2. INTRODUCTION
5–10 % of all patients seen in general practice
Dizziness/vertigo/unsteadiness accounts for 25 % of
referrals to ENT and neurology clinics [Bronstein, 2008]
Associated symptoms include nausea, emesis, and
diaphoresis
Vertigo should be distinguished from “mimickers”, viz
imbalance (disequilibrium), light-headedness (giddiness),
presyncope
3. Latin word ‘vertere’ : ‘to turn’
Unpleasant feeling of subjective sense of movement of body
(subjective vertigo) or of surrounding environment (objective vertigo)
DEFINITION
American Academy of Otolaryngology - HNS Foundation [AAO-HNSF]-
2017 Update: “An illusory sensation of motion of either self or
surroundings in absence of true motion”
4. Positional Vertigo:
“A spinning sensation produced by changes in head position relative to
gravity”
- [AAO-HNSF]-2017 Update
BPPV:
“A disorder of the inner ear characterized by repeated episodes of
positional vertigo”
- [AAO-HNSF] - 2017 Update
5. “Dizziness” – lay term; non specific
Denote lightheadedness / giddiness / faintness
Causes include medical conditions
Can often accompany vertigo, but can appear
independently
Light headedness/ giddiness – non specific
Range from uneasy feeling/nauseating feel/imbalance
Presyncope – feeling of upcoming swoon/collapse with
darkening sight or tinnitus; without LOC.
If LOC (+) - syncope
8. Features of a Vestibular Disorder
Pathways Cardinal features
Vestibulo-ocular tracts (VOR) Nystagmus
Vestibulospinal tracts (VST) Falling to side
Vestibulocerebellar tracts (VCT) Ataxia, imbalance
Emetic pathways Nausea, vomiting
Parietotemporal cortex Vertigo
Vestibulohypothalamic tracts Autonomic features
9.
10. Vertigo implies dysfunction of vestibular system [4 events]
Postural imbalance (dystaxia)
Ocular motor movts (nystagmus)
Autonomic symptoms (Nausea/vomiting/sweating)
Perceptal alterations (vertigo)
11. HISTORY
EXAMINATION
GENERAL
HEAD AND NECK
EAR
NEURO-OTOLOGICAL
VOR TEST –DIX HALLPIKE & LATERAL SEMICIRCULAR CANAL TEST
HEAD THRUST TEST ,CALORIC TEST
CRANIAL NERVE EXAMINATION
COORDINATION &POSTURE
GAIT & SPECIAL TEST
12. HISTORY
• Key history points
• Is it vertigo?
• Duration
• What are precipitating factors?
• Accompanying symptoms
14. PERIPHERAL VS CENTRAL ORIGIN VERTIGO
Feature Peripheral Central
Severity Severe vertigo/nausea &
vomiting
Less severe
Onset Acute Subacute or slow
Duration Short duration; subsides Persists
Otological
symptoms
Common Rare
Asso neurological
symptoms
Absent Present
Change with OF Reduces No change
Abolition of OF Aggravates No change
OF : optic fixation
16. DURATION OF VERTIGO
TIME PERIPHERAL CENTRAL
Seconds BPPV VB-TIA ,aura of epilepsy
Minutes Perilymph fistula VB-TIA ,aura of migraine
Hours Meniere’s disease
Vestibular migraine
Basilar migraine
Days Vestibular neuritis
labyrinthitis
VB- stroke
Weeks , months Acoustic neuroma
Drug toxicity
Multiple sclerosis,
cerebellar degenerations
Varies SSCD
17. SINGLE VERTIGO EPISODE
Hearing Possible cause
Hearing spared Vestibular neuritis
Or viral labyrinthitis
Head injury
Hearing involved Head injury
Labyrinthine fistula
Viral infection( mumps , Ramsay hunt)
Vascular(labyrinthine stroke)
18.
