DIZZINESS AND VERTIGO

DR.Budhi Suwarma SpS

FK Unjani October 2014
 Introduction
• 2,5 % of all primary care visits : dizziness
• 1 % of all primary care visits : vertigo
• Diverse etiologies
• A broadly based approach is necessary
 Symptoms in dizziness and vertigo
Primary Symptoms Secondary Symptoms Non-specific Symptoms

Vertigo Nausea, emesis, diarrhea Giddiness

Impulsion and rocking Pallor, Bradycardia Light-headedness

Oscillopsia Fatigue

Ataxia Headache

Hearing Symptoms Visual sensitivity

 Vertigo
• A sensation of rotation, either of the person or
of the world (“blurring”, “jumping”)
• Horizontal, vertical or rotatory
• Horizontal is the most common type
(dysfunction of the inner ear).
Movement of the visual scene opposite the
direction of the slow-phase
• Vertical is rarer,
transient (BPPV), constant ( central)
• Rotatory is the least frequent,
transient (BPPV), chronic (central)
 Vertigo
•The illusion of rotation
caused by asymmetry of
neural activity between
the right and the left
vestibular nuclei
 Impulsion
• A sensation of translation ( “being pushed or
tilted”)
• Variant include rocking, floating, perceived
changes in the direction of up and down
• Dysfunction of otolithic apparatus or its
central processing
 Oscillopsia
• An illusory movement of the world evoked by
head movement.
• Bilateral vestibular loss : unable to see when
their head are in motion.
• Unilateral vestibular loss : “the world doesn’t
keep up” when head rotate rapidly to the side
of the ear.
 Ataxia
• Unsteadiness of gait
• Nearly universal in otologic or central vertigo
• Variably observed in medical and unlocalized
vertigo
 Hearing symptoms
• Often accompanied by tinnitus, hearing
reduction/distortion and aural fullness
 Secondary symptoms
• Visual sensitivity : “grocery store syndrome”,
dizziness related to the types of patterned
visual stimulation ( views grocery store aisles,
drives past picket fences or through bridge, or
views large-screen movies )
 Etiology
•Otologic
•Central
•Medical
•Unlocalized
 Otologic Vertigo
• About 1/3 of all patients with vertigo
• Benign Paroxysmal Positional Vertigo (BPPV)
• Vestibular Neuronitis and Labyrinthitis
• Meniere disease
• Bilateral vestibular paresis or loss
• Superior canal dehiscence & perilymph fistula
• Tumors compressing the 8th CN
 BPPV
• 20 % of vertigo of all cause
• 50 % of all otologic cases
• Brief vertigo provoked by changes in
the orientation of the head to gravity
• Caused by loose debris within the
posterior canal of the inner ear
 Vestibular Neuritis (Labyrinthitis)
• About 15 % of all otologic vertigo
• Vertigo
• Nausea
• Ataxia
• Nystagmus
• Viral infection of the vestibular nerve
• Labyrinthitis (the same symptom complex +
tinnitus and/or hearing loss)
 Meniere’s disease
• About 15 % of otologic vertigo
• Intermittent vertigo accompanied by hearing
loss
 Bilateral Vestibular Paresis
• Oscillopsia and ataxia caused by loss of
vestibular hair cells
• Post several weeks th/ i.v. or intraperitoneal
ototoxic antibiotic (e.g. gentamicin)
• Much more rarely autoimmune disorders such
as Cogan’s syndrome (bilateral hearing loss)
 Superior Canal Dehiscence Syndrome
(SCD) and Perilymph Fistula (PLF)
• Vertigo induced by sound (Tullio phenomen)
• Ataxia provoked by activity or straining
• New diagnostic : Vestibular-evoked myogenic
potentials (VEMP)
• SCD : bone over the superior SCC is absent
• PLF : rupture between the fluid-filled inner ear
and the air-filled middle ear (e.g. barotrauma
scuba diving, ear surgery for otosclerosis or
cholesteatome)
 Tumors Compressing the 8th CN
• Asymmetric hearing loss combined with mild
ataxia
 Central Vertigo
• 2 – 23 % of vertigo
• In a majority of cases, is caused by vascular
disorders such as stroke, TIA, Vertebrobasilar
• Basilar artery migraine
• Seizures
• Multiple sclerosis
• Chiari malformation
 Stroke and TIA
• About one third of all central dizziness cases
 Basilar migraine
