Vestibular system-II

Physiology of Balance
Body balance by different systems:
Vestibular
Proprioceptive
Visual

Coordination in CNS
Cortex
Cerebellum
Reticular formation
Extra-pyramidal system

Peripheral Vestibular
Disorders
1. Benign Paroxysmal Positional Vertigo
(BPPV)
2. Vestibular Neuronitis
3. Labyrinthitis
4. Menieres disease
5. Acoustic Neuroma
6. Fistula-perilymph, labyrinthine

 Peripheral vestibular disorders

Vertigo With hearing loss- Menieres
disease, labyrinthitis, fistula,ototoxicity
Vertigo Without hearing loss- BPPV,
Vestibular neuronitis

Central Vestibular Disorders

Vascular
Wallenbergs Syndrome
Head Injury
Cerebellar Infarct

Postconcussive Syndrome
Demyelinating Disease
Congenital

Vestibular Function Tests

Clinical
Spontaneous nystagmus
Fistula test
Romberg test
Gait
Past pointing/fall

Laboratory
Caloric test
Electronystagmography
Rotary Chair test
Posturography

VFT

Balance maintained by :
1. Vestibular system
2. Eyes
3. Proprioceptors in the muscles

VFT
Investigating the vestibular system
consists of the following,
1. Testing the vestibulospinal reflexes
2. Testing spontaneous and provoked
nystagmus
3. Tests on vestibular and optokintic
systems

Vestibulospinal Reflexes
ROMBERGS TEST
Patient stands with feet together, arms
by the side with eyes open then
closed
Peripheral vestibular lesions- the
bodys centre of gravity is displaced
to the side of the labyrinthine lesion
Central disturbances- pattern of
unsteadiness of gait and direction of
fall are irregular.

Vestibulospinal Reflexes
UNTERBERGERS Stepping Test
Stepping on the spot with the eyes
closed and arms outstretched for 30
sec
Peripheral disorders- rotation of body
axis to the side of the labyrinthine
lesion
Central disorders the deviation is
irregular

Vestibulospinal Reflexes
POSITIONAL TESTS ( cerebellar
lesions)
1.Parallel supine arms- arm on side of
cerebellar lesion sinks down as a
result of loss of tone
2. Finger-nose pointing- overshooting
indicates cerebellar lesion
3. Dysdidokinesia- central cerebellar
lesion

Nystagmus
Involuntary rhythmical oscillation of
eyes away from the direction of gaze,
followed by return of eyes to their
original position.
The direction of the fast component
determines the direction of the
nystagmus ( towards the dominant
vestibular centre, inhibitory impulses
are suppressed i.e the side of the
lesion )

Spontaneous Nystagmus
First Degree nystagmus present
only when the eyes deviate to the
side of the lesion
Second Degree nystagmus present
when patient looks straight ahead
Third Degree nystagmus present in
both directions

Positional Nystagmus
Hallpike Manouvre
Patient sits on bed, head turned 45
degrees to left or right.
Patient is rapidly laid back with head
over edge of bed 30 degrees below
the horizontal. Eyes open look for
nystagmus.
After 30 sec return patient to upright
position
Repeat with head to other side

Vestibulo-ocular reflex
ROTATIONAL TESTS
Nystagmus Induced by accelerating
and decelerating rotating chair, tests
both labyrinths simultaneously
CALORIC TESTS
COWS- cold water opposite side,
warm water same side, direction of
nystagmus
Extent of caloric response indicates
function of labyrinth

Vestibulo-ocular Reflex
Electronystagmograghy
Positive potential between the
cornea and retina recorded as eyes
move from straight ahead gaze
Test includes different head positions,
eyes open, closed and caloric tests

Results of Vestibular
Function Tests
Presence of complete vs. incomplete
loss
Presence of peripheral vs. central
dysfunction
Direct patient management
Help in outcome prediction

Nystagmus
Rapid alternating movement of eyes in
response to continued rotation of the
body
Involuntary, rhythmically,oscillatory eye
movement
Primary diagnostic indicator in
identifying vestibular lesions
Physiologic nystagmus
vestibular, visual, extreme lateral gaze

Pathologic nystagmus
spontaneous, positional, gaze evoked

Labeled by
the direction
of the fast
component

Spontaneous Nystagmus
First Degree nystagmus present
only when the eyes deviate to the
side of the lesion
Second Degree nystagmus present
when patient looks straight ahead
Third Degree nystagmus present in
both directions

