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 DR. MADAN
JUNIOR RESIDENT
5 dictinct sesory organs :
 3 semicircular canals
 2 otolith organs
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
otocyst
Endolymphatic lateral
diverticulum utriculosaccular
chamber
Utricular chamber sacular chamber
Utriculus scc.ducts
(35 days)
Sup. Post. Lateral
sacculus cochlea
 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
Macula : 14-16wks
Cristae : 23wks
Organ of corti :
25wks
Vertical canals : 45*
Horizontal canal : 30*
Function pair
 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
Na+ K+ Ca2+ ( meq / litre )
Perilymph 140 5 .68
Endolymph 5 150 .025
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
 Perilymph : ultrafiltrate of either CSFCSF or bloodblood .
Reaches by vestibular aqueduct or preivascular
or perineural channels
 Drainage is through venules & middle ear
mucosa
INTERNAL AUDITORY
( LABYRINTHINE ) A.
(45%)Anterior inferior
cerebellar A.
Superior cerebellar
or
Basilar A.
Rotational acceleration =
semicircular canal respond in 3
planes
Linear acceleration = horizontal
through utricle, vertical through
saccule
 AMPULLA : Crista ampularis – saddle
shaped ,across floor ,at right angles to long
axis.
 Cupula
 Supporting cells
 Blood vessels
 Nerve fibres
Cupula : gelatinous mass of mucopolysaccharides
in keratin meshwork
Sub cupular space
Fluid –tight
Sp.gravity – 1
( post alcoholic
nystagmus )
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
Actin filaments
Hair cells : supporting cells – tight
junction or desmosomes
Simple & complex calyx ( striola )
Type 1 : 2 - 1:1
 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
 Dimorphic 70%
 Bouton 20%
 Calyx 10%
 Aminoglycosides kill hair cells
 Loop diuretics and NSAIDS are hair cell
toxins
 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
Stabilizes eye in space
Necessary to see while head is in motion
Stabilizes body
Helps maintain desired orientation to
environment
 Semicircular Canals
are angular rate
sensors.
 Otoliths (utricle and
saccule) are linear
accelerometers
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
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.
Principle 3: Stimulation of a semicircular canal
produces eye movements in the plane of that
canal. Ewald’s 1st
law.
Push – pull
arrangement of
canals
 B.P.P.V
 Slow phase eye movement
downward in the plane of
affected pc.
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
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 )
 Pc- BPPV-Exitation of PC afferent
 Superior canal dehiscence syndrome
 Caloric testing :
 COWS (cold opposite, warm same) – direction
of the nystagmus
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.
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
Principle 7: The response to simultaneous canal
stimuli is approximately the sum of the
responses to each stimulus alone
RIGHT HAND
RULE
 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.
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.
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
 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
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
Ocular tilt reaction
Head tilt
Disconjugate deviation ( skew)
Counter roll
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
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
 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)
 Jerky-direction, true , vestibular system
 Pendular- direction ,not true , visual system
 Irregular- jerky or pendular , cns leasion
Direction –detemined by direction of fast phase.
Horizontal plane- H nystagmus , V system
Vertical plane- vertical nystagmus ,CNS
 First degree
 Second degree
 Third degree
 Peripheral vestibular pathology-decrease on
optic fixation & increase on optic fixation
withdrawal(eye closed)
 Central vestibular pathology-
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
Peripheral Central
Latency + -
Duration < 1 min > 1 min
Fatigability Yes No
Reversal with upright
position
Yes No
 Seasaw nystagmus –parasellar lesion(Pituitary
leasion)
- rostral midbrain lesion
 Multiple sclerosis
 Arnold chiari malformation
 Vertbrobasilar insufficiency
 Drug –alcohol, antiseizure
 BPPV
 Medullar leasion
 Mid brain anomalies---in child pineal tumor
,mid brain vascular malformation
Hind brain anomalies—chiari malformation
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
 Seconds to minutes to hours
 Perilymphatic fistula
 Benign paroxysmal positional vertigo
 Otosclerosis
 Vascular
• Migraine
• Vertebrobasilar insufficiency (AICA)
• Wallenberg syndrome
• Hyperviscosity syndromes
Hours:
 Ménière's disease
 Migraine
 Metabolic
 Iatrogenic
 Syphilis
 Days:-
 Labyrinthitis
 Temporal bone trauma
 Iatrogenic
 Viral neuronitis
 Vertebrobasilar infarction
 Cerebellar/brainstem hemorrhage
 Autoimmune neurolabyrinthitis
 Multiple sclerosis
 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
 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.
 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.
. 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
 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.
 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
 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.
 distortion of the membranous labyrinth
 perisaccular ischemia and fibrosis(pathologic
study)
 hypoplasia of the endolymphatic sac and
duct(imaging study)
 Autoimmune processes
 Pathogenesis:
1. utricular destruction
2. Cupulolithiasis
3. based on the fatigability of the nystagmus
 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)
 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
 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.
Pathophysiology of vestibular system
Pathophysiology of vestibular system

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Pathophysiology of vestibular system

  • 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
  • 9.
  • 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
  • 22.
  • 23.
  • 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.
  • 30.
  • 31. Principle 3: Stimulation of a semicircular canal produces eye movements in the plane of that canal. Ewald’s 1st law.
  • 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
  • 40.
  • 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
  • 59.  Mid brain anomalies---in child pineal tumor ,mid brain vascular 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)
  • 75.
  • 76.
  • 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.