Disorders of vestibular system 04.04.16-dr.davis

1. DR. DAVIS THOMAS

2. 2
Introduction
 Basic inputs - vision, proprioception, and
vestibular system
 Provide ocular stability, gait control, and
balance
 Disorders of vestibular system are major
disruptors causing spatial disorientation
 Many causes of dizziness, vertigo when
caused by a loss of vestibular function
 Management strategies for vestibular
disorders has continued to evolve

3. 3
Pathophysiology
 Balance requires –
 Normal functioning vestibular system
 Input from visual system (vestibulo-ocular)
 Input from proprioceptive system (vestibulo-spinal)
 Central causes compromise central circuits that
mediate vestibular influences on posture, gaze
control, autonomic fx
 Disruption of balance between inputs results in
vertigo
 Goal of treatment: restore balance between
different inputs

4. 4
Pathophysiology
 Vestibular system influences autonomic
system
 Intimate linkage in brainstem pathways
between vestibular and visceral inputs
 Alteration of vestibular inputs results in:
 nausea, vomiting
 Pallor
 Respiratory/circulatory changes

5. 5
Vestibular Neuritis
 Sudden onset of peripheral vertigo
 Usually without hearing loss
 Period of several hours - severe
 Lasts a few days, resolves over weeks
 Inflammation of vestibular nerve -
presumably of viral origin
 Spontaneous, complete symptomatic
recovery with supportive treatment
 Treatment aimed at stopping inflammation

6. 6
BPPV
 Most common cause
 Dysfunction of posterior SCC
 Cupulolithiasis vs. Canalithiasis
 Cupulolithiasis
 Calcium deposits embedded on cupula
 PSCC becomes dependent on gravity
 Canalithiasis
 Calcium debris (otoconia) displaced into PSCC
 Does not adhere to cupula

7. 7
BPPV
 Head movements
 Looking up
 Lying down
 Rolling onto affected ear
 Result in displacement of “sludge” / otoconia
 Vertigo lasting a few seconds
 Treatment approaches
 Liberatory maneuvers
 Particle repositioning
 Habituation exercises

8. 8
BPPV
 Epley
 Canalithiasis
 Canalith repositioning
 Move into vestibule
 Cure rates
 80% - one treatment
 100% - multiple

9. 9
BPPV - Epley

10. 10
Vertebrobasilar insufficiency
 Vertigo, diplopia, dysarthria, gait ataxia
and bilateral sensory & motor
disturbance
 Transient ischemia - low stroke risk
 Antiplatelet therapy - aspirin 325mg qD
 Ticlid
 Platelet aggregate inhibitor
 Risk of life-threatening neutropenia
 Only in patients unable to tolerate aspirin

11. 11
Migraine
 Concomitant vertigo and disequilibrium
 Headache control improves vertigo
 Diagnostic criteria
 Personal/family history
 Motion intolerance
 Vestibular symptoms - do not fit other
causes
 Theories - vascular origin, abnormal
neural activity (brainstem), abnormal
voltage-gated calcium channel genes

12. Meniere’s Disease

13. History
 1861 – Prosper Meniere describes classic symptoms
and attributes to labyrinth
 1871 – Knappin theorizes dilatation of membranous
Labyrinth
 1938 – Hallpike and Portman confirm endolymphatic
hydrops via temporal bone histology
 1972 – AAOO defines the disease criteria
 1985 – AAO-HNS revises the definition and establishes
reporting protocols
 1995 – AAO-HNS revises the definition and reporting
protocols again

14.  Definition:
A disease of the membranous inner ear
characterised by deafness, vertigo and
usually tinnitus , which has as its pathologic
correlate hydropic distension of the
endolymphatic system.

