1.  DR. MADAN
JUNIOR RESIDENT

2. 5 dictinct sesory organs :
 3 semicircular canals
 2 otolith organs

3. 4th
25th
week of gestation
Surface ectoderm
Otic placode
Otic pit
(30 days)
Otic vesicle / otocyst
Acoustico facial ganglion
(neural crest cells : 4wks )
Vestibuolo geniculate
cochlear ganglion

4. otocyst
Endolymphatic lateral
diverticulum utriculosaccular
chamber
Utricular chamber sacular chamber
Utriculus scc.ducts
(35 days)
Sup. Post. Lateral
sacculus cochlea

5.  Arrival of afferent N.endings precedes hair cells
 (3rd
wk) common macula
 Upper end : utricular macula + crista
ampularis
sup. & lat.SCC
 Lower end : saccular macula +crista ampularis
post.SCC
Mesoderm : otic capsule / Bony labyrinth
9wks : hair cells are well developed with synapses

6. Macula : 14-16wks
Cristae : 23wks
Organ of corti :
25wks

7. Vertical canals : 45*
Horizontal canal : 30*
Function pair

8.  Vestibular ( scarpa’s ganglion )
SuperiorSuperior InferiorInferior
 Ant. & lat. Cristae Post.crista
 Utricular macula Saccular macula
Central regions : large ganglion cells
Peripheral regions : small ganglion cells

10. Na+ K+ Ca2+ ( meq / litre )
Perilymph 140 5 .68
Endolymph 5 150 .025

11. Endolymph : marginal cells of stria vascularis
( deeply invaginated,Free ribosomes, vesicles ,
Na+K+ ATPase , adenylate cyclase ,carbonic
anhydrase )
 Dark cells of crista & macula have similar
characters.
 Endolymphatic sac : columnar cells for
absorption

12.  Perilymph : ultrafiltrate of either CSFCSF or bloodblood .
Reaches by vestibular aqueduct or preivascular
or perineural channels
 Drainage is through venules & middle ear
mucosa

13. INTERNAL AUDITORY
( LABYRINTHINE ) A.
(45%)Anterior inferior
cerebellar A.
Superior cerebellar
or
Basilar A.

14. Rotational acceleration =
semicircular canal respond in 3
planes
Linear acceleration = horizontal
through utricle, vertical through
saccule

15.  AMPULLA : Crista ampularis – saddle
shaped ,across floor ,at right angles to long
axis.
 Cupula
 Supporting cells
 Blood vessels
 Nerve fibres

16. Cupula : gelatinous mass of mucopolysaccharides
in keratin meshwork
Sub cupular space
Fluid –tight
Sp.gravity – 1
( post alcoholic
nystagmus )

17. Inorganic crsytalline deposits of calcium
carbonate .
0.5 – 30 µm ( 5-7 )
Sp.gravity : 2.71 – 2.94
Very small in striola region
Utricular macula : kinocilium
towards striola
Saccular macula : away from striola

18. Actin filaments
Hair cells : supporting cells – tight
junction or desmosomes
Simple & complex calyx ( striola )
Type 1 : 2 - 1:1

19.  Crista : central & peripheral zone
 Modified columnar epithelial cells
In horizontal canal kinocilium is
located towards utricle ,where as in
vertical canals the kinocilium is
placed away from the utricle

20.  Dimorphic 70%
 Bouton 20%
 Calyx 10%

21.  Aminoglycosides kill hair cells
 Loop diuretics and NSAIDS are hair cell
toxins

24.  Vestibular - Holds images of the seen world steady on
the retina during brief head rotations
 Optokinetic - Holds images of the seen world steady on
the retina during sustained head rotations
 Smooth pursuit - Holds the image of a moving target
on the fovea
 Nystagmus (quick phases) - Resets the eyes during
prolonged rotation and direct gaze toward the
oncoming visual scene
 Saccades - Brings images of objects of interest onto the
fovea
 Vergence - Moves the eyes in opposite directions so
that images of a single object are placed simultaneously
on both foveas

25. Stabilizes eye in space
Necessary to see while head is in motion

26. Stabilizes body
Helps maintain desired orientation to
environment

27.  Semicircular Canals
are angular rate
sensors.
 Otoliths (utricle and
saccule) are linear
accelerometers

28. Principle 1: The vestibular system primarily
drives reflexes to maintain stable vision and
posture
 VOR / VCR / VSR
 Input to autonomic centres
 Cerebellum
 Cortical areas
Vestibular deficit can thus be unmasked by
very dynamic head movements

29. Principle 2: By modulating the non-zero
baseline firing of vestibular afferent nerve
fibers, semicircular canals encode rotation of
the head, and otolith organs encode linear
acceleration and tilt.

