PERIPHERAL VESTIBULAR DISORDERS ALONG WITH TREATMENT AND DIAGNOSIS

1. PATHOLOGY OF
EQUILIBRIUM
DR ADITYA GOEL
RSO 3RD YEAR

2. The vestibular system
• The main function of the vestibular system is to generate information
to the central nervous system with a four fold purpose:
• To ensure Gaze stabilization
• Enable balanced locomotion and body position
• Provide general orientation of the body with respect to gravity
• Readjust autonomic functions after body reorientation

3. Equillibrium

4. Otolith organs
The Otolithic Organs include:
• the utricle
• the saccule

5. The otolith organs saccule and utricle are
orthogonally oriented to each other, with the
utricle relatively horizontal and the saccule
predominantly vertical (tangential in the
head).
Both the saccule and the utricle sense linear
accelerations caused by translational
movements of the head as well as static tilts
of the head.

6. • The detection of
translational movements
and static tilts is enabled
by means of an otolith
membrane.
• Hair cells embedded at the
base of gelatineous
membrane and any
movement cause
deflection which in turn
sends signals to the brain.

8. Physiology of equilibrium
• The semicircular canals (SCCs) measure predominantly rotations and
are responsible for the dynamic equilibrium whereas the maculae of
the utricle and saccule detect mainly translations and are responsible
for static equilibrium.
• The moving endolymph in the SCCs is the key trigger for movement
detection of the head.
• The configuration of the SCC allows the movement of the endolymph
only in the direction along the cylindrical canalicular cavity.

9. •The cupular deflection is
ultimately the signal that is
fed to the brain, because this
deflection triggers hair cell
depolarization or
hyperpolarization.
•Depolarization of the
ipsilateral hair cells occurs
during angular head
movements and
simultaneously the
hyperpolarization of
contralateral hair cells occurs.

10. Pathways

11. Vestibulo ocular reflex
• 1. During head rest, hair cells in both SCCs have a resting discharge rate of 90 spikes
per second.
• 2. Head rotation is to the right.
• 3. Endolymph fluid lags behind, i.e. moves relative to the left within each SCC due to
inertia.
• 4. The cupula bends to the left in each canal.
• 5. In the (leading) right SCC the stereocilia bend towards the kinocilium.
• 6. In the (following) left SCC the stereocilia bend away from the kinocilium.
• 7. The discharge rate increases in the leading right ear (e.g. from 90 to 300 spikes per
second).
• 8. The discharge rate decreases in the following left ear (e.g. from 90 to 20 spikes per
second).
• 9. The vestibular nuclei interpret the difference in discharge rates between left and
right SCCs as movement to the right, and therefore trigger the oculomotor nuclei to
drive the eyes to the left to maintain gaze stabilization.

12. Vertigo
• Vertigo is defined as a false illusion of either onself or the
environment is rotating.
• It indicates the involvement of angular motion sensing system i.e. The
semi circular canals and their central projections, such involvement
can occur from labyrinth to vestibular cortex.
• Additional symptoms like hearing loss and tinnitus indicate
involvement of labyrinth and 8th nerve , linear vertigo such as falling
vertically downwards may indicate involvement of otolith system
whereas frank diplopia, facial numbness and dysarthria indicates
involvement of brainstem.

14. • Dizziness : a sensation of spinning around and losing one's balance.
• Altered sense of balance and place, possibly described as lightheaded,
feeling faint or as if head is spinning.
• Motion sickness: Motion sickness is a sensation of wooziness. It usually occurs
when you’re traveling by car, boat, plane, or train. Your body’s sensory organs
send mixed messages to your brain, causing dizziness, lightheadedness, or nausea.