15. Meniere’s disease
 Synonym – endolymphatic hydrops
 Idiopathic
 Menier’s syndrome – secondary
Trauma
Viral infections
Syphilis
Cogan’s syndrome
Otosclerosis
Autoimmune diseases

16. AAO-HNS CHE 1995
 Meniere’s is diagnosed by
 Episodic Vertigo
○ Spontaneous, lasting minutes to hours
○ Recurrent, must have 2 episodes > 20 min.
○ Nystagmus during episodes
 Fluctuating Hearing loss
○ Avg (250, 500, 1000) 15 dB < Avg (1000, 2000, 3000)
or
○ Avg (500, 1000, 2000, 3000) 20 dB > than other ear
○ For bilateral disease Avg (500, 1000, 2000, 3000) > 25
dB in the studied ear
 Roaring Tinnitus
 Aural pressure

17. Lermoyez syndrome
 Variant of meniere`s
 Reversed meniere`s
 Initially hearing loss and tinnitus develop
which persist for prolonged periods.
 Then vertigo develops with improvement of
hearing and tinnitus
 TUMARKIN CRISES: sudden unexplained
fall without loss of consciousness or
associated vertigo.
 deformation of otolithic membrane of
utricle or saccule

18.  Cochlear hydrops
- only features of cochlear involvement
- vertigo is absent
- block at the level of ductus reunions
 Vestibular hydrops
- typical episodic vertigo
- cochlear functions are normal

19. CLASSIFICATION OF ENDOLYMPHATIC
HYDROPS
I. 1.PRIMARY
2.SECONDARY(SYPHILIS)
II. 1.EARLY ONSET
2.DELAYED ONSET
III. 1.TYPICAL
2.ATYPICAL
IV. 1.VESTIBULAR
2.COCHLEAR

20. AAO-HNS CHE 1995
 Definite Meniere's disease
 Two or more definitive spontaneous episodes of vertigo
20 minutes or longer
 Audiometrically documented hearing loss on at least
one occasion
 Tinnitus or aural fullness in the treated ear
 Other causes excluded
 See staging chart
 Certain Meniere's disease
 Definite Meniere's disease, plus histopathologic
confirmation
 See staging chart Stage PTA
1 <=25
2 26-40
3 41-70
4 >70

21. AAO-HNS CHE 1995
 Possible Meniere's disease
 Episodic vertigo of the Meniere's type without documented
hearing loss, or
 Sensorineural hearing loss, fluctuating or fixed, with
dysequilibrium but without definitive episodes
 Other causes excluded
 Probable Meniere's disease
 One definitive episode of vertigo
 Audiometrically documented hearing loss
on at least one occasion
 Tinnitus or aural fullness in the treated ear
 Other causes excluded
Stage PTA
1 <=25
2 26-40
3 41-70
4 >70

22. Aetiology
 Genetic
 Anatomical
 Traumatic
 Viral infection
 Allergy
 Autoimmune
 Psychosomatic

23. Pathophysiology
 Endolymphatic hydrops leads to distortion of membranous
labyrinth
 Reisner’s membrane can be seen bulging into the scala
vestibuli in some histologic studies
 Microruptures may lead to episodic attacks which resolve when
the tears heal

24. Pathophysiology
 Theories behind endolymphatic hydrops
 Obstruction of endolymphatic duct/sac
 Hypoplasia of endolymphatic duct/sac
 Alteration of absorption of endolymph
 Alteration in production of endolymph
 Autoimmune insult
 Vascular origin
 Viral etiology

25. Pathophysiology
Prodromal stage of gradual distension of endolymphatic system
Distension progress leading to thinning & atrophy of Reissner’s
membrane &saccular wall
Rupture &sudden release of large volume of endolymph in small
perilymph space
Sensory & neural structure exposed to K + rich endolymph
Sudden HL & vertigo
When perilymphatic compartment is restored to normal, symptoms
subside
Aided by the collapse, the rupture heals & the process is repeated.

27. AAO-HNS CHE 1985
 Meniere’s is diagnosed by
 Vertigo
○ Spontaneous, lasting minutes to hours
○ Recurrent, must have more than 1 episode
○ Associated with nystagmus
 Hearing loss
○ Fluctuating sensorineural
○ Low-frequency or flat
 Tinnitus
 Vertigo treatment reporting standard
 0 = Complete control
 1-40 = Substantial control
 41-80 = Limited control
 81-120 = Insignificant control
 > 120 = Worse
 Hearing treatment reporting standard
 PTA reported 500, 1000, 2000, 3000 kHz
 If multiple pre and post levels are available, the worst is always used
 PTA is considered improved / worse if a 10 dB difference is noted
 SDS is considered improved / worse if a 15% difference is noted
Avg spells/month post-treatment
(24 mon recommended)
x 100 =
Control LevelAvg spells/month pre-treatment
(6 mon recommended)