31. Principle 3: Stimulation of a semicircular canal
produces eye movements in the plane of that
canal. Ewald’s 1st
law.

32. Push – pull
arrangement of
canals

33.  B.P.P.V
 Slow phase eye movement
downward in the plane of
affected pc.

34. Principle 4: A semicircular canal is normally
excited by rotation in the plane of the canal
bringing the head towards the ipsilateral side.
Horizontal : ampulopetal flow is excitatory
Vertical : ampullofugal flow is excitatory

35. Principle 5: Any stimulus that excites a
semicircular canal's afferents will be
interpreted as excitatory rotation in the plane
of that canal.
 Vertigo
 Nystagmus ( brief changes )

36.  Pc- BPPV-Exitation of PC afferent
 Superior canal dehiscence syndrome
 Caloric testing :
 COWS (cold opposite, warm same) – direction
of the nystagmus

37. Principle 6: High accelerations head rotation in
the excitatory direction of a canal elicits a
greater response than does the same rotation in
the inhibitory direction. Ewald’s 2nd
law.
Excitation inhibition asymmetry:
Hair cells asymmetry. Vest.aff. baseline firing
rate 50 – 100 spikes / sec. while they can be
increased they cannot be driven below 0.

38. Acceleration must be 3000 degrees/sec2 , and the peak velocity must be 150 to 300
degrees/sec, meaning that the rotation must be finished in 150 milliseconds , 10 to 15
degrees.
HEAD THRUST
TEST

39. Principle 7: The response to simultaneous canal
stimuli is approximately the sum of the
responses to each stimulus alone
RIGHT HAND
RULE

41.  Vestibular neuronitis : Fetter & Dieghan’s et al
proposed that vestibular neuritis is usually a
disorder of organs innervated by
sup.vestibular N. 21% occurrence of
ipsilateral Pc-BPPV.

42. Principle 8: Nystagmus due to dysfunction of
semicircular canals has a fixed axis and
direction with respect to the head
Central nystagmus direction may change with
direction of gaze , where as peripheral
nystagmus has a fixed axis & direction.

43. Principle 9: Brainstem circuitry boosts low-
frequency VOR performance through "velocity
storage" and "neural integration.“
In humans the time constant of the decay of
angular VOR for constant velocity of rotation is
about 20sec longer.
Arise from medial & descending vestibular
nucleus whose axons cross midline

44.  Pre & post rotatory nystagmus (due to
exitation& inhibition asymmetry net result not
zero-sensed by brain stem)
 Head –shake nystagmus
 Alexander’s law -Amp of nystagmus
Video Frenzel Goggles

45. Principle 10: The utricle senses both head tilt
and translation, but loss of unilateral utricular
function is interpreted by the brain as a head
tilt toward the opposite side

46. Ocular tilt reaction
Head tilt
Disconjugate deviation ( skew)
Counter roll

47. Principle 11: Sudden changes in saccular activity
evoke changes in postural tone.
Activates the extensor muscles & relaxes the
flexors to restore postural tone
VEMP---short latency relaxation potential by
click or tone burst

48. Principle 12: The normal vestibular system can
rapidly adjust the vestibular reflexes according
to the context, but adaptation to unilateral loss
of vestibular function may be slow and
susceptible to decompensation

49.  It is rhythmic repetitive oscillation of eye ,
initiated by a slow eye movement that drives
the eye off target , followed by a fast movement
that is corrective(jerky movement) or another
slow eye movement in the opposite direction.
(pendular nystagmus)

50.  Jerky-direction, true , vestibular system
 Pendular- direction ,not true , visual system
 Irregular- jerky or pendular , cns leasion

51. Direction –detemined by direction of fast phase.
Horizontal plane- H nystagmus , V system
Vertical plane- vertical nystagmus ,CNS

52.  First degree
 Second degree
 Third degree

53.  Peripheral vestibular pathology-decrease on
optic fixation & increase on optic fixation
withdrawal(eye closed)
 Central vestibular pathology-

54. Features peripheral central
Direction -fast phase away from
leasion
-unilateral disease of
vestibular organ or nerve
Labyrinthitis
Meniere’s disease
-changes with gaze
-disease of brain stem
Any cns disorder
Visual fixation Inhibit nystagmus
Always diminishes or
even disappear
Either no effect or
increase nystagmus

55. Peripheral Central
Latency + -
Duration < 1 min > 1 min
Fatigability Yes No
Reversal with upright
position
Yes No

56.  Seasaw nystagmus –parasellar lesion(Pituitary
leasion)
- rostral midbrain lesion

57.  Multiple sclerosis
 Arnold chiari malformation
 Vertbrobasilar insufficiency
 Drug –alcohol, antiseizure

58.  BPPV
 Medullar leasion

59.  Mid brain anomalies---in child pineal tumor
,mid brain vascular malformation

60. Hind brain anomalies—chiari malformation

61. A sensation of spinning or motion
Time course : helps to discriminate between
otologic and nonotologic causes of vertigo
Vertigo that lasts for less than 1 minute can
represent benign paroxysmal positional vertigo
Vertigo that is prolonged for hours is typical of
Ménière's disease or endolymphatic hydrops