 Cold or warm water or air is irrigated into

the external auditory canal, usually using
a syringe. The temperature difference
between the body and the injected water
creates a convective current in the
endolymph of the nearby horizontal
semicircular canal. Hot and cold water
produce currents in opposite directions
and therefore a horizontal nystagmus in
opposite directions.[4]

In patients with an intact brainstem:

If the water is warm (44C or above) endolymph in the ipsilateral
horizontal canal rises, causing an increased rate of firing in the
vestibular afferent nerve. This situation mimics a head turn to the
ipsilateral side. Both eyes will turn toward the contralateral ear,
with horizontal nystagmus to the ipsilateral ear.
If the water is cold, relative to body temperature (30C or below),
the endolymph falls within the semicircular canal, decreasing the
rate of vestibular afferent firing. The eyes then turn toward the
ipsilateral ear, with horizontal nystagmus (quick horizontal eye
movements) to the contralateral ear.[5][6]
Absent reactive eye movement suggests vestibular weakness of
the horizontal semicircular canal of the side being stimulated.

Caloric test

Benign Paroxysmal
Positional Vertigo
(BPPV)

The Ear

27

The Inner Ear

28

Benign Paroxysmal Positional Vertigo

(BPPV)

Inner ear problem that results in short

lasting, but severe, room-spinning
vertigo.
Benign: not a very serious or
progressive condition
Paroxysmal: sudden and
unpredictable in onset
Positional: comes with a change in
head position
29
Vertigo: causing a sense of dizziness.

Benign Paroxysmal Positional

Vertigo (BPPV)
5 criteria crucial in diagnosis (Hallpike-Dix
Test):
torsional/linear-rotary nystagmus; reproduced
by provocative positioning with affected ear
down
nystagmus of 1-5 sec. latency
nystagmus of brief duration (5-30 sec.)
reversal of nystagmus direction on returning
to upright position
response diminishes with repetition of
maneuver (fatigability)
(Massoud 96)

Canalolithiasis Theory
The most widely accepted theory of the pathophysiology
of BPPV
Otoliths (calcium carbonate particles) are normally
attached to a membrane inside the utricle and saccule
The utricle is connected to the semicircular ducts
These otoliths may become displaced from the utricle to
enter the posterior semicircular duct since this is the
most dependent of the 3 ducts
Changing head position relative to gravity causes the
free otoliths to gravitate longitudinally through the canal.
The concurrent flow of endolymph stimulates the hair
cells of the affected semicircular canal, causing vertigo.

31

Canalolithiasis Theory

32

Causes

Idiopathic
Infection (viral neuronitis)
Head trauma
Degeneration of the peripheral end organ
Surgical damage to the labyrinth

33

Symptoms
Starts suddenly
first noticed in bed, when waking from
sleep.
Any turn of the head bring on dizziness.
Patients often describe the occurrence of
vertigo with
tilting of the head,
looking up or down (top-shelf vertigo)
rolling over in bed.

nausea and vomiting.

There is no new hearing loss or tinnitus.
34

Diagnosis
Lab Studies:
No pathognomonic laboratory test for BPPV
exists. Laboratory tests may be ordered to rule
out other pathology.

Imaging Studies:
Head CT scan or MRI.

Procedures:
The Dix-Hallpike test, along with the patient's
history, aids in the diagnosis of BPPV.

35

The Dix-Hallpike test

36

Treatment
Medications
The Canalith Repositioning Procedure
(CRP)
Surgery

37

Medications
Antiemetic
Antihistaminic
Anticholinergic

38

Canalith Repositioning
Procedure ( CRP )

The treatment of choice for BPPV.

Also known as the Epley maneuver,
The patient is positioned in a series of steps so as to slowly
move the otoconia particles from the posterior semicircular
canal back into the utricle.
Takes approximately 5 minutes.
The patient is instructed to wear a neck brace for 24 hours
and to not bend down or lay flat for 24 hours after the
procedure.
One week after the CRP, the Dix-Hallpike test is repeated.
If the patient does experience vertigo and nystagmus, then
the CRP is repeated with a vibrator placed on the skull in
order to better dislodge the otoconia.
39

The Epley Maneuver

40

Clinical Trial
Ruckenstein (2001) Therapeutic efficacy of the Epley
canalith repositioning maneuver. Laryngoscope

Eighty-six patients
74% of cases that were treated with one or two canalith
repositioning maneuvers had a resolution of vertigo as a
direct result of the maneuver.
A resolution attributable to the first intervention was
obtained in 70% of cases within 48 hours of the maneuver.
An additional 14% of cases that were treated had a
resolution of vertigo.
Only 4% of cases (three patients) manifested BPV that
persisted after four treatments.