• About 15 % of central vertigo
• Presents with vertigo and headache
• Or isolated vertigo
• Women in their thirties
 Seizure
• About 5 % of central vertigo
• Present with vertigo combined with motor
symptoms or confusion
• Dizziness is a common symptom in epilepsy
 Multiple Sclerosis
• About 2 % of central vertigo
• Present with vertigo and other central signs
such as cerebellar dysfunction
 Chiari I malformation
• About 1% central vertigo
• Hindbrain malformation
• Cerebellar tonsils herniate ≥ 5 mm below the
foramen magnum
• Vertigo, ataxia, occipital headache, down beat
nystagmus
• Symptom may be precipitated by straining
 Cervical Vertigo
• After whiplash injury  vertigo, tinnitus and
neck pain.
• Neck movement limited by pain and nausea or
vertigo on neck positioning
• No strong nystagmus
• No definitive clinical or laboratory test
• Compression of vertebral artery are unusual
 Medical Vertigo
• Caused by altered BP, low BS and/or metabolic
derangements e.c. Medication/systemic infect
• About 33 % of all dizziness
• Postural hypotension
• Cardiac arrhytmia
• Hypoglycemia and DM
• Medication effects
• Viral syndrome
 Postural hypotension
• Presents as giddiness, light-headedness or
syncope
• Dizziness occurs only while upright
 Cardiac arrhythmia
• Presents as syncope or drop-attacks
• Symptoms present only while upright
 Hypoglycemia
• About 5 % of dizziness in general medical
setting
• Presents with giddiness or light-headedness
• Often accompanied by autonomic symptoms
such as palpitation, sweating, tremor, pallor
Medication effect or Substance Abuse
• About 16 % of the dizzy in the emergency
setting
• Present with giddiness or light-headedness,
sometime true vertigo
• Antihypertensive agent (α-1 adrenergic
blocker/terazosin, CCB/nifedipine), sedatives,
benzodiazepine (alprazolam withdrawl),
alcohol intoxication, vestibular suppresant
(meclizine and scopolamine)
 Viral syndrome
• About 4-40 % of all cases in emergency room
• GE, influenza-like illnesses
 Unlocalized Vertigo / Psychiatric
• Between 15-50 % of all dizziness and vertigo
• Psychogenic, HV syndrome, Posttraumatic,
Nonspecific dizziness
• Anxiety and Panic
• Posttraumatic vertigo
• HV
• Malingering
• Unknown
 Psychogenic
(anxiety, panic,posttraumatic stress)
• Dizziness, ataxia and autonomic symptoms
• Anxiety is the sole cause or a reaction?
• In somatization disorder, symptoms may be
present without anxiety
 Posttraumatic vertigo
• PTV is common
• No findings on examination or vestibular
testing
• BPPV is excluded by a negative Dix-Hallpike
maneuver
 HV syndrome
• Vertigo after HV without other findings or
nystagmus
 Multisensory Disequilibrium of the
elderly
• Age-related multisensory impairment
• Examination is otherwise normal
 Malingering
• Vertigo may be claimed in attempt to obtain
compensation
 Evaluation : History
• Vertigo (spinning), secondary symptom (nausea),
non-specific symptom ( giddiness or light-
headedness), something entirely different
(confusion)
• Timing (constant or episodic). If episodic, how
long do they last ?
• Triggering or exacerbating factors ( positional
changes of head or body), (standing up), (rapid
head movements), (walking in a dark room),
(loud noises), (coughing, nose blowing, sneezing ,
straining or laughing), (underwater diving,
elevators, airplane travel), (exercise),
• Triggering or Exacerbating factors (cont.),
(shopping malls, narrow or wide-open spaces,
grocery stores, escalators), (food, salt, msg),
(fasting), (alcohol), (menstrual periods), (boat
or car travel), (anxiety and stress)
• Otologic history (hearing loss, tinnitus,
fullness). If any positive  audiogram.
“Roaring” tinnitus suggests Meniere’s disease
• Medication history (ototoxic drug, AEDs, anti-
hypertensives, sedatives)
• Family history
• System review : psychiatric, vasc, Ca, neuro
logic, otologic surgery, general medical history
 Examination Procedures for Dizziness and Vertigo
Procedures Triggers for addition

