs frequently in central
vestibulopathies
Neurotologic examination in dizzy Pts.
 Goals of Vestibular function test
1) to detect of lesion site
2) to evaluate of balancing ability using various sensory inputs
3) to decide the degree of compensation
 Vestibular function test
1) Static Vestibular Balance : Nystagmus
2) Proprioceptive / Vestibulo-spinal reflex
3) Dynamic Vestibular Function Test
4) Provocative Measures
Neurotologic examination in dizzy Pts.

1) Static Vestibular Balance

• Spontaneuous Nystagmus
Check direction
Check wave form whether torsional component or not
Check for static visual fixation & suppression
• Interpretation
• Peripheral: Horizontal-lotary jerk nystagmus, suppresses
with visual fixation
• Central: direction changing, horizontal, vertical, torsional,
or pendular nystagmus, enhances with visual fixation
Neurotologic examination in dizzy Pts.
Nystagmus interpretation
1) spontaneous nystagmus (with Frenzel goggles or
camera)
+ : Direction fixed, mostly horizontal, rotatory, less
vertical
 Peripheral : Acute – lesion side, Chronic – healthy side
+ : direction changed, mostly rotatory or vertical
 Central lesion
2) fixation suppression test
+ : peripheral
- : central
Neurotologic examination in dizzy Pts.
 Nystagmus interpretation
3) Gaze evoked nystagmus (5 points, 50cm, <30’, frequency, amplitude)
+ : direction change : central
- : direction fixation but degree change (Alexander’s law): peripheral
4) Saccade & pursuit test (saccade – quick chage, pursuit – slowly)
+ : central lesion
- : mostly peripheral
5) Positional nystagmus (with Frenzel’s goggles or ENG)
+ : nystagmus in a certain position of head : peripheral
6) Positioning nystagmus (with Frenzel’s goggles or ENG)
+ : nystagmus induced or changed in turning or positioning of head
Differentiation between peripheral and central
nystagmus
Characteristics peripheral Central

Direction Mixed torsional-horizontal Varies : pure vertical,

torsional, or horizontal
mixed
Change of direction Unidirectional Varies : unidirectional or
direction change
Effect of fixation Suppression Varies : increased,
decreased, or no effect
Adaptation Within days Often persists

Other neurologic No Often

deficits
Differentiation between peripheral and central
nystagmus
• Alexander’s law
: Nystagmus from peripheral lesions and some central lesions
: is more intense (slow-phase velocity is higher) when the
eyes are turned in the direction of the quick phase.
: due to the combination of gaze-evoked nystagmus (by the
initial loss of the neural integrator after a peripheral lesion)
+ the vestibular nystagmus caused by the static asymmetry
of the lesion itself.
: The two factors add on looking away from the lesion and
cancel each other on looking toward it.
Nystagmus in left peripheral vestibulopathy. In unilateral vestibular
neuritis, mixed torsional-horizontal nystagmus beats to the intact side.
Nystagmus typically increases during gaze in the direction of nystagmus
and decreases during gaze in the opposite direction (Alexander’s law), but
never changes directions.
Differentiation between peripheral and central
nystagmus
• Bruns’ nystagmus
: found in patients with cerebellopontine angle tumors
: is a combination of gaze-evoked nystagmus with low-
frequency, large-amplitude, fast phases on looking toward
the side of the lesion + jerk nystagmus with high-frequency,
small-amplitude, fast phases on looking the other side.
Differentiation between peripheral and central
nystagmus
• Horizontal gaze–evoked nystagmus
: is a hallmark of lesions in the medial vestibular nucleus and
nucleus prepositus hypoglossi complex.
• Low-amplitude gaze-evoked nystagmus
: often is a side effect of many types of medications
- including hypnotics, sedatives, and anxiolytics.
 Nystagmus of stimulating SCCs
Schematic summary of
nystagmus of stimulating
individual semicircular
canals and combinations of
canals, with arrows
representing slow phases
from the observer's
perspective.
Stimulation of a single
canal produces slow-phase
movements of the eyes in a
plane parallel to one in
which the canal lies.
 Nystagmus of stimulating SCCs

Purely vertical nystagmus

can only be induced by
simultaneous stimulation of
the same canal on both sides.
Purely torsional nystagmus
can only be produced by
stimulation of both vertical
canals, but not the lateral
canal, on one side.
 Nystagmus of stimulating SCCs