41

Brandt-Daroff Exercises

method of treating BPPV, usually used when the office

treatment fails.
These exercises should be performed
for two weeks, three times per day
for three weeks, twice per day.
In each time, one performs the maneuver as shown five
times.
1 repetition = maneuver done to each side in turn (takes 2
minutes)

42

Brandt-Daroff Exercises

43

BPPV
Epley canalolilith/ particle repositioning
procedure
The most commonly used for posterior canal
BPPV
Seated position with the head turned
toward the affected ear

BPPV
Epley canalolilith/ particle repositioning
procedure Rapidly lower the patient to DixHallpike position (reclined 30 degrees beyond
the level of the table)

The otoconial particles move and come to

rest at midpoint of duct
Leave the patient in this position for 40
seconds after the nystagmus subsides

BPPV
Epley canalolilith/ particle repositioning
procedure Slowly roll the patient to the

opposite side pausing briefly every 45

degrees until the affected ear is up

The otoconial particles are entering into

the crus communis

BPPV
Epley canalolilith/ particle repositioning
procedure Slowly roll the patient onto

the right shoulder

The otoconial particles are falling via the

crus communis into the vestibule

BPPV
Epley canalolilith/ particle repositioning
procedure

Turn the head another 90 and the

procedure is completed by sitting the
patient upright

The otoconial particles are repositioned

BPPV
Epley canalolilith/ particle repositioning
procedure Contraindications :
Severe neck diseaseSevere carotid
stenosis

Post-procedure instructions:
Wait 10 minutes before allowing the
patient to go home
Do not let the patient drive home if
possible
Not to let patient sleep with affected
ear down

Surgery
Singular neurectomy
Vestibular Nerve Section
Posterior Canal Plugging Procedure

50

Singular neurectomy
Old procedure
Section the nerve that transmits
information from the posterior
semicircular canal ampulla toward
the brain.
Can cause hearing loss in 7-17% of
patients and fails in 8-12%.

51

Clinical Trial
Gacek (1995) Technique and results of singular
neurectomy for the management of benign
paroxysmal positional vertigo. Acta Otolaryngol

One hundred thirty-seven patients

1972-1994.
(94%) experienced complete relief of vertigo following SN.
(2%) experienced partial relief of positional vertigo
following SN and
(4%) failed to have any improvement of symptoms
following SN.
(3%) had a partial sensorineural following SN.

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Posterior Canal Plugging

Procedure

Replaced the singular neurectomy.

A mastoidectomy is performed through an incision made
behind the ear.
The balance center is then uncovered and
The posterior semicircular canal is opened, exposing the
delicate membranous channel in which the crystalline
debris is floating.
The canal is then gently, but firmly packed off with tissue so
the debris can no longer move within the canal and strike
against the nerve endings.
The canal is then sealed and the incision closed.
One-night hospital stay is advised.
The patient returns in one week for suture removal.
less than 20% hearing loss.
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Clinical Trial
Walsh (1999)Long-term results of posterior semicircular
canal occlusion for intractable benign paroxysmal
positional vertigo. Clin Otolaryngol

13 patients who
All patients reported complete and immediate resolution of
their positional vertigo, which has been maintained in the
long term.
All patients developed a transient mild conductive hearing
loss secondary to a middle ear collection, which usually
resolved within 4 weeks.
Five patients developed a transient mild high frequency
sensorineural hearing loss which resolved in all cases within
6 months.
There were no reports of sensorineural hearing loss nor
tinnitus in the long term.
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Vestibular Nerve Section

Done when the attacks of vertigo cannot
be controlled with medication.
An incision is made behind the ear and
balance-hearing nerve is located.
The balance part of the nerve is cut.
The operation is done with a neurosurgeon
and takes two hours.
The success rate (no vertigo attacks) is
over 90%.
The hearing is usually not affected.
55

Vestibular Nerve Section

56

Clinical Trial
Thomsen et al, (2000) Vestibular neurectomy Auris
Nasus Larynx

42 patients.
The vertigo was controlled in 88% of the patients
postoperative imbalance occurred in 14 patients

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Summary
BPPV
Common complain
Vertigo when changing head position
Diagnosed by Dix-hallpike
Treated by CRP
Surgery if CRP fails

58

Mnires
disease

Mnires disease
aka Idiopathic Endolymphatic Hydrops
refers to a condition of increased hydraulic
pressure within the inner ear endolymphatic
system
Tetrad of symptoms:
(1) fluctuating hearing loss,
(2) occasional episodic vertigo (usually a spinning
sensation, sometimes violent),
(3) tinnitus or ringing in the ears (usually low-tone
roaring)
(4) aural fullness (eg, pressure, discomfort, fullness
sensation in the ears).