15. • Central vestibular disorder :
• Vascular
-Ischemic stroke/transient ischemic attack
-Subclavian steal syndrome
– Vertebrobasilar transient ischemic attacks
– Wallenberg’s syndrome
– Lateral pontomedullary infarction
– Cerebellar infarction
– Hemorrhage: Brainstem and cerebellar
– Migraine: Basilar migraine and vestibular migraine

16. • Inflammatory
– Multiple sclerosis
– Cerebellitis
• • Infectious
– Intracranial complications of otitis media
– Meningitis
– Cerebellar abscess (fungal or bacterial)
• • Craniocervical Junction Disorders
– Chiari malformation

17. • Metabolic
– Wernicke’s encephalopathy
– Diabetes
– Vitamin B12 deficiency
– Hypothyroidism
– Hypoparathyroidism
– Hypoglycemia
– Hyperventilation
• • Toxic
– Medications (methotrexate) and alcohol
• • Degenerative
– Parkinson’s disease

18. • Trauma
– Post-concussion syndrome
• • Physiologic
– Motion sickness
• • Psychophysiologic
– Chronic anxiety
– Panic disorder
– Phobic postural vertigo
• • Multisensory Disturbances
– Peripheral neuropathy and visual loss
– Aging: Cerebellar atrophy and diffuse small vessel ischemia

20. DISEASES OF EQUILIBRIUM
• PERIPHERAL VESTIBULAR DISORDERS
• BENIGN PAROXYSMAL POSITIONAL VERTIGO
• MENIERE’S DISEASE
• SUPERIOR SEMICIRCULAR CANAL DEHISENCE
• VESTIBULAR NEURITIS
• LABYRINTHITIS

21. Benign paroxysmal positional vertigo
• This is the most common cause of vertigo.
• Incidence
• Benign paroxysmal positional vertigo is the most
common
• cause (20–40%) of peripheral vertigo.
• Age: 11–84 years; mean age of onset fourth to
fifth decades.
• Incidence increases with age.
• Pediatric BPPV patients have association with
migraine.
• Slightly increased incidence in females.

22. Benign paroxysmal positional vertigo
Etiological Factors
• In about 52% of cases, one or more of the following etiological
factors are present.
• Most common are closed head injury and vestibular neuronitis
(vertigo lasting days).
• Infections
• Old age
• Surgery (stapedectomy)
• Prolonged bed rest and inactivity
• Benign paroxysmal positional vertigo can develop in cases of
Ménière’s disease, viral labyrinthitis and recurrentvestibulopathy.

23. Benign paroxysmal positional vertigo
• Pathogenesis
• Otoconia gets displaced from utricle to semicircular canal (SCC) usually
posterior.
• Cupulolithiasis: Deposition of otoconia on the cupula of posterior SCC.
• Canalithiasis: Free floating material (debris) within the lumen of posterior
SCC.
• Lateral canal BPPV (17% of cases): The pathogenesis is usually
cupulolithiasis with or without canalithiasis. Particles are usually in the long
arm of the lateral canal (canalithiasis) far from ampulla (geotropic
nystagmus) or near the ampulla/on the opposite side of cupula (ageotropic
nystagmus), floating within the endolymph or embedded in the cupula
(cupulolithiasis).

24. Benign paroxysmal positional vertigo
• Clinical Features
• Sudden brief (seconds) spells of severe vertigo associated with change in
head position, such as
• Rolling over in the bed.
• Getting into bed and assuming a supine position
• Arising from a bending position
• Extending the neck
• Turning rapidly
• Vertigo spell lasts for seconds and never more than a minute. |However
patients usually complain of longer subjective feeling of dizziness..

25. Benign paroxysmal positional vertigo
• Bouts of vertigo are clustered in time. Remissions may last for
months or more.
• The active spells may be associated with the feeling of light
headedness or mild imbalance, which is worsened by head
movement.
• Some patients have chronic balance problem, which may be
worse at the time of awakening from the sleep

26. Benign paroxysmal positional vertigo
• Types
• Though following three types of BPPV are described but the
most common is posterior canal BPPV.
• 1. Posterior semicircular canal BPPV
• 2. Lateral semicircular canal BPPV
• 3. Superior semicircular canal BPPV

27. • Diagnosis
• Dix-Hallpike test: The BPPV is classified as active if rotatory
nystagmus is elicited by Dix-Hallpike test. Patients with a typical
history of BPPV, but a negative Dix-Hallpike test and whose
symptoms had settled are diagnosed as resolved BPPV.
• Differential Diagnoses
• Vascular compression of cranial nerve VIII complex
• Multiple sclerosis
• Acoustic neuroma