Thus, disease of the

labyrinth seldom produces
purely vertical or purely
torsional nystagmus.
Combined involvement of
all three canals on one side
causes a mixed horizontal-
torsional nystagmus.
Neurotologic examination in dizzy Pts.
 Vestibular function test
2) Proprioceptive / Vestibulo-spinal reflex test
a. Righting reflex test
b. Deviation test
Neurotologic examination in dizzy Pts.
 Vestibulo-spinal reflex test
a. Righting reflex test
- Romberg test
: check of vestibular & proprioceptive function in eye closed
: stand with feet together with open & close eyes in 1 min each
: fall or step : (+)
: fall or deviated side  lesion side
: (+) with eye close  lesion of vestibulo-spinal reflex, labyrinthine
(+) with eye open  cerebellar ataxia
: lower specificity(accuracy)  need to modify  the other test
Rhomberg Test
Neurotologic examination in dizzy Pts.
 Vestibulo-spinal reflex test
a. Righting reflex test
- one leg stance Romberg test
: eye fixation 1m away, 30s stand with EO, EC; EO=15±9, CO=4.5±3
- Romberg test on sponge
- Romberg tandem test (Mann’s test)
: arm cross on chest, heel-to-toe stand
: 49-60% sensitive and 95% specific for static imbalance
 Clinical Test for Sensory Integration in Balance - modified (CTSIB-m)
: in six positions, 2 Romberg + 2 on sponge + 2 one leg stance
: 90% sensitivity and 95% specificity
Modified Clinical Test of Sensory
Interaction on Balance

- Mann’s test
Figure 3: mCTSIB—Normal stability, eyes open (NSEO).
Figure 4: mCTSIB—Normal stability, eyes closed (NSEC).
Figure 5: mCTSIB—Perturbed stability, eyes open (PSEO).
Figure 6: mCTSIB—Perturbed stability, eyes closed (PSEC).
Figure7: Single leg stance golf swing take-away position.
Figure 8: Single leg stance golf swing follow-through position.
Neurotologic examination in dizzy Pts.
b. Deviation test (Lim coordination test)
- past pointing test
: 10 times with EO then more
10 times with EC : (+) > 10cm
: both lateralization  peripheral
: widen or deviation  central
- tandem walk test
: heel to toe walk on line
Neurotologic examination in dizzy Pts.
b. Deviation test

- vertical writing test

- Fukuda stepping test

: 100 step with eyes close

& hands out in fronts

 >45(90)’ / 1m or fail : (+)

 body deviated side – weak vestibular side

: but lower specificity, localization false (+)

Neurotologic examination in dizzy Pts.
 Vestibular function test
3) Dynamic Vestibular Function Testing:
: Head turn (head impulse, head thrust) test
- Tests the gain of the vestibulo-ocular reflex
: Head shaking test
- Utilizes a central pathway that “remembers”
angular velocity
 Head impulse test (HIT)
gazing to examiner’s nose  10~15°
rapidaly turning of Pt. head 
observe Eye movement
A : in healthy subjects, HIT normally
induces a rapid compensatory eye
movement in the opposite direction,
and steady fixation is attained
B : in patients with unilateral peripheral
vestibular hypofunction, HIT toward
the affected side produces a
corrective saccade after head rotation
because the eyes move with the head
due to a defective vestibule-ocular
reflex, thus losing the target with
head rotation
“positive” head thrust sign for the right HC indicating
normal left HC function & abnormal hypofunction Right HC.
Head shaking test (post head shaking nystagmus test)
• Eye movements are observed in darkness for 10 seconds
• The examiner grasps the patient’s head and moves it briskly back and forth in
the yaw plane (around the vertical axis)
: for a frequency of about 2 Hz
: displacement of the head of 30 ° to either side.
: the head should be pitched about 30° downward to being parallel
to the axes of the lateral canals
: is continued for 20 cycles and then abruptly stopped.
• Normal or bilateral vestibulopathy – Nys (-)
• Unilateral vestibular imbalance – Nys (+) away from the lesion side.
Neurotologic examination in dizzy Pts.
 Vestibular function test
4) Provocative Measures:
Hyperventilation
Dix-Hallpike (positioning), supine roll test
Valsalva
Calorics
Neurotologic examination in dizzy Pts.
 Provocative Measures
1) positioning nystagmus (Dix-Hallpike test with Frenzel’s goggles)
: 45’ open eyes  20~30’ 45’ 30~45s  sitting position
+ : Vertical nystagmus. : brainstem, cerebellum
+ : Rotatory & direction-fixed, : BPPV
cf) fast c. of eye’s top geotrophic : Post. SCC, ageotrophic : Lat. SCC
: latency - nystagmus after 5-15s,
: fatigue – held position  weak
: Habituation - repeat  weak
2) supine roll test
: for Dx of BPPV of lat. SCC
Dix Hallpike T.
Dix Hallpike T.
Diagnosis with Dix Hallpike test in BPPV of
PSCC
• Delay seconds latency
• Downward (upbeat) torsional beating (geotrophic)
Nystagmus in affected ear test.
• Duration < 1 minute
• Directional change in reverse sitting
• Dizziness (subjective)
• Disappear fatigability after several times again

 Hager 6D for diagnosis of BPPV

 Physical examination in dizziness Pts.