General examination : Orthostasis

Arrythmia

Balance Assessment : Observe gait

Eye-closed tandem Romberg test
Pulsion and retropulsion Parkinsonian gait

Otologic Examination : Hearing

Tympanic membrane

Neurologic Examination : Cranial nerves, long tract signs

Cerebellar
Position sense testing Fails Romberg test

Nystagmus Assessment : Spontaneous nystagmus Goggles/ophthalmoscop

Vibration, VA, Dix-Hallpike,
Head-shake, Valsava, HV
VOR Gain Assessment : Dynamic illegible “E” test Fails Romberg test
Ophthalmoscope test Fails “E” test
• General examination : Blood pressure and
pulse (standing), arrhythmia ?,
If standing BP is low  check BP lying flat.
Auscultate the heart, carotid and subclavian a.
• Balance assessment : observation of gait,
eye-closed tandem Romberg test ( young
adult able to perform for 30”  declines with
age, low normal performance 6”).
Bilateral vestibular loss (moderately ataxic,
unsteady with eye-closed + narrow base, can
not stand for 6” in the eye-closed tandem R.
• Balance ass. (cont.) Bi
Additional superimposed position sense
deficit (unsteady with eyes open + narrow
base).
Chronic unilateral vestibular loss (very little
ataxia, normal on the eyes-closed tandem
Romberg)
Basal ganglia function (pulsion-retropulsion
test)
• Otologic examination :
Hearing / high-tone (arm’s length finger rub,
record the distance, most elderly able to hear
6”),
Inspect tympanic membranes (wax,
perforation, otitis, discoloration, mass lesion)
• Neurologic examination :
Cranial nerves
Long tract signs
Cerebellar
Position sense testing
• Nystagmus Assessment
Optimally requires use of Frenzel goggles (g)
worn by the patient to obscure the patient’s
vision and magnify the examiner’s view.
Spontaneous N (observe 10”) : inner ear
dysfunction (S deviate off center and Q back
to the center), central (sinusoidal, gaze-
evoked, saccadic).
If (g) are not available,use ophthalmoscopic
examination to monitor movement of the
back of the eye.
Visual suppression in inner ear dysfunction
 Peripheral origin sp. nystagmus
• Horizontal with a torsional component
• Does not change direction w. a change in gaze
• S toward affected ear,Q toward unaffected ear
• Decreased by visual fixation ( using Fresnel ,
blank sheet of paper in front of patient’s eyes)
Central origin spontaneous Nystag
• Often purely horizontal/vertical/torsional
• Changes in direction with changes in gaze
• Visual fixation has little effect
• Dix-Hallpike positional test
to precipitate nystagmus of BPPV
(SCC post rapidly brought into vertical position),
# Sit  move rapidly to the head-hanging pos.
Wait 20”, if no dizziness/nystagmus,
# Sit back up, head 45◦ right  move rapidly to
head-right supine. Wait another 20”
# Sit up again, head 45◦ left  move rapidly to
head-left supine. Wait another 20”
The nystagmus beats upward + rotatory
component the top part of the eye beats toward
the down ear. Latency 2-5”, lasts 5-60” 
downbeat when sat up
Variant BPPVs with different vectors.
Lateral-canal variant : strong horizontal
nystagmus that changes direction between
head left and right
Anterior-canal variant : downbeating
nystagmus
Nystagmus test requires video Frenzel
• Head-shake test : If no spontaneous or
positional nystagmus, wearing Frenzel’s
goggles, patient’s head is rotated in horizontal
plane, back and forth 20 cycles, 45◦, 2 cps 
nystagmus lasting ≥ 5”  organic disorder of
the ear or CNS.
• Neck vibration test to SCM 10” first on one
side and then on the other. A strong
nystagmus away from the lesion
(compensated peripheral vestibular)
• Vertebral artery test (cervical vertigo) : patient
upright and wearing the goggles, the ead is
rotated to the end of rotation on either side
and left there for 10”. Positive if a nystagmus
provoked by the position of the head.
• Valsava test : Wearing the goggles, valsava 10”
Nystagmus at the onset and release of
pressure
• HV test 30 times : inspect nystagmus with
Frenzel goggles and ask the patient if the
procedure has reproduced the symptom.
Nystagmus induced  tumor VIII or MS
• Assessment of VOR gain : bilateral vestibular
loss, eye-closed tandem Romberg test failed.
Dynamic illegible “E” test : Eye chart LogMar
unit calibrated at a distance ≥ 10’.
Record 1st visual acuity with head still.
Record 2nd visual acuity after gently moves
head horizontally, 1 Hz, ± 30◦
Normal drop 0-2 lines
Partial/complete bilat vest loss drop 3-7 lines
Ophthalmoscope test : when illegible “E” +,
focuses on the optic disk, moves head as
above, if the disk moves with the head abN
 The Head Thrust test
• A bedside test of the horizontal VOR
• Absent SCC lateral function on affected side
• Catch-up saccade occurs in one direction and
not the other
• Indicates a peripheral vestibular lesion on that
side or 8th nerve
 Fukuda or Unterberger test
• Marching in place (60 step) with eyes closed
and arms out
• Positive : veers to side of the lesion > 45o
• Cerebellar lesion are unable to stand unaided
 Laboratory Procedures for Dizziness and Vertigo
Test Indication
Audiologic Tests : Audiogram Vertigo, hearing symptoms
Otoacoustic emmision Hearing symptoms
ECOG Secondary test for Meniere’s disease
Vestibular Tests : VEMP Vertigo
ENG Vertigo
Rotary chair test Bilateral loss, secondary to confirm ENG
Posturography Malingering