19. RED FLAGS IN ACUTE VERTIGO
INDICATION FOR BRAIN IMAGING
Modified from Seemungal and Bronstein
Acute Unilateral deafness
Acute (occipital headache)
Any central symptoms or signs
A negative (normal )head –impulse test
24. Nystagmus :
Greek word – “tired/sleepy”
Involuntary rhythmic oscillating & conjugate movt of eyes, due
to defect in vestibular system
Slow drift in 1 direction (vestibular/visual induced component),
then fast flicking movt in opp direction (centrally controlled
movt-cerebral compensation) : Jerk nystagmus
Paradoxically nystagmus direction termed wrt fast movt
Horizontal/rotatory/vertical
25. Physiological nystagmus
• Continuation of visual fixation. A form of OKN
Induced nystagmus
• Caloric/position tests
Spontaneous nystagmus
• Always pathological
26. Optokinetic nystagmus (OKN):
Involved in maintainance of visual fixation on moving object
in absence of head movts
Movt of image across retina results in compensatory eye
movts which keep image fixed on fovea
Slow movt (smooth pursuit) & restorative fast movt (saccade)
27. Ewald’s law
Regarding relationship b/w labyrinthine receptors & vestibular reflexes which they mediate
1st law – Head & eye movements always occur in plane of canal being stimulated & in direction of
endolymph flow
2nd law - In LSCC, ampullopetal endolymph flow causes a greater response than ampullofugal flow
3rd law - In PSCC, ampullofugal endolymph flow causes a greater response than
ampullopetal response
• Excitatory stimuli & their responses are of greater amplitude than inhibitory stimuli
• Fast component of nystagmus always opp to direction of flow of endolymph
28. ALEXANDER’S LAW
Vestibular nystagmus, if present, can be enhanced by moving the eyes in direction of fast
phase, & decreased by moving eyes to direction of slow phase
For peripheral origin nystagmus
Direction of nystagmus is dependent on the direction of fast component
A second/third degree nystagmus will enhance on gaze deviation in the direction of fast
phase
29. NYLEN’S CLASSIFICATION
Severity of nystagmus wrt fast component
According to Alexander’s law, holds ground for nystagmus of peripheral origin
1st degree – Present when pt looks in direction of fast component. Weak
nystagmus
2nd degree – Present when pt looks straight ahead (neutral gaze)
3rd degree – Present even when pt looks in direction of slow component. Most
severe
30. LSCC: maximally excited by rotation toward side of canal &
inhibited by rotation in opposite direction
Results in excitatory slow phase movt toward opp side & a resetting saccade
towards canal (Horizontal nystagmus)
SSCC: excited by rotation downward and to side, in the plane of canal
Results in vertical-torsional nystagmus, with slow phase of vertical component
upward & resetting saccade downward (Downbeat torsional nystagmus)
PSCC: excited by upward rotation & to side, in plane of canal, so that slow phase
is downward & resetting phase upward (Upbeat torsional nystagmus)
31. Feature Peripheral Central
Latency 2-20 s No latency
Duration < 1 mt > 1 mt
Direction of
nystagmus
Fixed (towards
undermost ear)
Changing
Fatigablility Fatiguable Non fatiguable
Habituation Yes No
Acc symptoms Severe None or slight
Fatiguability – Response remit spontaneously as position maintained
Habituation – Attenuation of response as position repeatedly assumed
32. Elicit nystagmus
• Pt seated comfortably in front
• Examiner keeps finger 30 cm in front of pt’s eye in central position, &
moves it sideways & upward-downward within 30 degree (never beyond
30 degree)
• Keep finger in each position for about 5 sec
• Frenzel glass
33. • Positive
1.Erosion of horizontal semi circular canal
2.Fenestration surgery
3.Post stapedectomy fistula
4.Rupture of round window membrane
• False positive
1. Congenital syphilis (Hennebert sign)
2. Menieres ds
3. SSCC dehiscence
FISTULA TEST
35. Head shaking nystagmus test
• Test of dynamic vestibular function
• Pt asked to shake head vigorously 30 times horizontally, with chin placed about 30
degree downward
• Stop head shaking abruptly – w/f nystagmus
• (N) – no or occassionally 1-2 beats