Central origin

BPPV
BPPV diagnosis in variable SCC

Diagnosis
Type
Maneuver Induced nystagmus
Dix-Hallpike Upbeating torsional
PSCC
Side-lying geographic Ny.

LSCC - canalithiasis Supine roll Geotrophic Ny.

LSCC - cupulothiasis Supine roll Apogeotrophic Ny.
SSCC Dix-Hallpike
 Supine roll test
• The mechanism of
displacement of the ampullar
crista that is responsible for
the origin of geotropic
nystagmus in canalithiasis(a),
or for apogeotropic
nystagmus in cupulolithiasis
(b).
• 1 - ampullar crista, 2 -
fragments of otoliths. The
arrows indicate the direction
of displacement of the cupula
by gravity with the
lateralization movement of
the head.
Supine test
Supine roll test in BPPV of LSCC

• Latency no more than 3 sec,

• No fatigability
• may beat toward or away from side of the cupula
• increases in magnitude while maintaining the test
position
• Cupulolithiasis > canalithiasis
• Cupulolithiasis – apogeotrophic Nystagmus
• Canalithiasis – geotrophic nystagmus
Superior canal BPPV

• Dix-Hallpike positioning testing

• Rt PSCC = Lt SSCC vice versa
• Least common
Physical examination in dizziness Pts.
 Provocative Measures
2) Nystagmus vibration to mastoid area or SCM muscle
: (+) – the same direction horizontal Nys (+) to the both side vibration
 Nys away from the lesion side
: normal – different side Nys (+)
3) hyperventilation nystagmus test
: breath deeply and rapidly for 30 breaths, or for 30 s to 3 min
: in NL, 50~100% low amplitude downbeating nystagmus
: in unilateral vestibular lesion, usually Nys.(+) toward the lesion side
: an indicator of damage to the vestibular nerve or central vestibular
pathways
4) Valsalva nystagmus test
: perilymphatic fistula  Nys (+)
Physical examination in dizziness Pts.
5) Caloric test (with Frenzel’s goggles)
: less accurate than ENG/VNG
: with 30’ head up supine position
: stimulate lat. and post. SCC with convection theory
: measure & compare the duration of nystagmus
: % caloric paresis
= 100 * [(LC + LW) –(RC + RW)/(LC + LW + RC + RW)]
: fixation test for ddx peripheral from central
: water or air
Mono-thermal test - near 20’, after 30s,
Bi-thermal test - 20’&0’ / 30’&44’(Hallpike), after 30s,
 Physical examination in dizziness Pts.
- Caloric test (with Frenzel’s goggles)
Physical examination in dizziness Pts.
- Caloric test (with Frenzel’s goggles)

Schematic illustration of
Hallpike’s bithermal caloric test
Physical examination in dizziness Pts.
• General neurologic examination

: Evaluation of abnl tension in head, neck and shoulder m. & joint

: Deep tendon reflex

: cranial nerve examination

: Vascular exam for possible posterior circulation problem

: cerebellar function (disdiadokinesis)

Physical examination in dizziness Pts.
 Cerebellar function test
Speech test
- deep breathing & “Ahhhhhha” as long as possible ; vocal cord
- “la la la” as fast as possible ; tongue
- “me me me” as fast as possible ; lip
Upper extremity
- passively flex and extend of elbow ; muscle tone
- rebound reaction ; coordination
- Rapid alternation test
- Finger-nose-finger alternating test
Lower extremity
- stand up and walking
- tandem walking test (heel to toe)
- heel knee tap, heel shin test
Vestibular laboratory tests
Role of the vestibular laboratory testing
• Determination of extent and site of lesion within the peripheral
and central vestibular system
• Determination of the functional limitations in static and dynamic
postural control (these may be related directly to gait
abnormalities) and functional performance of the vestibuloocular
reflex (VOR)
• Assessment of the status of the compensation process
• Along with symptom presentation to aid in the prognosis and
design of vestibular and balance rehabilitation

 vestibular laboratory testing is never a replacement for a detailed

neurotologic history and physical examination. but needs to be
interpreted in context of the history and physical examination.
General laboratory test in dizziness
• Routine lab.