Pathophysiology

Overproduction
Malabsorption
of endolymph
gross enlargement of membranous labyrinth
endolymphatic hypertension
Periodic rupture of membranous labyrinth
Mixing of K+ rich endolymph with perilymph
Inactivation of hair cells and neurons of VIIIth nerve
sudden change in the rate of
vertigovestibular nerve firing

Age - 40-50 yrs

Sex F>M
20% family history
Racial variation Caucasians= Blacks

Clinical features
Rotatory vertigo

Sudden
24 min to 24 hours
Nausea, vomiting
Preceded by aura
Aural fullness
Increasing tinnitus
Hearing loss
No neurological
deficits
Nystagmus +

Sensorineural
hearing loss
Fluctuating low freq
Progressive

Tinnitus
Continuous/intermittet

Henneberts signfalse positive fistula

test without presence
of fistula
Remission period

Mnires disease- causes

Metabolic disturbances,
Hormonal imbalance,
Trauma
Various infections (eg- otosyphilis and
Cogans syndrome , interstitial keratitis).
Autoimmune diseases, such as lupus and
rheumatoid arthritis

Audiogram

Age - 40-50 yrs

Sex F>M
20% family history
Racial variation Caucasians= Blacks

Investigations

Pure tone
audiogram
Low freq SNHL

Speech audiometry
Discrimination
score-55 to 85%

Special audiometry
test s/o cochlear
lesion
Transtympanic
electrocochleograp
hy- best objective

Glycerol test
Hearing improves
on giving glycerol

Caloric test
Canal paresis

Medical treatment
Acute episodes bed rest, hydration
Vestibular sedatives prochlorperazine,
promethazine hydrochloride, cinnarizine, diazepam

Prophylaxis

Salt restriction
Diuretic therapy - hydrochlorthiazide
Vasodilators - betahistine
Steroids and immunological therapy
Intratympanic gentamicin chemical ablation of
vestibular function

Hearing loss hearing aids

Tinnitus reassurance, masker

Surgical treatment
Endolymphatic absorption
Endolymphatic sac decompression-1
Endolymphatic sac-CSF shunt

Selective dennervation of vestibular

1
labyrinth
Vestibular nerve section-2

Labyrinthine destruction
Labyrinthectomy-3

2
3

LABYRINTHITIS

 Inflammation of labyrinth
Classification
Bacterial

Acute toxic (serous)

Acute suppurative
Chronic suppurative
Fibrosseous

Viral

Bacterial labyrinthitis
Routes of spread of infection

Round window, oval window, labyrinthine

fistula
AOM, COM, malignancy of middle ear, trauma

Internal auditory meatus, cochlear aqueduct,

vestibular aqueduct
Meningitis
Organisms

B hemolytic strep, pneumococci, H. influenzae

- acute
Gram ve bacilli - chronic

Pathology
Acute serous labyrinthitis
Chemical changes in perilymphatic space
Reversible
Acute suppurative labyrinthitis
Invasion of perilymphatic space by bacterial
organisms
Irreversible destruction
Chronic suppurative labyrinthitis
Fibrosseous
Fibrosis calcification osteoneogenesis

 Not common in post antibiotic period

Otogenic suppurative labyrinthitis any age
group with cholesteatoma or untreated AOM
Meningogenic suppurative labyrinthitis
children < 2yrs

Clinical features
In presence of AOM,COM,meningitis sudden
onset
Severe rotatory vertigo days to weeks
Unilateral severe hearing loss
Unilateral tinnitus
o/e acute phase
Immobile, infected labyrinth upwards
Nystagmus +
Disequilibrium persists ~ 6wks
Hearing loss
Serous improves
Suppurative total and permanent.