28. Ewald’s law
• Characteristics eye movements during the tests is based on
fundamental principle of Ewald :
• The direction of eye movement is in the plane of canal or canals that
are stimulated.
• In the horizontal canal , endolymph flow towards the ampulla
(ampullopetal) is excitatory and stronger response than the flow
away from the ampulla (ampullofugal) ,which is inhibitory.
• The opposite holds true for vertical canals

29. Dix hallpike test
• Dix hallpike test- for vertical canals
Procedure : explain the procedure with counselling of the pateint
about dizziness but they have to maintain their eyes open for
examination.
Pateint should be seated along the couch ,feet up and the head is
turned to 45 degree to the side being tested.
This cause alignment of vertical canals with the saggital plane.
The head is brought down 30 degrees below the horizontal plane
while maintaining the position 45 degrees to the side being tested .

30. • Interpretation : LARP (left anterior and rt posterior) are stimualted
during rt dix hallpike and RALP( right anterior and left posterior) are
stimulated in left dix hall pike.
• Normally during rt dix hallpike there is ampullofugal (excitatory) flow in
RT PSCC and ampullopetal (inhibitory) in LT ASCC ,it balances out and
there is no nystagmus.
• In rt PSCC BPPV – If there were particles in rt PSCC ,ampullofugal force is
greater resulting in net excitaory effect and eye movement consistent
with the plane of canal.
• Nystagmus is produced with slow phase eye movement towards rt ear
or downwards and outwards, fast phase - upwards and outwards.

31. • Treatment
• Treatment consists of repositioning maneuvers. There is no role
of any medicine. The following maneuvers are effective in
majority of the BPPV patients.
• Repositioning Maneuvers
• After the maneuver, patients are told to sleep with 45°elevated
head and avoid bending.

32. • For Posterior SCC
• Epley maneuver : It is effective in 90% cases of posterior canal BPPV.
Meclizine or benzodiazepine 1 hour before may be given in anxious
patients. First two positions (upright and supine position with extended
neck turned 45°) are similar to Dix-Hallpike maneuver .Then head is rolled
180° in two 90° increments so that the offending ear is up. From this
position, patient is brought to the sitting position. The repositioning
maneuver is repeated again and again until no nystagmus is produced.
Head remains in that particular position until any nystagmus resolves.

34. • video

35. • Semont maneuver : The patient is turned rapidly into the
position that provokes vertigo and kept in that position for 4
minutes. Then patient is move quickly to opposite position with
normal ear down. After some time, patient is asked to sit slowly
in upright position.

37. • video

38. • For Lateral SCC
• Geotropic nystagmus: Lying on the normal side with affected
ear up for 12 hours—effective in 92% cases.
• Modified Epley: Patient lies on the affected side with normal ear
up. Then, patient is moved in 90° increments to supine, affected
ear up, prone and at last affected ear down.

40. • Surgical Treatment
• The following surgical procedures are considered in cases that
are refractory to the above mentioned maneuvers and the
symptoms are disabling to the patient:
• Singular neurectomy
• Posterior SCC occlusion

42. SUPERIOR SEMI-CIRCULAR CANAL DEHISENCE
• Dehiscence (opening) in the bone overlying the superior semicircular
canal of the inner ear. This clinical syndrome—superior canal
dehiscence syndrome (SCD).
• Described by Minor and collegues in 1998.
• Causes vestibular and auditory symptoms.

44. • Vestibular symptoms :
• Vertigo
• Oscillopsia (the apparent motion of objects that are known to be
stationary)
• Coughing, sneezing, running can raise intracranial tension and thus
increases symptoms
• Auditory symptoms:
• Autophony
• Hypersensitivity of bone conducted sound
• An apparent conductive hearing loss, revealed on audiometry.

45. • Some patients can have exclusive vestibular symptoms , some can have
both and a few can have only auditory symptoms.
• Pathophysiology
• With a dehiscence in the bone that is supposed to cover the superior
semicircular canal the fluid in the membranous superior canal (which is
located within the lumen— tubular cavity—of the bony canal) can be
displaced by sound and pressure stimuli.
• There are normally only two points of increased compliance (yielding to
pressure) in the inner ear: the oval window, through which sound
energy is transmitted into the inner ear via the stapes bone; and the
round window, through which sound energy is dissipated from the
inner ear after traveling around the cochlea.