: Autoimmune lab, VDRL for syphilis, TFT

• Audiologic test

: PTA,

Impedance Audiometry (acoustic stapedial reflex, tone decay),

Spheech audiometry (SRT with sppondee, SD),

BERA
 Specific Laboratory test in dizziness Pts.
1. Electronystagmogram (ENG)
: Measure orbital movement electrically using charge difference between
retina and cornea to detect eye movement
: Compare Time and amplitude graph between Rt. & Lt.
: Electrodes are typically placed at each lateral canthus and above and below
at least one eye with a common electrode on the forehead.
: Available to correlate with
Oculomotor test (spontaneous N., Gazing stability, Smooth pursuit, Saccade )
Positional test (Dix Hall pike test, supine roll test)
Positioning test
Caloric test
Provocation test (Valsalva maneuver, Rotatory chair)
 Specific Laboratory test in dizziness Pts.
2. Video-nystagmography (VNG) : Video gauided computerizing ENG
: Eye movements are recorded directly using infrared camera and digital
video image technology.
: for binocular recording. a reflected image of the eye is captured by cameras
mounted above, in front of each eye or adjacent to the lateral canthi
Example 1
• Gaze evoked nystagmus
Example 2
Normal Saccades results
Example 3-1
• Caloric Test
Example 3-2
• Bithermal Caloric Test result
 Specific Laboratory test in dizziness Pts.
3-1. Rotatory chair
• The purpose of the test
: to expand the investigation of the peripheral vestibular system
by applying natural head movements and using 3 outcome parameters
to characterize the peripheral vestibular system together with its central
projections
(a) the timing relationship between eye movement and steady state
(sinusoidal protocol) or transient (a step test) head movement,
(b) the overall responsiveness of the system to the stimulus,
(c) the responsiveness when rotating to the right versus the left.
: In this manner, the test expands across frequency (beyond that of stimulation
by caloric irrigations) the investigation of the function of the peripheral
vestibular systems.
Specific Laboratory test in dizziness Pts.
3-2. Rotatory chair
: 0.01 ~ 0.64 Hz rotation cf) ordinary
environment 1~5Hz
: Advantage
1) test stimuli are similar to ordinary
times
2) less N/V, Sx. and more controllable
than caloric test
: But It’s hard to test fast stimuli > 1 Hz
and unilateral disease
 Specific Laboratory test in dizziness Pts.
4-1. Vestibular-Evoked Myogenic Potential (VEMP)
• The purpose
: to provide information regarding VIII nerve and otolith organ function
: to potentially separate superior from inferior vestibular nerve and
likewise utricular from saccular involvement.
• Advantage
: it provides ear-specific information as like Caloric test .
• oVEMP - is measured at the inferior oblique muscle (directly under the eye) and
is reflection of the VOR
• cVEMP - is measured at the sternocleidomastoid muscle (SCM)
- is a reflection of the ipsilateral vestibule-collic reflex.
( measuring the pathway from the saccule, down the inferior vestibular
nerve to the brainstem, and then to motorneurons in the SCM, which
result in a relaxation of the contracted SCM muscle)
 Specific Laboratory test in dizziness Pts.
4-2. Vestibular-Evoked Myogenic Potential (VEMP)

<Rt. meniere’s disease>

Specific Laboratory test in dizziness Pts.
5. Computerized Dynamic Posturogram
: integral analysis of visual, proprioceptive, vestibular system
: evaluate sensory cognition & voluntary motor function
- motor control test (MCT)
Autonomic postural reflex (spinal reflex)
Dx of extravestibular Ds and psychiatric Ds
- seneory organization test (SOT)
Proprioception(2) * Vision(3,open+close+comfued)
Dynamic Posturography
• Conditions Tested:
Specific Laboratory test in dizziness Pts.
6. Epley onmiax system : Diagnoses + treatment
MNUMS protocol of vestibular out Pt.
• HX.
• General P/Ex
• Vestibular P/Ex c Franzel glass
: vision, spontaneous Ny, gaze Ny, saccade/pursuit Ny,
positional & positioning Ny
• Periperal Vestibular test
: Past point test, Romberg test, stepping test
• Central Vestibular test : alternative test, nose finger test
Case Study
• 26 y/o woman presents to the emergency room several hours after the
sudden onset of severe “dizziness” with nausea and vomiting.
• You call her up to your clinic.
Case Study
• History – reveals no associated symptoms.
• No report of hearing loss
Case Study
• Physical Exam: Dix hallpike test
Case Study
• ENG:
Case Study
• ENG:
Case Study
• ENG