Investigations

Audiogram
Serous labyrinthitis
unilateral high-frequency hearing loss
Suppurative labyrinthitis
severe-to-profound unilateral hearing loss
Meningitis - often bilateral
Caloric test
Absent caloric response
Xray mastoid, CT scan

Treatment
Bed rest, hydration, antivertiginous
drugs
IV broad spectrum antibiotics
Surgical management
AOM myringotomy, cortical
mastoidectomy
COM- MRM

Viral labyrinthitis

Common than bacterial labyrinthitis

Organisms - mumps virus, adenovirus, influenza virus
Route of spread - blood borne, subarachnoid space.
Preceeded by URTI, viral infection
Presenting features similar to bacterial labyrinthitis

Hearing loss mild to moderate

Resolution of vertigo earlier
Treatment

Medical treatment as in bacterial labyrinthitis

Steroids role in hearing recovery
No role of antiviral agents

 What if one labyrinth is destroyed !

Acute stage- vertigo,vomiting,
horizontal nystagmus( slow phase
towards lesion)
Chronic stable stage- most patients
experience no symptoms at all
Chronic progessive

 If both labyrinths are destroyed !

Acute stage- may not experience vertigo because of
no asymmetry in vestibular neural activity
Long term effect- Dandys syndrome
Cannot walk securely in dark in uneven ground loss of
VSR
Cannot see clearly while head is moving quickly
(oscillopsia)- loss of VOR
Disoriented when visual and propioceptive input is
ambiguous- loss of VCR
A patient with bilateral vestibular loss---never be motion
sick

Vestibular neuritis
(Epidemic vertigo)
Definition:
Self limiting inflammation of the
vestibular part of the vestibulocochlear nerve
Etiology:

Unknown but neurotropic viruses

Herpes simplex virus is thought to
exist in latent form in human vestibular
ganglia.

Vestibular neuritis
Clinical features:
H/O preceding sore throat and other
acute URTI
Both sexes are equally affected
Between the ages of 30 and 50
Vertigo
Violent, rotatory with nausea and
vomiting
Aggravated by head movement
Less by keeping the head still and
eyes shut.

Vestibular neuritis
Clinical features contd.

Nystagmus is typically unidirectional

with the quick phases beating towards
the unaffected side.
Typical absence of auditory symptoms
Absence of other neurological symptoms
and signs.
Unilateral reduced or absent caloric
response

Vestibular neuritis
Treatment:
Symptomatic by labyrinthine sedatives
Prochlorperazine
Cinnarazine
Promethazine
Early mobilization and vestibular
rehabilitation exercises facilitate
compensation

Acoustic Neuroma
(Vestibular Schwannoma)

Commonest CPA angle tumour- about

78 %
Accounts -8-10 % of all intracranial
tumour
Benign non-capsulated tumour arising
from schwann cells at glial
neurilemmal junction in IAM
60-80 % of which arise from the
superior vestibular nerve

Acoustic Neuroma
(Vestibular Schwannoma)

Clinical features:
Slow growing no vertigo usually
Unilateral SNHL, sometimes sudden and / or
tinnitus
Trigeminal nerve involvement - numbness of face
Headache, ataxia and facial weakness -advanced

A patient presenting with an asymmetrical

SNHL of unknown origin should be considered
to suffer from a VS unless proved otherwise

Acoustic Neuroma
(Vestibular Schwannoma)

Investigations:
High tone SNHL
Poor speech discrimination test
Tone decay test positive
Tests of recruitment negative
Canal paralysis but normal if from
inferior vestibular
Abnormal ABR
Gadolinium enhanced MRI diagnostic

Acoustic Neuroma
(Vestibular Schwannoma)

Treatment:
Surgery Various approaches
Translabyrinthine
Middle fossa
Retrosigmoid

Streotactic radiotherapy ( Gamma

Knife )
in less than 3 cm

single high dose of radiation with

precise targeting

Perilymph and labyrinthine

fistula
Perilymph fistula
Leak through round and oval window
Following
Severe nose blowing
Strenuous exercise
Barotrauma/ Surgical trauma
Labyrinthine fistula
Leak through an abnormal third window
Following
Chronic ear disease/surgery

Perilymph and labyrinthine

fistula
Clinical Features
Brief episodes of vertigo with progressive
SNHL
Sudden or fluctuating hearing loss at
times
Tinnitus
Fistula sign positive-in minority of patients
Treatment
Removal of the cause
Conservative initially-bed rest, head
elevation