46. • SCD creates a third mobile window into the inner ear. The signs and symptoms in this
syndrome are due to the physiological consequences of this third window.

47. • Dehiscence of bone over semicircular canal and consequently
forming connections with middle cranial fossa
• Causes formation of 3rd window , which is mobile , in the inner ear.
• Due to loud sound, cough , Valsalva , there is movement of this 3rd
window in the inner ear.
• Leads to alteration of inner ear fluid dynamics and causes increased
firing of vestibular afferents and causes transient momentary vertigo

48. • There are constellation of symptoms :
• There can be two movements in the inner ear fluids and these
movements are responsible for different types of symptoms.
• Two main movements are
1. Marked inward movement of stapes / outward movement of 3rd
window
2. Inward movement of dehiscence

49. Marked inward movement of stapes /
outward movement of 3rd window in
superior semicircular canal (vertical
canal)
There is increased ampullofugal flow (
flow away from the ampulla ) on affected
side of vestibule
There is excitatory response which causes
Tonic upward eye movement and
ipsilateral intorsion

50. inward movement of dehiscenece
( negative pressure on external ear, pressing
the jugular vein, raised ICT, deep breaths
Ampulopetal flow ( flow towards ampulla)
on affected side
There is inhibitory response which causes
tonic downward eye movement and
ipsilateral extorsion

51. • Epidemiology
• Prevalence is 4-8 %
• Mean age is 45yr and there is increased prevalence with increasing
age .
• It can be congenital or acquired.
• Congenitally it can be due to improper ossification of petrous bone.

52. • Clinical features :
• Vestibular and auditory symptoms
• If dehiscence is <= 2.5 mm – there are combined symptoms.
• Vestibular symptoms :
• Thevestibular symptoms in SCD can be debilitating and often provoke
patients to seek medical attention.
• Patients may note that loud noises cause them to see things moving or
that they experience a similar sensation when they cough, sneeze, or
strain to lift something heavy. They may perceive that objects are moving
in time with their pulse (pulsatile oscillopsia).
• Some individuals can bring on the sensation of motion—and cause their
eyes to move—by pressing on their tragus (positive fistula test )
• Patient have feeling of constant disequilibrium and imbalance.

53. • Auditory symptoms :
• The auditory symptoms and signs in SCD may mimic those in other ear
disorders like otosclerosis i.e conductive hearing loss for low frequency.
• Patients with SCD may also complain of symptoms such as hearing
their eye movements, hearing their own voice too loudly in the affected
ear (autophony), or having a distorted sensation of sound in the
affected ear during activities such as running.
• Pulsatile tinnitus
• Bone-conducted sounds are amplified by the effects of the dehiscence,
whereas the energy from air-conducted sounds is Partially shunted
away from the cochlea and through the dehiscence

54. • Investigations
1. HRCT temporal bone – gold standard . It is done in two views :
a. In plane of semicircular canal – poschl view
b. In orthogonal plane- stenver’s view

56. 2. Vestibular evoked myogenic potential (VEMP):
Record response to high intensity narrow band clicks/ tone burst.
In superior semicircular dehiscence – VEMP response present at
lower than normal threshold in affected ear both for AC and BC.

57. • MANAGEMENT
• Mild symptoms :
• Conservative management: avoid trigger or stimuli
Ventillatory tube insertion – reduces pressure changes.
• Surgical management : plugging capping and resurfacing
• Round window reinforcement
• Severe disability symptoms: surgical management .

59. ACUTE VESTIBULAR NEURITIS
• Also known as vestibular neuronitis / acute viral labrynthitis
• Second most common cause of peripheral vertigo after BPPV.
• It is the inflammation of the vestibulocochlear nerve in the inner ear
which sends balance and head position information from inner ear to
the brain.
• When this nerve is swollen , it can cause difficulty in conduction of
information.
• It leads to sudden severe vertigo, dizziness, balance problems ,
nausea , vomiting.

61. • Etiology :
• Exact cause is not known.
• 50% pt have history of upper respiratory tract infection.
• Due to some microrganisms like: mumps virus , varicella zoster virus ,
influenza, Epstein barr virus , borrelia burgdorferi, treponema
pallidum.
• It can also precedes herpes infection.