28. AUDIOLOGICAL INVESTIGATION
 TFT – Reveals SN loss
 PTA – Early disease - low frequency SN
loss – Late disease - high frequency
SN loss
0
10
20
30
40
50
60
70
80
90
100
110
500 1000 2000 4000 8000
0
10
20
30
40
50
60
70
80
90
100
110
500 1000 2000 4000 8000
0
10
20
30
40
50
60
70
80
90
100
110
500 1000 2000 4000 8000
Early Stage Later Stage

29. AUDIOLOGICAL INVESTIGATION
 Speech reception threshold very closely
matching PTT in over 90%
 Speech discrimination score
 Between attacks – 55 – 85 %
 During attacks – Low
 Test for Recruitment
 SISI – better than 70 %
 Stapedial replex +ve
 Tone Decay Test – less than 20 dB
 Bekesy Audiometry – Type II curve

30. AUDIOLOGICAL INVESTIGATION
 Electrocochleography
It’s a diagnostic and prognostic test
 Summating Potential (SP) is larger and more
negative
 SP/AP Ratio more than 30 % (Normal – 20%)
Normal M.D

31. GLYCEROL TEST
 To confirm the diagnosis and useful mainly on
prognosis
 Procedure
 1.5 ml / kg glycerol with equal amounts of water
 +ve Test – 10 dB or more @ 2 or more frequency or
speech discrimination improves 12% or more
 -ve Test – Do not reach +ve criteria
 Decremental – Threshold worse by 10 dB
 +Ve Glycerol Test – C.I for Labyrinthectomy

32. ASSESMENT OF
VESTIBULAR FUNCTION
 Caloric Test
 30 – 50 % of M.D shows canal paresis on the
affected side
 Electronystagmography

33. RADIOLOGICAL INVESTIGATION
 X-Ray temporal bone
 Hypocellularty, sigmoid sinus placed more medially and
anteriorly
 CT Scan
 To see the size, position of VA and see the size and location
of Endolympotic sac or dehiscent sup semi circular canal.
 To see peri aqueduct and perilabyrithine penumatization.
 MRI Scan (With and without contrast)
 Evaluation of skull base tumours / C.P. angle
lesions / vascular lesions / multiple sclerosis /
vascular compression of 8th N / acoustic neuroma
(with Gadolinium)

34. Special Tests
 Vascular imaging
Non invasive : a) Doppler Ultra Sonography
b) Colour Doppler
c) M.R. Angiogram (M.R.A)
Invasive : a) Conventional Angiogram
b) C.T. Angiogram

35. Estimation of the followings
 Full Blood Count
 ESR
 T3, T4 & TSH
 Urea, Electrolytes
 Cholesterol & Triglycerides
 Glucose & GTT
 VDRL & FTA-ABS

36. TREATMENT
 General measures
 Medical treatment
 Surgical treatment

37. General measures
 Dietary restriction of salt, caffeine,
alcohol, nicotine
 Cessation of smoking
 Intermittent dehydration
 Avoid activities requiring body balance
 Reassurance
 Bed rest

38. Medical Therapy
 Diuretics - Frusemide
 Vasodilators– Carbogen,
Histamine,
Betahistine,
Nicotinic acid
 Labyrinthine sedative– Promethazine,
Dimenhydrinate,
Prochlorperazine

40. SYMPTOMATIC RELIEF DURING ACUTE EPISODES
 VESTIBULAR SUPPRESSANTS:
i. Phenothiazines-
prochlorperazine,perphenazine
ii. Antihistamine-cinnarizine,
cyclizine,dimenhydrinate,promethazine,mec
lizine
iii. Benzodiazepines-reduce activity in
vestibular nuclei & relieve anxiety
associated with the attack-
diazepam,lorazepam
iv. Transdermal scopalamine hydrochloride, an
anticholinergic agent

41. PROPHYLAXIS BETWEEN ACUTE EPISODES
TO REDUCE ENDOLYMPHATIC
ACCUMULATION
 SALT RESTRICTION
 DIURETIC THERAPY(hydrochlorthiazide,
chlorthalidone,acetazolamide)
 HYPEROSMOLAR DEHYDRATION

42. Intratympanic Ablation
 Fowler (1948) and Schuknecht (1957)
established role of aminoglycoside therapy.
 Streptomicin used initially
 Vertigo eliminated in all patients
 Profound hearing loss in all patients
 Gentamicin treatment now preferred
 Theoretical targets of therapy are
○ Dark cells of the stria vascularis
○ Planum semilunatum of the semicircular canals
 Higher doses destroy the hair cells of the
cochlea