Blood Tests : FTA-ABS Vertigo with hearing symptoms

GlycoHb, ANA, TSH Hydrops symptom complex
Lyme serology Vertigo in person from endemic area

Radiologic Tests : MRI Central Vertigo, abN BAER

MRA vertebro basiler TIA
CT temporal bone Pressure sensitive,Tullio,asymetrical VEMP
mastoiditis,head trauma,congenital abN
Other Tests : EEG Quick spins, head trauma
Holter monitoring Cardiogenic syncope
Tilt-table test Syncope
 Audiogram
• Measures hearing
• Abnormalities suggest otologic vertigo
• To separate otologic from other sources of
vertigo
 Otoacoustic emissions (OAE)
• Measure sounds generated by the ear itself
• Detecting malingering, central hearing deficit,
auditory neuropathy
• Not helpful in ≥ 60 yrs
 Electrocochleography (ECOG)
• An evoked potential, the recording electrode
is positioned on the ear drum
• Requires reasonable high-frequency hearing
• Abnormal ECOG is suggestive of Meniere’s dis
 Electronystagmography (ENG)
• Is helpful when there is no clear diagnosis
after history and examnination
• A battery of procedures that can identify
vestibular asymmetry (vestibular neuritis) and
document spontaneous or positional
nystagmus ( BPPV)
• Are gradually being displaced by VEMP
• Long and difficult test, little standardization, if
abN ≠ clinical picture  confirmed by rotatory
chair or in combination with VEMP testing
Vestibular-Evoked Myogenic Potentials
(VEMP)
• Basic vestibular test
• Good balance between diagnostic utility and
patient tolerability
• Sensitive to SCD syndrome, bilateral vestibular
loss, acoustic neurinoma
• Normal result in vestibular neuritis and
Meniere’s dis
 Rotatory chair testing
• Measures vestibular function of both inner
ears together
• Highly sensitive and specific for bilateral
vestibula loss
• In unilateral loss, it is sensitive but nonspecific
Does not identify the side of the lesion
• Is likely to be largely replaced by VEMP testing
 Posturography
• Is an instrumented Romberg test
• It is very useful in documenting malingering
• Has some utility in following the progress of
treatment
 Blood tests
• There is no routine set
• Triggered by specific symptom complex
 MRI
• Is not routinely needed to evaluate vertigo
without other accompanying neurologic
finding
 CT scan of the temporal bone
• Provides higher resolution of ear structures
than MRI and also is better for evaluating
lesions involving bone
• High-resolution direct coronal is best suited to
diagnose SCD
 Electroencephalography (EEG)
• Is used to diagnose seizures
 Ambulatory event- or Holter monitoring

• Is used to detect arrhythmia or sinus arrest

 Tilt-table testing
• For diagnosis of neurocardiogenic syncope
• The appropriate role is presently unclear
 Differential Diagnosis
• Approach based on specific symptom
complexes

• Approach based on timing only

These categories are less useful for diagnosis
than those based on symptom complexes, but
can be used when patients do not fall into any
category
 Specific Symptom Complexes
Positional Headaches and Hydrops Pressure Medicolegal
Vertigo Vertigo Symptom Sensitivity Situation
(bed spins) Complex Complex

Malingering
BPPV Basilar Meniere’s dis SCD and disability
Migraine evaluations

Central vertigo Post traumatic Perilymph Perilymph

Vertigo fistula fistula

Meniere’s dis
Vestibular Chiari I Post traumatic Chiari I
neuritis malformation hydrops malformation