• U/L peripheral vestibular deficit – nystagmus (initial phase with slow phase towards
lesion side; then reversal )
• Cerebellar defects – vertical nystagmus (cross coupled nystagmus)
36. • Patient is asked to follow series of vertical stripes on a moving drum
(moving in alternate directions)
• Normally produces nystagmus- slow component in the direction of
moving strips, & fast component in opp direction
• Useful to detect central lesions (brainstem/cerebral hemisphere
lesions)
OPTOKINETIC TEST
38. CALORIC TEST
• Induce nystagmus by thermal stimulation of labyrinth
• Allow separate testing of each labyrinth
• Stimulates LSCC
Modified Kobrak test-
1. Pt seated with head tilted 60 deg backward (place LSCC in vertical position)
2. 5 ml of ice water instilled for 60 sec. If no response; then 10ml, 20ml, 40ml
3. (N)-nystagmus to opp side with 5 ml water
4. Response with increased quantities - hypoactive labyrinth
5. No response at 40ml – dead labyrinth
39. Fizgerald Hallpike test (bithermal caloric test)
• PRINCIPLE: thermal change induces convection currents in LSCC
(when placed vertically) and thus cupular deflection
• Patient is made to lie down with head raised 30 deg above
horizontal
• each irrigation lasting 40 sec alternatively with water at 30 deg & 44
deg C
• Gap of 5 min is given between the irrigation
• If no response – repeat with 20 deg C water for 4 mts before
labelling the labyrinth dead
40. • “COWS” – Cold water – nystagmus to opp side
Warm water – nystagmus to same side
• Observe for nystagmus till its end point
• Chart time taken from start of irrigation to end point of nystagmus on
calorigram
41. Cold air caloric test
• In TM perforations (irrigation C/I)
• Dundas Grant tube : coiled copper tube wrapped in cloth
• Air in tube cooled by pouring ethyl chloride, & then blown into ear
42. • Method of detecting & recording of nystagmus
• Used in caloric/positional/rotational/optokinetic stimulus
• Detects corneoretinal potentials by placing electrodes
around eyes
Uses-
• Permanent record
• Detect nystagmus not seen with naked eye
ELECTRONYSTAGMOGRAPHY
43. Typical pattern of nystagmus to the left. This trace
represents the eye movement amplitude in degrees
(vertical) as a function of time in seconds (horizontal)
44. • Patient seated in Barany’s revolving chair with head tilted
300 forward
• Rotated 10 turns in 20 sec
• Nystagmus (25-40s) observed on abrupt stopping of
chair
• Uses – congenital EAC stenosis/agenesis : when caloric
tests cannot be done
• Disadvantage- both labyrinths are stimulated
ROTATION TEST
45. • The only vestibular test differentiating end organ lesion from
vestibular nerve lesions
• Pt erect with feet together, eyes closed & arms outstretched
• Current of 1mA passed to one ear
• If Current is positive- person sways towards the stimulated ear
• If current is negative – person sways away from the stimulated ear
GALVANIC TEST
46. • Method to evaluate vestibular function by measuring postural
stability
• Principle- maintenance of posture depends on 3 sensory inputs –
visual, vestibular, somatosensory
POSTUROGRAPHY
49. TREATMENT OF VERTIGO
• TREATMENT OF CHOICE DEPEND ON THE CAUSE OF VERTIGO
General rehabilitation measures
• Physical exercise programs
• Rehabilitation : Correction/remedial measures
• Psychological support
• Pharmacotherapy
• Social/familial/economic rehabilitation
• Monitoring, feedback & follow-up
50. General rehabilitation measures :
• Individualized program of physical rehabilitation
• Mx of musculoskeletal disorders, retraining of gait & stance
• Correction of optic disorders
• Biofeedback : retraining in age related disequilibrium
51. Physical exercise regimens
• Systematic exercise program
Cooksey Cawthorne regimen
• Customized exercise program
Individualized program based on functional difficulties
Pts instructed to work at limit of their ability
Initial home training program – by physiotherapist
• Specific therapies
Epley/Semont/Brandt Daroff maneuvers
52. Cooksey Cawthorne regimen :
• For peripheral vestibular disorders (1940s)
• Aimed at encouraging head & eye movts that provoked dizziness