62. • Clinical features :
• Patient have dramatic sudden onset of severe vertigo with vegetative
symptoms like nausea , vomiting , sweating, with gradual and
definitive improvement throughout the course.
• Sometimes patients have bouts of attacks for over several weeks with
complain of ear stuffiness.
• Nystagmus : which horizontal or horizontal- rotatory nystagmus and is
towards the healthy ear.
• There is no subjective hearing loss, but audiogram can show hearing
loss at high frequencies.

63. • Investigations:
1. calorie test: it is absent or reduced in the side of involvement.
2. CSF study : usually normal
3. videonystagmography/electronystagmography
4. Audiogram: to find out any hearing loss.
5. vemp: it is used to detect which branch of the nerve is affected ( the
superior or inferior nerve )
• Prognosis:
• Vertigo Usually last for many hours to 1-2 weeks and then
spontaneously disappears over weeks to months.
• Imbalance by rapid head movement can remain persistent for months
till the resolution of acute disease.

64. • Diagnostic criteria of COATS :
1. Acute onset of non-recurrent vertigo often accompanied by nausea
and vomiting.
2. Absence of cochlear symptoms (hearing loss or tinnitus) or signs of
CNS involvement .
3. Commonly unilateral partial or complete peripheral vestibular
lesion .
4. Complete subsidence of symptoms within 6 months.

65. • Diffential diagnosis :
• Vestibullopathy
• Multiple sclerosis
• Acoustic neuroma
• Haemorrhage parietoinsular cortex or superior or medial temporal
gyri (vestibular cortex).

66. • Treatment :
1. Hospitalization and iv fluids
2. Antiemetics
3. Anticholinergics
4. Vestibular rehabilitation : gait training , exercises
5. Cognitive beahvioural therapy

67. MINIERE’S DIEASE
• Also k/a endolymphatic hydrops.
• Disorder of the inner ear.
i. Periodic episodes of vertigo or dizziness
ii. Fluctuating, progressive, unilateral or bilateral hearing loss
iii. Unilateral or bilateral tinnitus
iv. Sensation of fullness or pressure in one or both ears.
v. Nausea, vomiting, sweating.

68. • Idiopathic i.e primary endolymphatic hydrops where cause is not
known is termed as Meniere’s disease.
• When cause of endolymphatic hydrops is known such as infections
(measles, mumps , syphilis), trauma (ear surgery, head injury),
autoimmune diseases or otosclerosis., then it is termed as secondary
endolymphatic hydrops or Meniere’s syndrome.

69. What causes meniere’s disease?
• Due to swelling of the
endolymphatic sac in the
vestibular system of the inner ear
• The endolymphatic duct may be
obstructed by scar tissue, or is
narrow since birth
• Due to too much fluid secreted
by the stria vascularis

71. • Incidence :
• Age 35-60 years
• Slight female preponderance
• It can be hereditary with autosomal dominance mode.
• 45% people have bilateral disease
• Mostly it is a unilateral disease.
• 10 % of patients present with dizziness.
• Etiology :
• It is a multifactorial disease whose exact cause is not yet known.
• Some factors are listed as below:

72. Idiopathic endolymphatic hydrops (meniere’s
disease
• Increased production of
endolymph
- Allery
- Autoimmune
- Endocrine- hypothyroidism,
hypopituitarism, diabetes
- Increased sympathetic
activity.
- Sodium and water retention
- Viral infection- HSV, VZV
Decreased absorption of
endolymph
- Inner ear trauma
- Ischaemia of
endolymphatic sac.
- Obstruction of
endolymphatic sac
- Small size of
endolymphatic sac

73. Secondary endolymphatic hydrops ( Meniere’s
Syndrome)
• Meniere’s disease after a known established cause:
1. Chronic otitis media
2. Cogan syndrome – interstitial keratitis, audiovestibular symptoms,
systemic vasculitis
3. Leukemia
4. Otosclerosis
5. Post stapedectomy
6. Syphilis and granulomatous diseases