Stapes
Postural Unlocalized Syphilis malformation
hypotension vertigo or prosthesis
 BPPV
• Bed spin, a brief burst of rotatory vertigo
when getting into or out of bed or on rolling
over from one side to the other
• Typical nystagmus is observed on Dix-Hallpike
 no other diagnoses need to be considered
• Roughly 95% of all positional nystagmus is
caused by BPPV
• MRI when an atypical BPPV refractory to th/
 Central disorders
• Strong positional nystagmus
• Combined with an abnormal neurologic
examination
• When an atypical BPPV is refractory to
treatment
 Vestibular neuritis
• A weak horizontal positional nystagmus
• ENG and audiogram are indicated
 Postural hypotension
• Dizziness on getting out of bed, but never
occurs in bed
• Supine  standing BP ↓ ≥ 20 mmHg or
pulse rate ↑
 Migraine
• Women in their thirties with perimenstrual
exacerbations
• Food triggers
• Motion sickness
• Positive family history
• Empirical trials of antimigraine medication
 Posttraumatic vertigo
• Audiometry
• ENG
• CT scan of the head
 Chiari malformation
• Occipital headache
• Downbeat nystagmus
• Ataxia
• Sagittal T-1 MRI
 Unlocalized vertigo
• Audiometry and ENG for vertigo component
• The headache component consider tension,
migraine, sinus
 Hydrops Symptom Complex
• Spells of vertigo
• Roaring tinnitus
• Transient hearing loss
• Preceded by aural fullness
• Audiometry, FTA-ABS, ESR, TSH in all patients
 Meniere’s disease
• Duration of vertigo is 2 hours (vary second-
weeks)
• Audiogram : fluctuating low-tone
sensorineural hearing loss
• ECOG test in difficult cases
• About 10% of bilateral Meniere’s disease are
autoimmune
• Thyroid disease is frequent in Meniere
 Perilymph fistula
• History of barotrauma
• Fistula test
 Posttraumatic hydrops
• A variant of Meniere’s disease symptom
complex
• Appears after a significant blow to the ear
• Bleeding into the inner ear?
 Syphilis
• Bilateral hearing loss
• FTA-ABS
Pressure Sensitivity Symptom Complex
• Diziziness or ataxia evoked by nose blowing,
high-speed elevator, cleaning of the ear with a
cotton swab, straining as at stool, after the
landing of an airplane, after diving
• Vertigo induced by loud noise (Tullio’s
phenomen) and by exercise
• Audiometry and VEMP test
 Superior Canal Dehiscence (SCD)
• The main source of pressure sensitivity
• Vertigo and nystagmus can be provoked by
loud noise or pressure
• VEMP is nearly always abnormal (asymmetry)
• High-resolution CT scan of the temporal bone
 Perilymph fistula
• A history of barotrauma
• Unable to clear their ear during scuba diving
or airplane travel
• Audiometry and ECOG
• Trial of a ventilation tube in the suspect ear
 Meniere’s disease
• Mild pressure sensitivity occurs in about 1/3
Chiari malformation and Platybasia
• Vertigo is correlated with straining but not
with pressure in the CAE
• Downbeat nystagmus
• Abnormal MRI
 Stapes malformation
• Congenital malformation of the stapes
footplate
• Stapes prostheses (for otosclerosis) of
excessive length
• Remarkable pressure sensitivity with torsional
movement of the eye
• High-resolution CT scan of the temporal bone
 Medicolegal situations
• Disability evaluations
• Worker’s compensation cases
• Legal situations
• No objective evidence on PE and testing, resist
examination (closing their eyes), refusing to
perform positional maneuvers.
• Posturography  “nonphysiologic” pattern
Typical Duration of Conditions Causing Dizziness
1-3” < 1’ Minutes-Hours Hours – days ≥ 2 weeks
(quick spin)