62.  Seconds to minutes to hours
 Perilymphatic fistula
 Benign paroxysmal positional vertigo
 Otosclerosis
 Vascular
• Migraine
• Vertebrobasilar insufficiency (AICA)
• Wallenberg syndrome
• Hyperviscosity syndromes

63. Hours:
 Ménière's disease
 Migraine
 Metabolic
 Iatrogenic
 Syphilis

64.  Days:-
 Labyrinthitis
 Temporal bone trauma
 Iatrogenic
 Viral neuronitis
 Vertebrobasilar infarction
 Cerebellar/brainstem hemorrhage
 Autoimmune neurolabyrinthitis
 Multiple sclerosis

65.  most common infectious cause of acute
vertigo is viral labyrinthitis
 Traumatic causes of vertigo include temporal
bone fractures, labyrinthine concussion, and
perilymphatic fistula
 Systemic metabolic abnormalities that can
affect vestibular function include
hyperviscosity syndromes (hyperlipidemia,
polycythemia, macroglobulinemia,sickle cell
anemia), diabetes mellitus,
hyperlipoproteinemia, and hypothyroidism

66.  A number of collagen vascular disorders have
been associated with vestibular dysfunction as
a form of autoimmune inner-ear disease.
Common disorders of this type include
rheumatoid arthritis, polyarteritis nodosa,
temporal arteritis,nonsyphilitic interstitial
keratitis, lupus, sarcoid, relapsing
polychondritis, dermatomyositis, and
scleroderma.

67.  Ischemia of small labyrinthine vessels will
cause isolated infarction of the vestibular
labyrinth and vertigo; occlusion of larger
vessels anterior inferior cerebellar artery or its
branches will cause sudden and profound loss
of both auditory and vestibular function and
regional infarction of the brainstem.

68. . Endolymphatic hydrops or Ménière's disease is
defined by the well-recognized symptoms of
vertigo, hearing loss, tinnitus, and aural
fullness. The underlying mechanism(s) that
cause abnormal homeostasis of endolymph
resulting in distention and rupture of the
membranous labyrinth
. Histopathologic findings suggest that fibrosis
of the endolymphatic sac,
. Altered glycoprotein metabolism,
. viral infections may be pathogenic

69.  Otoconia or calcium carbonate crystals
normally attached to the macula of the utricle
become free floating within the endolymph of
the posterior semicircular canal. These free-
floating particles become gravity sensitive and
cause a hydrodynamic shift in endolymph that
affects the posterior semicircular canal cupula
in response to provocative head movements,
resulting in positional vertigo.

70.  The peripheral vestibular system includes : (1)
sensory receptor structures that are responsible
both for sensing the motion and position of the
head in space and converting (transducing) the
sensory stimulus into an electricalsignal;
 (2) the vestibular portion of the eighth cranial
nerve that carries the encoded sensory
information from the receptors to the central
nervous system (CNS) in the form of neural
activity

71.  Ménière's disease (idiopathic endolymphatic
hydrops) is a disorder of the inner ear
associated with a symptom complex consisting
of spontaneous, episodic attacks of vertigo;
sensorineural hearing loss that usually
fluctuates; tinnitus; and
 often a sensation of aural fullness.

72.  distortion of the membranous labyrinth
 perisaccular ischemia and fibrosis(pathologic
study)
 hypoplasia of the endolymphatic sac and
duct(imaging study)
 Autoimmune processes

73.  Pathogenesis:
1. utricular destruction
2. Cupulolithiasis
3. based on the fatigability of the nystagmus

74.  canalithiasis mechanism-latency
 nystagmus duration ---lowest part of canal
 the vertical (upbeating) and
torsional nystagmus
 reversal of nystagmus
 fatigability of the nystagmus(repeated Dix
Hallpike - dispersion of material with
in the canal)

77.  syndrome of vertigo and oscillopsia induced by
loud noises or by stimuli that change middle
ear or intracranial pressure
 Tullio phenomenon--- eye movement-- loud
noise
 Hennebert's sign
 "third mobile window

78.  Loud sounds, positive pressure in the external
auditory canal, and the Valsalva maneuver against
pinched nostrils --- ampullofugal deflection
---nystagmus that has slow phase components that
are directed upward with torsional motion of the
superior pole of the eye away from the affected
ear.
 Conversely, negative pressure in the external
canal, Valsalva against a closed glottis, and jugular
venous compression ----oppositelydirected eye
movements with slow phase components directed
downward with torsional motion of the superior
pole of the eye toward the affected ear.