74. Pathogenesis
• Inadequate absorption of fluid from endolymphatic sac – due to ischaemic fibrosis
• Overaccumulation of endolymph – ischaemia of neuroepithelium and anoxia of
stria vascularis leads to increase transudation of fluid and leads to bulging of
Reissner’s membrane to scala vestibuli
• Membrane rupture theory : rupture of membranous labyrinth
k+ rich fluid mix with perilymph
sustained depolarisation and inactivation of hair cells and neurons of 8th nerve
This is the cause of acute attack of hearing loss and vertigo and healing of membrane
resolves the symptoms

76. Clinical features
• TRIAD of MENIERE’S disease
Triad
VERTIGO
TINNITUS
FLUCTUATING
HEARING LOSS

77. • Vertigo attacks usually preceded by aural of fullness of ear, increased
tinnitus . Attacks may wake up patient from sleep.
• Cluster of attacks are separated by long remission.
• Attacks are accompanied by nausea vomiting, sweating.
• Vertigo is exacerbated by any head movement.
• Hearing loss is fluctuant and progressive. It is associated with
Displacusis( difference in perception of pitch between ears ) and
Recruitment (intolerance to loud sound).
• Tinnitus is non pulsatile and it may be Whistling or roaring, continuos
or intermittent
• Ear fullness- mainly during attack.

78. • Lermoyez attack- in this, increased tinnitus and hearing loss precede
vertigo episode and resolve after onset of vertigo.
• Drop attacks -also known as otolith crisis of Tumarkin – it is the
sudden unexplained falls without loss of consciousness or associated
vertigo.
• Tulio phenomena: loud sounds produces vertigo.
• Nystagmus :
The direction of nystagmus is horizontal and it varies with course of
time.

79. • Differential diagnosis
1. Migrain and basilar migrain
2. Otosclerosis
3. Cogan syndrome
4. Cardiogenic
5. Trauma
6. Acoustic neuroma
7. Vertebral basilar insufficiency
8. Labyrinthitis
9. Drug induced – alcohol, smoking, anticonvulsants,
aminoglycosides,sedatives

80. Diagnostic scale for Ménière's disease of the American Academy of Otolaryngology-Head and Neck Surgery

81. Examination
• Otoscopy – No abnormality.
• Nystagmus
• Fistula test – False +ive in 30% pt. (Hennebert’s sign)
• Tuning Fork test –
a) Rinne test – Positive (AC>BC)
b) Weber test – Lateralize towards better ear.
c) ABC test – Decreased in deceased ear.

82. Investigations
. Pure Tone Audiometry – SNHL
• In early stage – Lower frequencies affected.
curve is rising type.
• In later stages – when higher frequencies involved Flat or Falling curve
obtained.

84. • Other Audiological tests –
a) Speech discrimination score – 50-80% much impaired during attacks.
b) SISI - more than 70% in 2/3 patients.
c) Recruitment test - Positive.

85. . Electrocochleography - changes are diagnostic.
a) Summating potential : action potential >30% (N=30%)
b) Widened SP-AP waveform. (>2ms)
c) Distorted cochlear microphonics.
3. Caloric test – Reduced response on affected side in 75% pt.

88. . Glycerol test -Dehydrating agent.
-1.5 ml/ kg mixed in lime orally.
-PTA and SDS done prior and
after 2 hrs
a) Pure tone threshold improves >10 db.
b) SDS increases >15%.
c) SP/AP ratio in ECoG decreases >15%.

89. • Imaging :
• CT scan
• MRI

90. • TREAMENT :
A. General measures –
i. Reassurance
ii. Cessation of smoking.
iii. Low salt diet. ( < 1.5-2 gm/day)
iv. Avoid excess intake of water.
v. No coffee, tea or alcohol.
vi. Avoid stress.

91. B. Acute attack :
1. Reassurance and bedrest
2. Vestibular sedatives : prochlorperazine , promethazine
3. Vasodilators : inhalation of carbogen, betahistine
C. Chronic phase:
1. Dietary modification : salt restriction , intermittent dehydration
2. Diuretics

92. 3. Vasodilators
4. Hormone replacement therapy
5.Meniett device : it is pulsed positive pressure in EAC
and pressure equalization tube . In this through
grommet , pressure waves are delivered to round
window. This displaces endolymph and relieves
symptoms.
6. Immunosuppressants

93. • Surgical management:
1. Non- Ablative Procedure – intratympanic injection of steroids
2. Partially ablative procedure - Intratympanic inj of gentamycin –
(Chemical labyrinthectomy)
Microwick – a microwick of polyvinyl acetate is passed through grommet. Through
it gentamicin or steroid is instilled.