43. Meniett Device
 Transtympanic “Micropressure”
Treatment
 FDA approved in 1999 as a class II
device
 Treatment self-administered TID
 Each treatment is three 1-minute
cycles
 Applies intermittent, alternating
pressure 0-20 cm H20
 Requires a tympanostomy tube

44. Meniett Device
 Criteria: “active symptoms of vestibular or
cochleovestibular hydrops”
 Improvement in tinnitus, vertigo & ear fullness
 Improvement in hearing
 Requires tympanotomy tube
 Problems
○ Tube otorrhea, blockage, extrusion
○ Recurrence of disease after therapy cessation

46. Precautions & Prerequisites for Surgery
 Accurate diagnosis
 Failed medical management
 Risks Vs Benefits
 Bilaterality of the disease
 Health status

47. Meniere’s Disease.
 Classification
 Conservative
 Ablative
 Miscellaneous

48.  Conservative surgery for Meniere’s
Residual hearing preserved-50dB SRT,50%SDS
1) Sac surgery :
a) Endolymphatic sac decompression
b) Endolymphatic mastoid
shunt(shea,Arenberg.morrison)
c) Endolymphatico subarachnoid shunt(austin)
2) Selective vestibular nerve section
3) Sacculotomy
4) Cody Tack procedure
5) Otic periotic shunt
6) Cochleosacculotomy
Meniere’s

49. Ablative
 Residual hearing sacrificed
1)Labyrinthectomy
2) Labyrinthectomy with cochleo
vestibular neurectomy
Meniere’s

50. Unilateral Disease
1. Serviceable hearing
Conservative surgery-Sac surgery
2. Poor hearing
Ablative surgery-Labyrinthectomy/Nerve section
Bilateral Disease
1. Both ears good hearing
Sac surgery-Uni/Bilateral
2. Only Hearing Ear
Sac surgery
3. Both poor
Rehabilitation exercise/Nerve section
Meniere’s

51. Meniere’s
Endolymphatic Sac Surgery
Aim
To preserve both auditory & vestibular
function
Principle
Decompress or open Sac
Increase drainage & Resorption
Eliminate hydrops
Decrease sequelae & symptoms

52. Meniere’s
Endolymphatic Sac Surgery
 Indications
 Failed medical
treatment with
serviceable hearing
 Only hearing ear
 Fluctuating hearing
loss 2-3yrs with
medical treatment
 Contraindications
 Poor hearing
 Decrimental glycerol
test

53. Meniere’s
Procedure
•Cortical mastoidectomy done
•Identify
-Lateral & post semicircular canal
-Vertical segment of 7th nerve
-Posterior fossa dural plate
•Donaldsons line drawn
•Sac identified and opened

54. Advantages of Sac Surgery
 Better hearing
 No post op disequilibrium
 Less risk
 Preserves both components

55. Complications
 Facial nerve injury
 Hearing loss
 CSF leak
 Meningitis

56.  Final surgical option for control of vertigo
 1904 described
 Transcanal, transmastoid
 PTA 70, discrim 20%
 Indications
- Unilateral poor hearing
- Negative Glycerol test
Labyrinthectomy

57. Overview
 Acute Therapy
 Long-Term Stabilization
 Non-invastive medical
treatments
 Alternative options
 Non-Destructive Therapy
 Medical: IT Steroids
 Surgical: Mastoid shunt
 Destructive Therapy
 Medical: IT Gentamicin
 Surgical
○ Nerve section
○ Labyrinthectomy
Vestibular
Suppressants
Diuretics
Salt Restriction
Vasodilators
? Water Therapy
Alternative Therapies
Meniett
Herbal
Hypnosis
?
Intratympanic
Steroid Therapy
Intratympanic
Gentamicin Therapy
Surgical Ablation
Nerve Section
Labyrinthectomy
Mastoid Shunt

58. 58
Conclusions
 Vestibular complaints common to ENT
 Thorough evaluation and understanding
 Dx and treat acute symptoms
 Wean vestibular suppressants
 Specific pharmacotherapy instituted
 Chronic, uncompensated disease
benefits from early VRT

59. THANK U