2. • Vertigo is the sense of hallucination of rotation of self or its
environment .
• Results from imbalance between occular ,proprioception and
vestibular system.
3. How do we maintain equilibrium?
Visual input
Proprioceptiual
input
Vestibular input
labyrinths.
equilibrium
7. Diagnosis
History
- important to differentiate TRUE or FALSE vertigo
- peripheral or central causes
So ,Detailed history taking is essential!
8. Character
Periperal - acute , episodic attack
Cenral – persistent , no episodic attack
Duration
Sec or min in BPPV
Min to hour in Meniere’s disease
Days in central causes
9. Associated symptoms
Peripheral - associate with nausea , vomiting and sweating
- hearing loss and tinnitus in Meniere’s disease
Central - neurological deficit
Precipitating factors – such as position of head , work , timing
Drugs history- aminoglycosides , NSAIDS , Asprin ,Chemotherapy,
Psychiatric drugs , anti-malaria drugs
10. Physical examination
• Detailed and thorough neurological ,ophthalmological and otological
examination should be done.
• Ear examination - External Auditory Canal ,TM to exclude active
CSOM with labyrinthine erosion
- Tunning Fork Tests
-Audiograms
11. Specific clinical examination of vestibular disorder
• Vestibulo-ocular tests
• Vestibulo- spinal tests
• Special vestibular tests
13. Caloric test
• Exposure of cold (30 degree C ) or warm (44 degree C) water to TM
nystagmus is observed
Normal healthy labyrinth – Nystagmus directed to opposite (cold) and
same in warm.
This test indicates the presence or absence of function in a particular
labyrinth .
14. Rotation test
• This test access the vestibular response to angular acceleration by
measuring nystagmus from surface electrodes around the ocular
muscles.
• Nystagmus is induced by acceleration and deceleration in ratating
chair.
15. Electronystamography
• This test gives information about central mechanisms and disorders
of vestibular nuclei in the brain stem.
16. Dix –Hallpike test
• Patient sits near end of exam: couch.
• Pt’s head is held firmly between examiner’ s hands and turn 45degree
to Rt or Lt and then
carried pt rapidly backwards so that pt’s head is protruded at the end
of the couch and Nystagmus is observed 2-3 mins and then returned
to upright position.
• Procedure is then repeated with opposite direction.
17. • In BPPV – nystagmus occurs 2-20 sec latent period ,directed to
undermost ear and disappear in 50 sec and fatiguability disappear in
repeatation and vertigo (+) .
• In central cause – more persistent Nystagmus and variable direction
18. Vestibulo-spinal tests
Romberg’s Test
• To assess pt’s ability to stand well
• Placing feet together and hands by the side and eyes closed.
• Pt sway to affected side in peripheral cause
19. Unterberger test
• Marching up & down on the spot for 30sec with eyes closed and arm
outstretched
• Will sway > 30 degree in peripheral cause
Gait
• Assess pt’s walking with closed or opened eyes
• Hemiplegic or ataxic gait in central causes
Posturography
• modern balance- testing equipment allows recording of postural
sways using force platforms.
20. Special Vestibular Tests
Head shake test
• Shake vigorously ~30 times horizontally with chin placed ~30 degree
downward and stop abruptly and nystagmus is observed.
• Slow phase to hypoactive ear (peripheral )
• Vertical Nystagmus (central)
Occilopsia test with Snellen’s chart
Vestibulo ocular reflex (VOR) suppression test – abnormal in central d/o
Horizontal Head thrust test
21. Other Investigations
• RBS
• Blood Pressure
• Complete pictures
• Thyroid function tests
• CT/ MRI to exclude CNS lesion
22. Benign paroxysmal positional vertigo
Definition
BPPV is characterized by brief but violent attacks of paroxysmal
vertigo provoked by certain positions of the head, with no auditory
symptoms .
23. Aetiology
• Frequently arises with no apparent antecedent cause
• Most common vestibular disturbance after closed head injury or
sometimes stapes surgery.
• May be due to degenerative changes in the labyrinth of the aged and
vestibular artery occlusion.
24. Mechanism is explained by 2 theories.
Cupulolithiasis
CaCO3 from otilith organs becomes deposited on the cupula of the
posterior SCC.Changing the head position from erect to the supine
position displaces the cupula away from utricle due to gravity.
Canalolithiasis
Debris of CaCO3 crystals forms in the most dependent portion of
posterior canal.When a critical head postion is assumed, the debris
moves in ampullofugal direction , having a ‘Plunger’ effect within
narrow post SCC , causes movement of cupula with a brief paroxysm of
vertigo & nystagmus.
25. Characteristics of BPPV
Latent period - 2-20 sec
Adaptation - disappear in 50 sec
Fatiguability - disappear in repeatation
Vertigo - always (+)
Direction of Nystagmus- to undermost ear
Incidence - relatively common
26. Treatment
Reassurance about nature of disease and natural resolution.