in systematic manner
• 80% pts – effectively benefitted
• Perform with eyes open & closed – promote compensation using
vestibular & propioceptive mechanisms
• Resting, sitting, standing & moving about positions
• Eye & head movts; throwing ball from 1 hand to other; walk across
room; walk up & down stairs; bending forward to pick up objects
53. Pharmacotherapy
• Vestibular sedatives/Vasodilators/Anti emetics/ Central depressants
• GABA – Inhibitory NT in vestibular system
• Avoid chronic use & in C/c symptoms : suppress central vestibular activity which is crucial for
development of compensatory mechanisms
• Use judiciously in acute symptomatic pts to enable initiation of exercise regimes. To be withdrawn
as soon as possible
• In anticipated position testing, withdraw medications at least 48 hrs prior to test
54. Commonly used agents for the management of
vertigo
Agent Dose
Antihistamines
Meclizine 25-50 mg 3 times a day
Dimenhydrinate 50 mg 1-2 times daily
Promethazine 25 mg 2-3 times daily
Benzodiazepines
Diazepam 2.5 mg 1-3 times daily
Clonazepam 0.25 mg 1-3 times daily
Anticholinergic
Scopolamine transdermal Patch
55. Agent Dose
Others
Diuretics or low sodium diet (1g/d)
Methylprednisolone 100 mg daily (1-3) days
Anti migrainous drugs
Dopamine blocker :
Prochlorperazine
5 mg TID (30 mg daily)
Vasodilators
Betahistine 4/8/16/32 mg BD/TID
Cinnarizine 25 mg 1-2 times daily
Flunnarizine 5/10 mg OD
56. Betahistine
Reduce endolymphatic pressure by improved microcirculation in stria vascularis
of cochlea or inhibit activity of vestibular nuclei
Prochlorperazine (Stemetil)
Dopamine antagonist
Block CTZ & hence vomiting center
Antihistaminics
H1 blockers – act on vomiting center
Sedation
57. Surgery : reserved for those severe cases where medical therapy fails or
debilitate person affected
Over the years, several surgical options have evolved from endolymphatic sac
surgery, labyrinthectomy to vestibular neurectomy to singular neurectomy and
now vestibular implants
58. Surgery for SSCC dehiscence
• Plugging the dehiscence via MCF approach
• Dehiscence detected by HRCT temporal bone parasagittal cut
Surgery for Perilymph fistula
• Exploratory tympanotomy
(LA with IV sedation to enable valsalva manuevre to detect leaks)
• EUM repair by sealing suspected area with fat; fascia & sealed with bone
wax
59. Surgery for Meniere’s disease
• Cochleosacculotomy (endolymphatic shunt procedure)
Connect endolymphatic sac with subarachnoid space- drain excess endolymph
• Portman procedure (decompression of endolymphatic sac)
Create permanent fistula in endolymphatic sac : ensure expansion of endolymph sac during
crisis
• Sacculotomy (Fick’s operation)
Puncturing distended saccule via stapes footplate
62. 50 yr female c/o recurrent brief periods of rotatory vertigo ; often with nausea
& vomiting. They aggravated with certain head positions & also rolling over in
bed. The episodes typically came in spells, and lasted < 1 mt
O/E- TM (N), Position test (+), PTA (N), CT & MRI (N)
63. MC disorder of peripheral vestibular system
50-70 % - idiopathic
Secondary BPPV- Trauma (7-17 %)
Viral neumolabyrinthitis
Meniere’s disease
Migraine
Ischemic processes
Iatrogenic – otological surgery;
reposition manouevres
5th – 7th decade
♀ > ♂ (in young onset BPPV ♀ =♂)
BPPV
64. Posterior Canal BPPV – MC (> 90%)
Lateral canal BPPV
Superior canal BPPV (rare)
2 etiopathologies attributed
Canalolithiasis : free floating otolith debris within SCCs. Now identified as the major
mechanism of all subtypes of BPPV
Cupulolithiasis : deposits adhering to cupula (proposed by Schuknecht in 1969). More
significant role in lateral canal BPPV
65. BPPV
• Cupulolithiasis theory (Schuknecht;1969)
Degenerated end pdts of otoconia dislodged from utricular macula
Cause – trauma including iatrogenic; viral inf;vascular insufficiency
Deposit on cupula : density differential b/w perilymph & cupula
Gravity dependent deflection of cupula – continues as long as provocative
orientation was maintained – sustained nystagmus
66. • Canalithiasis theory (Hall 1979; Epley 1980)
Canaliths – loose otoconia debris dislodged from utricle
