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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
Postconcussive Syndrome
Demyelinating Disease
Congenital
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
Caloric test
Benign Paroxysmal
Positional Vertigo
(BPPV)
The Ear
27
28
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.
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
36
Treatment
Medications
The Canalith Repositioning Procedure
(CRP)
Surgery
37
Medications
Antiemetic
Antihistaminic
Anticholinergic
38
Canalith Repositioning
Procedure ( CRP )
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
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)
BPPV
Epley canalolilith/ particle repositioning
procedure Slowly roll the patient to the
BPPV
Epley canalolilith/ particle repositioning
procedure Slowly roll the patient onto
BPPV
Epley canalolilith/ particle repositioning
procedure
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
52
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.
54
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
57
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
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
Metabolic disturbances,
Hormonal imbalance,
Trauma
Various infections (eg- otosyphilis and
Cogans syndrome , interstitial keratitis).
Autoimmune diseases, such as lupus and
rheumatoid arthritis
Audiogram
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
Surgical treatment
Endolymphatic absorption
Endolymphatic sac decompression-1
Endolymphatic sac-CSF shunt
Labyrinthine destruction
Labyrinthectomy-3
2
3
LABYRINTHITIS
Inflammation of labyrinth
Classification
Bacterial
Viral
Bacterial labyrinthitis
Routes of spread of infection
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
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
Vestibular neuritis
(Epidemic vertigo)
Definition:
Self limiting inflammation of the
vestibular part of the vestibulocochlear nerve
Etiology:
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.
Vestibular neuritis
Treatment:
Symptomatic by labyrinthine sedatives
Prochlorperazine
Cinnarazine
Promethazine
Early mobilization and vestibular
rehabilitation exercises facilitate
compensation
Acoustic Neuroma
(Vestibular Schwannoma)
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
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