If symptoms last for more than few weeks,
Brandt – daroft head exercise –aim to move debris out of semicircular canal
to utricle.
postion I – sitting upright
II – side lying position (for 30 sec)
III- sitting (30 sec)
IV- opposite side lying position
3 sets /days x2 weeks
98% success after 3-14 days of exercise
28. Epley’s manoeuver
• pre-medication at night before examination
• Explain possibility of vertigo
• Pt put on examination table in supine position and Hallpike’s position
for affected ear and then after 2-3 min,slowly taken head to opposite
Hallpike’s position.
• After 2-3 min, pt is rolled onto unaffected shoulder with head turn
towards floor.
• After 2-3 mins, pt is returned to seated position and asked to remain
upright for 48 hrs after procedure.
Cure Rate – 80% after one treatment and 100% after muiltiple sessions.
29. If severe symptoms for many months or years , cannot be helped in any
other way,posterior ampullary nerve section, or posterior canal
obstruction can be done.
Posterior Ampullary (singular)nerve section
• This nerve carries sensory fibres of post SCC crista to inferior
vestibule.
• Through permeatal tympanotomy approach, the bony overhang of
the round window niche is drilled away,inferomedial to round window
is drilled further and the nerve is exposed and avulsed.
• It can relieve BPPV but high risk of SNHL(+)
30. Posterior canal obliteration
Compression of membranous post SCC can prevent movement of
material within it.
Thorough cortical mastoidectomy ,post SCC is exposed and opened
gently.Bone wax or bone paste is then filled the perilymph space to
squash the membranous tube within and prevent movement of
endolymph.
31. Meniere’s disease
A disorder due to abnormal accumulation of fluid in
endolymphatic labyrinth characterized by episodes of vertigo
associated with progressive SNHL and persistent tinnitus.
32. Etiology
• 75% idiopathic
• 25% secondary to disease of otic capsule(trauma,infection such as
CSOM ,syphilis and otosclerosis
• Age -30-60 yrs
• Sex – 1:1
• Family h/o -10%
• Usually unilateral but later bilateral
33. Causes of symptoms may be due to
• Rupture of membranous labyrinth allow contamination of perilymph
and endolymph .
• Altered constituents of endolymph d/t altered blood supply or to
delivery of nutrient or removal of by products.
34. Symptoms
Vertigo
• premonitory symptom of sensation of fullness of ear
• Each attach – violent and prostration
• Association with N &V
• Last ½ hr -12 hour
• No LOC
35. Deafness
Fluctuating SNHL( low frequency HL during attacks of vertigo and
improve or normal threshold during remission)
Tinnitus
Low pitch,rumbling or roaring
Changing intensity & pitch before attack of vertigo
36. Treatment
Natural remission -60-80%
Medical treatment
Vestibular sedatives
• Antihistamine – inhibit H3 receptor in brain stem
• Cinnarazine –antihistamine+Ca channel blocker
• DZ –reduce activity in vestibular nuclei
37. Vasodilators
• Betahistine – increase cochlear blood flow and lower endolymph pressure
• CO2 inhalation – cerebral VD
• Nicotinic acid –B3
Electrolytes water balance
• Fluid and salt restricted diet
• Diuretic drugs
Immunological
• Systemic steroid
• Injection steroid through TM
38. If failed to control symptoms ,consider surgical treatment.
Conservative surgical treatment
To relieve vertigo preserving auditory funtion.
Operations aimed at presumed cause of hydrops
• Endolymphatic sac decompression
• Grommet insertion
• Obsolete operation –cochlestomy, cochlear dialysis, sacculotomy,
sympathetic sympathetomy
39. Radical surgical treatment
• Total ablation of active labyrinth with total loss of hearing in aggted
ear.
• Indicated in patient with severe deafness and patient with >60 yrs
- surgical labyrinthectomy
- Medical labyrinthectomy –Intratympanic gentamycin until desired
result.
40. VESTIBULAR NEURITIS
• A type of peripheral vestibular disorder
• A common cause of spontaneous vertigo
• Definition
– disorder in which there is sudden,
– spontaneous, isolated, total or subtotal loss of
afferent vestibular input from one labyrinth
41. • Etiology
– Viral infection of vestibular nerve
• Selective neuron loss in vestibular ganglia
– Virus
• Herpes Simplex virus type 1 (latent infection)
42. • In acute phase
– Spontaneous horizontal torsional nystagmus
• Unidirectional
• Quick phase towards unaffected side
• Suppressed by visual fixation
43. • Patients charcteristically rotate towards the
affected side when attempting to march on
the spot with their eyes closed
– POSITIVE FUKUDA / UNTENBERGER TEST