Vestibular N BPPV VB TIA Meniere’dis Vest neuritis &

irritation labyrithitis

BPPV variants Cardiac Meniere’s dis BA migraine Central Vertig +

arrythmia structural lesio

Meniere’s dis Meniere’s dis Panic attacks, Anxiety

variants variants HV, anxiety

Epilepsy Orthostasis Malingering

Bilateral vest
paresis/loss

Multisensory
disequilibrium

Drug
intoxication
 Vestibular Nerve Irritation
• Due to the microvascular compression
syndrome / a residual from vestibular neuritis
• Extremely frequent spells
• HV may induce nystagmus (video Frenzel’s g.)
• MRA occasionally documents brainstem
compression by VB system
• Good response to OxCBZ suggests the
diagnosis
 Meniere’s disease variants
• “Shocks or Earthquake” sensastions
• Frequency of spells is daily
• Hearing is often affected
 BPPV variants
• Spells are no more than daily frequency
• Slip down of otoconial debris
• Diagnosis is by Dix-Hallpike maneuver
 Epilepsy
• Spells can be very frequent 20 per day
• There is often a history of head injury
• Cognitive impairment is frequent
 Classic BPPV
• There is positional vertigo
• Adopted sleeping strategies (e.g. 2 pillows)
• Looking up top shelf
• Diagnosis is by Dix-Hallpike maneuver
 Cardiac Arrhythmia
• Spells occur only while standing
• Light-headedness is a more prominent
symptom than spinning
• Ambulatory event monitoring
• Holter monitoring
 TIA
• Spells lasting 2-30’
• Abrupt onset and offset
• Significant vascular risk factors
• MRA of the VB circulation
 Meniere’s disease
• Attack lasts 2 hours
• There is hearing symptom
 Panic attacks, Situational anxiety, HV
• Last minutes to hours
• PD normal
• A detailed history is useful
• HV reproduces symptoms
 Basilar Migraine
• Age, female, family history
• Attacks provoked by unusual migraine triggers
 Vestibular Neuritis
• Long duration + spontaneous nystagmus or
abnormal ENG ( significant ≥ 40% vestibular
paresis)
• If vertigo > 2 mo  central vertigo ?  MRI
• Labyrinthitis = ves. neuritis + hearing symptom
Audiometry, serum FTA-ABS, ESR, Fasting BS
 Central Vertigo with a fixed structural
CNS lesion.
• There are neurologic signs or symptoms
(“central signs”)
• MRI
 Anxiety
• Duration > 2 weeks
• No spontaneous nystagmus is evident under
Frenzel’s goggles
• Nearly every trigger factors exacerbates their
symptoms
• “Everything except stress  triggers vertigo”
• A trial of a benzodiazepine supports this D/
 Malingering
• Symptom persist as long as necessary to
accomplish their purpose of obtaining
favorable court settlements or disability ruling
• Posturography and neuropsychological testing
very abnormal
• VEMP and ENG are nearly always normal
 Bilateral vestibular paresis or loss
• Fail the dynamic illegible ‘E” test and the eyes-
closed tandem Romberg test
• Ataxia is worse in the dark
• Audiometry only high-frequency is affected
• VEMP and rotatory chair testing is the best
 Multisensory disequilibrium
• Unlocalized vertigo in an elderly patient
• Usually a permanent condition
 Drug intoxication
• Withdrawal of medication
 Diagnostic Approach
• Perform history and examination
• 20-40% could be diagnosed immediately
BPPV (15-20%) on Dix-Hallpike maneuver
Orthostatic hypotension and fixed cardiac
arrhythmia (2-5%)
Bilateral vest paresis/loss (5%) on dynamic
illegible “E” test
SCD (0-2%) with positive Valsava test
Acute vest neuritis (2-5%) spontaneous nyst.
• The remaining patients proceed as follows
• If fits into a symptom complex category 
• If does not fit :
Symptoms are intermittent
Symptoms are constant :
< 2 weeks, treat symptomatically,
if > 2 weeks follow the procedures
 Treatment Dizziness and Vertigo
• Four major causes :
otologic/peripheral vestibular,
central vestibular
medical
unlocalized
• True vertigo (rotatory)  peripheral
• Presyncope and loss of consciousness 
cardiovascular or CNS
• Obtain an accurate history, frequency, inten-
sity, effect on patient’s ADL
 Otologic / Peripheral vestibular
• Benign Paroxysmal Positional Vertigo (BPPV)
• Vestibular Neuronitis and Labyrinthitis
• Meniere’s disease
• Perilymphatic fistula
• Superior SCC dehiscence syndrome
• Ototoxicity
• Tumors involving N.VIII
 BPPV
• Clinical features :
# short attacks associated with changes in
head position, recurrent, lasting ≤ 1’,
reproducible with repeated movement in the
same direction, Dix-Hallpike (d/ and side
origin),
# the result of stimulation of the posterior SCC
by loose debris (CaCO3) from the utricle,
this can result from trauma/labyrinthitis/
spontaneously
• Treatment :
# First bilaterally suppressing the vestibular
system
(benzodiazepine, anhistamine, anticholinergic)
# Followed by repositioning exercises to move
the debris from SCC (office-based and home
exercises).
# If unresponsive  surgery
# Epley maneuver :
 Sit upright, head is turned 45◦ to the