Gravitate into SCCs (MC PSCC)
hydrodynamic drag in endolymph
evidenced by presence of “densities” within SCC
67. Depiction of canalithiasis of the posterior canal and cupulolithiasis
of the lateral canal (left inner ear)
69. CANAL REPOSITIONING MANEUVER :
Epley maneuver
Semont(liberatory)maneuver
Brandt Daroff exercise
Cupulolithiasis : Little latency; slightly longer duration of
nystagmus (compared to canalithiasis)
Vertical upbeating & rotatory nystagmus towards downward ear : Position test (+)
70. • Canaliths aggregrate in PSCC near ampulla (Most dependent
location in upright position)
• Provocative head position : detached otoconia gravitate as bolus
(as canal assume vertical position)
• Ampullofugal hydrodynamic drag on endolymph (enhanced by
advantage offered by canal:ampulla cross section differential)
71. o Latency – Few sec needed prior to displacement of endolymph & cupula (to
overcome inertia & resistance of endolymph within canal,& elasticity of cupula
o Typical torsional nystagmus
Flouren’s law : axis of eyeball rotation from induced nystagmus parallels axis of
generating SCC, & direction of its slow phase conforms to direction of endolymph
(cupular) displacement
o Limited duration – canaliths stop gravitating when they reach the more horizontal
portion of canal (where drag on endolymph ceases). Elasticity returns cupula to its
neutral position, nystagmus & vertigo ceases (fatiguability)
72. o Reversal – head in upright position – canaliths gravitate back towards ampulla,
causing ampullopetal drag on endolymph.
After a period of latency cupular deflection cause torsional nystagmus in
direction but in same axis
o Habituation – response declines with repeated provocation.
Each procedure cause canalith to be more dispersed (traverse less length of
canal) – less effective endolymph displacement
76. Brandt Daroff exercise
• More of habituation rather than Rx
• 5 exercises = 1 set
• 1 set each in morning, noon & evening
• Do for 14 days
77. Supine log roll test
Purely horizontal nystagmus without a horizontal
(rotatory) component
Canalithiasis : Geotrophic nystagmus
Side with stronger response is the affected canal
Cupulolithiasis : Ageotrophic/apogeotrophic nystagmus
Side with weaker response is the affected canal
82. BPPV variant Test Direction of
nystagmus
Duration of
nystagmus
Rx of choice
PSCC
cupulolithiasis
Dix Hallpike Upbeat torsional
towards affected
side
Persistant > 1 mt
(immediate
onset)
Semont/
Brandt Daroff
PSCC
canalithiasis
Dix Hallpike Upbeat torsional
towards affected
side
5-45 s (latent ) Epley/Semont/
Brandt Daroff
LSCC
canalithiasis
Roll test Horizontal
(geotrophic)
Sec-mts Barbecue/Gufoni
LSCC
cupulolithiasis
Roll test Horizontal
(ageotrophic)
Sec-mts Convert to
geotrophic;
then as above
SSCC
canalithiasis
Dix Hallpike Downbeat
torsional towards
unaffected side
5-45 s Epley on opp
side/
Brandt Daroff
83. Malignant positional paroxysmal
vertigo (MPPV)
• Position changing nystagmus associated with PCF tumours
(MC : CPA tumours)
• Not self limiting
• Constant alteration of nystagmus characteristics on repeating
position test
• Presence of non BPPV symptoms :
persisting imbalance/tinnitus/SNHL/Facial paresthesia/Facial
paralysis
• Persistence of symptoms & signs beyond 1 month
84. Singular neurectomy –
• Selective division of br of inf vestibular nerve innervating PSCC ampulla
• Gacek’s technique : transcanal approach; drill inferior to RW
PSCC occlusion -
• Occlusion of bony lumen of dome of PSCC without disrupting lumen of
SCC
• Postaural mastoidectomy approach
• Identify dome of PSCC b/w LSCC & post fossa dural plate, drill it
& plug with small periosteal plugs
Procedures for BPPV
![INTRODUCTION
5–10 % of all patients seen in general practice
Dizziness/vertigo/unsteadiness accounts for 25 % of
referrals to ENT and neurology clinics [Bronstein, 2008]
Associated symptoms include nausea, emesis, and
diaphoresis
Vertigo should be distinguished from “mimickers”, viz
imbalance (disequilibrium), light-headedness (giddiness),
presyncope](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)