95. 3. Hearing conservative non vestibular ablative surgery-
a. endolymphatic sac decompression surgery- in this there is
decompression , drainage and shunting
Endolymphatic sac shunting –
i) Into mastoid cavity – Paparella & Hansen technique.
ii) Into subarachnoid space.
b. Sacculotomy – a) Fick’s needle puncture of footplate.
b) Cody’s tack puncture of footplate.
c. cochleo-sacculotomy

99. 4. Vestibular surgery: Vestibular neurectomy - much greater vertigo
control than shunt surgeries.
5. Total destructive surgery :
• Destroys both cochlear and vestibular functions.
• Done in pt with severe deafness not responded to conservative measures like
gentamycin inj.
• Types of surgery –
1. Section of vestibular + cochlear nerve.
2. Total labyrinthectomy –
a) Transcanal
b)Transmastoid - more common.

100. Labyrinthine fistula
• Also known as Circumscribed labyrinthitis.
• There is loss of endochondral bone without loss of perilymph, usually
due to cholesteatoma( mainly hz scc).
• Inflammation of bony labyrinth and endosteum.
• CAUSES:
• Chronic otitis media squamosal type.
• Congenital syphilis
• Glomus jugulare
• Fenestration operation for otosclerosis.

102. • Clinical features:
• May be asymptomatic
• Brief period of imbalance , disequilibrium or vertigo.
• FISTULA sign: transient vertigo induced by washing ear or pushing the
tragus into EAC.
• tullio’s phenomenon: loud sound provoke vertigo.

103. • Investigation:
1. Fistula test
2. Ct scan – bone erosion is seen.

104. Treatment :
Surgery : complete removal of cholesteatoma from fistula site.

105. Serous labyrinthitis
• It is transient non purulent inflammation or chemical irritation of
inner ear, which usually does not result in any permanent damage.
If diagnosed and treated at early stage.
The hearing loss and vestibular functions which are lost are completely
reversible.
The perilymph is only involved.

106. • Causes:
1. Labyrinthine fistula
2. Bacterial or viral toxin invasion through round or oval window.
3. Blood borne inflammation.
4. Meningeal infection
5. Ear surgery – following fenestration or stapedectomy surgery.

107. • Clinical features:
• Spontaneous vertigo
• Irritative type of nystagmus- quick component is directed towards
affected ear.
• Fistula sign positive
• Hearing loss

108. • Treatment –
• Active and prompt treatment can prevent its sequelae
• Eradicating the cause can relieve the disease symptoms

109. Suppurative labyrinthitis
• It is the sequalae of serous labyrinthitis.
• Characterised by permanent hearing loss and acute vertigo.
• Patients usually give history of ear discharge , ear pain preceding cold
cough or meningitis.
• Routes of infection :
1. Tympanogenic :otitis media, mastoiditis,petrositis,temporal bone
fracture, penetrating injury.
2. Meningogenic : meningitis
3. Hematogenic : from distant or systemic infections

110. • Clinical features:
• Three stages :
1. Acute (manifest) stage(1-2 weeks) : rapid onset tinnitus, whirling vertigo,
pallor, diaphoresis ,nausea ,vomiting.
Symptoms does not resolve and not respond to treatment.
- Brisk jerky nystagmus : hz rotatory with quick component on affected side.
- Vertigo
- Patient lies quietly on affected side and cannot sit or stand.
- Slight head movement- produces vomiting.
- Complete hearing loss

111. 2. Chronic (latent or fibrous) stage: 1-6 weeks
- Mild vestibular upset and positional vertigo
- Difficulty in walking
3. Healed (compensated or ossification) stage (labyrinthitis ossificans)-
-New bone forms
- Can take many years
TREATMENT – same as serous labyrinthitis

112. Thank you