offending side, neck extended 45◦
 Reclined supine, head hung over the edge
of the exam table, held 10-15”
 Head is then slowly rotated away from the
offending side to 45◦ to the opposite side
 Body and head are turned to face
downward opposite the offending side
 After 10-15” the patient is slowly lifted to a
seated upright position keeping the head
turned away from the offending side
 The head is then slowly turned to midline
# Modified Semont maneuver
( perform 3x daily, untill symptom-free 24 h )
 Sit upright on the edge of the exam table,
head turned 45◦ to the offending side
 Drop the patient quickly to the opposite
the offending side, keeping the head turned
45◦ to the offending side, waits 30”
 Then moves the head and trunk in a swift
movement, toward the other side without
stopping in the upright position, waits 30”
 Sit up again
Vestibular Neuronitis and Labyrinthitis
• Clinical features :
 Similar presenting features
 Vertigo last for hours to days, often severe
enough to induce nausea and vomiting
 Labyrinthitis ≈ hearing loss, whereas
vestibular neuronitis is not
 Self-limited conditions, viral ?
 After acute phase, vestibular equilibrium
gradually returns over a course of several
weeks, often, but not always to full recovery
• Treatment :
 Vestibular suppression :
Antihistamine : histamine-1 antagonist,
central anti Ch-ergic mechanism
Meclizine, promethazine
Anti Ch-ergic : (suppresses vestibular input).
Scopolamine
Benzodiazepine : potentiation of central inh.
GABA receptor (inh. of vestibular stimulation)
 anxiolysis, sedation, amnestic, anti-
convulsant, muscle relaxant. SE : amnesia,
depression, dependence, withdrawl symptom
Antiemetic : many of anti Ch-ergic and
antihistamine also exert an antiemetic effect.
Prochlorperazine is a phenothiazine
(strong antiemetic), SE : extrapyramidal
Metoclopramide is an anti DoA-R
(antiemetic and prokinetic)
Ondansetron is a 5-HT3R antagonis (a-nausea)
 Corticosteroid (hearing loss in labyrinthitis)
Antiviral (no additional benefit).
Antibiotic (suppurative labyrinthitis,OMA )
 Vestibular rehabilitation (simple head-
turning, complex postural and ambulation.
 Meniere’s disease
• Clinical features :
 Fluctuating hearing loss, tinnitus, vertigo +
“aural fullness”
 Episodes ≥ 20’, acute, repeating attack
 Over time, responsiveness of vestibular
system ↓ (“burns out”)
 Caucasian female, onset age 40-60
 Overaccumulation of endolymph (hydrops),
ruptures/leakiness of membranous labyrinth,
allowing endolymph (K >>) to mix with
perilymph (K<<)  disrupt conductivity
• Treatment : multidimensional
 Medical (acute) as in labyrinthitis,
antiemetic, antihistamine, antiCh-ergic,
benzodiazepine
 Medical (chronic) salt restriction and
diuretic (titrated HCT and triamterene) –
endolymph and its production ↓
 Surgical (if medical th/ failed ≈ 10%),
endolymphatic sac decompression – vertigo ↓
vestibular nerve section
labyrinthectomy
intratympanic vestibulotoxic medication
 Perilymphatic fistula
• Clinical features :
 Abnormal communication of perilymph
between the labyrinth and the middle ear via
the oval window, round window or an
aberrant pathway e.c. Spontan/Barotrauma/
Penetrating middle ear trauma/Stapedectomy
 Vertigo with extreme pressure sensitivity
and may be exacerbated by Valsava maneuver,
pneumatic otoscopy
 Resemble labyrinthitis, with a predisposing
insult (pressure sensitivity)
• Treatment :
 small fistula may heal spontaneously with a
short course of bed rest
 stable hearing/clinical diagnosis?, try
vestibular rehabilitation
 if a clear temporal relationship between a
predisposing insult (scuba diving, ear surgery,
penetrating middle ear trauma) and classic
symptom, exploratory tympanotomy. The goal
is the localization of a discrete fistula that may
then be patched with autogenous connective
tissue. Bed rest while healing of the graft
continues, minimize coughing and straining.
 Superior SCC dehiscene syndrome
• Clinical features : (confirmed by high-resol. CT)
 A sound- and pressure-induced vertigo
caused by bony dehiscene of the superior SCC,
congenital, no barotrauma, no otorrhea
 Characteristic torsional vertical nystagmus
 “Tullio’s phenomen” : vertigo associated
with pressure from coughing, sneezing, strain-
ing + conductive hearing loss.
 Overlaps with perilymphatic fistula,
acquired horizontal SCC dehiscene e.c.choles-
teatoma/COM
• Treatment :
 Surgical plugging of the canal or repairing
the dehiscene in the floor of the middle
cranial fossa
 Ototoxicity
• Clinical features :
 Associated with well over 100 medications
 Clinically significant is aminoglycoside
particularly gentamicin (vestibulotoxic)
 Ataxia and oscillopsia
 Loop diuretics can compound the toxicity
 Cessation of treatment will halt the
continued insult, but recovery is variable and
may be incomplete
• Treatment :
 Unsatisfying
 Do all possible to avoid it
 Gentamicin toxicity can be caused at
therapeutic serum level in some patients
 Vestibular rehabilitation may be of value
and supportive measures are necessary while
central compensation and enhancement of
vestibulospinal and vestibulocervical reflexes
occur
 Tumors N.VIII
• Clinical features :
 Tumors CPA (vestibular schwannomas) are
usually slow-growing proceeds from IAC  CP
cistern  brainstem compression
 VIII dysfunction (cochlear and vestibular)
both fr. local compression as well as disruption
of the blood supply to the labirynth and N.VIII
 Nearby nerves VII and V may be affected
 The progession is gradual, need detailed Q
 Vestibular c.l.and central compensation are
able to mask the vestibular loss
• Treatment :
 Be tailored to characteristics of the tumor,
the tumor’s associated symptoms and the
patient’s overall health.
 Young healthy patient, surgery, offers the
most complete treatment with the least
likelihood of recurrence.
Retrosigmoid or middle cranial fossa approach
depend on tumorsize/location,existing hearing
 Elderly patient with multiple comorbidities,
observation, radiosurgery
 Central Vertigo
• Ischemia or infarction
• Vertebrobasilar migraine and migrainous
vertigo
• Seizures
• Multiple sclerosis
• Chiari malformation
 Ischemia or Infarction
• Clinical features :
 disruption of VB circ. (brainstem,
cerebellum, peripheral vest syst)  dizziness
 vertigo + other focal neurologic findings
(weakness, facial paresthesia, dysarthria,
ataxia, diplopia, visual disturbance
• Treatment :
 general supportive, antiplatelet, anti-
coagulant
 evaluation vascular risk factors
 cardiac evaluation (embolic sources)
VB Migraine & Migrainous Vertigo
• Clinical features :
 adolescent female > male
 aura : hemianopic, vertigo, ataxia,
numbness, dysarthria; followed by a throbbing
occipital headache; often associated w.nausea
 Migrainous vertigo : episodic vertigo w.o.
Neurologic symptoms and even wo headache.
Relationship with migrainous triggers and
response to antimigraine medication
 Rule out other causes of vertigo
• Treatment :
 Abortive therapy : ergotamine and triptan
 Frequent attacks : preventive medication,
β-blocker, tricyclic antidepreassant,
antiepileptic, CCB
 Seizures
• Clinical features :
 Vertigo associated with complex partial
seizures (swallowing, lip-smacking, awareness)
 Tumor, brain injury, metabolic
• Treatment :
 AED
 Surgical procedures to remove or isolate
the epileptogenic focus
 Multiple Sclerosis
• Clinical features :
 young adult, vertigo, isolated weakness,
visual disturbance
 MRI, CSF analysis
• Treatment :
 Immunomodulating agents
 Chiari malformation
• Clinical features :
 Downbeat nystagmus in primary position
• Treatment :
 Surgical decompression of the posterior
fossa
 Medical Dizziness
• Postural hypotension
• Arrhythmias
• Metabolic causes incl. Hypoglycemia and DM
• Medication effect
• Infection
 Postural hypotension
• Clinical features :
# Elderly patients result from any causes
# Lightheaded or presyncopal feeling when
standing from sitting or lying
# Cardiac output ↓, antihypertensive (vaso-
dilatation, β-block), dehydration, autonomic
insufficiency (DM-neuropathy)
• Treatment :
# systematic review of causes, review and
modif. the medication, hydration, stocking etc
 Arrhythmias
• Clinical features :
# Palpitation w/wo chest pain. True vertigo -
# May be associated w presyncope or loss of
consciousness
• Treatment :
# ECG, refer to cardiologist
# Antiarrthythmia, pacemaker, radio-
frequency ablation of aberrant pathway of
conduction
 Metabolic causes
• Clinical features :
# Hypoglycemia  feeling of dysequilibrium
# True vertigo -
# A thorough history is of paramount
importance in identifying of metabolic causes
• Treatment :
# Directed to the underlying disorder
 Medication effect
• Clinical features :
# AED, benzodiazepine, psychogenic 
dysequilibrium

• Treatment :
# Identifying and removing the offending
medication
 Infection
• Clinical features :
# Labyrinthitis, Lyme, Lues, HIV, Influenza

• Treatment :
# Identification of the causative infectious
agent.
 Unlocalized Vertigo
• Psychogenic
• Malingering
• Postconcussive
• Multifactorial
• Unknown
 Psychogenic
• Anxiety, depression, personality disorder are
common codiagnoses of dizziness
( a bidirectional relationship)
 Malingering
• For secondary gain
• Posturography can be used
 Postconcussive
• Mild to moderate traumatic brain injury (TBI)
• Nausea, vomiting, headache and dizziness last
for weeks following the injury
• Cognitive, psychological, and emotional
dysfunction may be persist
• Supportive measures and vestibular
rehabilitation
 Multifactorial
• Elderly with multiple comorbidities