Pathophysiology of vestibular system

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Pathophysiology of vestibular system

  1. 1.  DR. MADAN JUNIOR RESIDENT
  2. 2. 5 dictinct sesory organs :  3 semicircular canals  2 otolith organs
  3. 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. 4. otocyst Endolymphatic lateral diverticulum utriculosaccular chamber Utricular chamber sacular chamber Utriculus scc.ducts (35 days) Sup. Post. Lateral sacculus cochlea
  5. 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. 6. Macula : 14-16wks Cristae : 23wks Organ of corti : 25wks
  7. 7. Vertical canals : 45* Horizontal canal : 30* Function pair
  8. 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. 9. Na+ K+ Ca2+ ( meq / litre ) Perilymph 140 5 .68 Endolymph 5 150 .025
  10. 10. 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
  11. 11.  Perilymph : ultrafiltrate of either CSFCSF or bloodblood . Reaches by vestibular aqueduct or preivascular or perineural channels  Drainage is through venules & middle ear mucosa
  12. 12. INTERNAL AUDITORY ( LABYRINTHINE ) A. (45%)Anterior inferior cerebellar A. Superior cerebellar or Basilar A.
  13. 13. Rotational acceleration = semicircular canal respond in 3 planes Linear acceleration = horizontal through utricle, vertical through saccule
  14. 14.  AMPULLA : Crista ampularis – saddle shaped ,across floor ,at right angles to long axis.  Cupula  Supporting cells  Blood vessels  Nerve fibres
  15. 15. Cupula : gelatinous mass of mucopolysaccharides in keratin meshwork Sub cupular space Fluid –tight Sp.gravity – 1 ( post alcoholic nystagmus )
  16. 16. 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
  17. 17. Actin filaments Hair cells : supporting cells – tight junction or desmosomes Simple & complex calyx ( striola ) Type 1 : 2 - 1:1
  18. 18.  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
  19. 19.  Dimorphic 70%  Bouton 20%  Calyx 10%
  20. 20.  Aminoglycosides kill hair cells  Loop diuretics and NSAIDS are hair cell toxins
  21. 21.  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
  22. 22. Stabilizes eye in space Necessary to see while head is in motion
  23. 23. Stabilizes body Helps maintain desired orientation to environment
  24. 24.  Semicircular Canals are angular rate sensors.  Otoliths (utricle and saccule) are linear accelerometers
  25. 25. 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
  26. 26. 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.
  27. 27. Principle 3: Stimulation of a semicircular canal produces eye movements in the plane of that canal. Ewald’s 1st law.
  28. 28. Push – pull arrangement of canals
  29. 29.  B.P.P.V  Slow phase eye movement downward in the plane of affected pc.
  30. 30. 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
  31. 31. 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 )
  32. 32.  Pc- BPPV-Exitation of PC afferent  Superior canal dehiscence syndrome  Caloric testing :  COWS (cold opposite, warm same) – direction of the nystagmus
  33. 33. 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.
  34. 34. 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
  35. 35. Principle 7: The response to simultaneous canal stimuli is approximately the sum of the responses to each stimulus alone RIGHT HAND RULE
  36. 36.  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.
  37. 37. 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.
  38. 38. 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
  39. 39.  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
  40. 40. 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
  41. 41. Ocular tilt reaction Head tilt Disconjugate deviation ( skew) Counter roll
  42. 42. 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
  43. 43. 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
  44. 44.  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)
  45. 45.  Jerky-direction, true , vestibular system  Pendular- direction ,not true , visual system  Irregular- jerky or pendular , cns leasion
  46. 46. Direction –detemined by direction of fast phase. Horizontal plane- H nystagmus , V system Vertical plane- vertical nystagmus ,CNS
  47. 47.  First degree  Second degree  Third degree
  48. 48.  Peripheral vestibular pathology-decrease on optic fixation & increase on optic fixation withdrawal(eye closed)  Central vestibular pathology-
  49. 49. 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
  50. 50. Peripheral Central Latency + - Duration < 1 min > 1 min Fatigability Yes No Reversal with upright position Yes No
  51. 51.  Seasaw nystagmus –parasellar lesion(Pituitary leasion) - rostral midbrain lesion
  52. 52.  Multiple sclerosis  Arnold chiari malformation  Vertbrobasilar insufficiency  Drug –alcohol, antiseizure
  53. 53.  BPPV  Medullar leasion
  54. 54.  Mid brain anomalies---in child pineal tumor ,mid brain vascular malformation
  55. 55. Hind brain anomalies—chiari malformation
  56. 56. 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
  57. 57.  Seconds to minutes to hours  Perilymphatic fistula  Benign paroxysmal positional vertigo  Otosclerosis  Vascular • Migraine • Vertebrobasilar insufficiency (AICA) • Wallenberg syndrome • Hyperviscosity syndromes
  58. 58. Hours:  Ménière's disease  Migraine  Metabolic  Iatrogenic  Syphilis
  59. 59.  Days:-  Labyrinthitis  Temporal bone trauma  Iatrogenic  Viral neuronitis  Vertebrobasilar infarction  Cerebellar/brainstem hemorrhage  Autoimmune neurolabyrinthitis  Multiple sclerosis
  60. 60.  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
  61. 61.  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.
  62. 62.  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.
  63. 63. . 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
  64. 64.  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.
  65. 65.  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
  66. 66.  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.
  67. 67.  distortion of the membranous labyrinth  perisaccular ischemia and fibrosis(pathologic study)  hypoplasia of the endolymphatic sac and duct(imaging study)  Autoimmune processes
  68. 68.  Pathogenesis: 1. utricular destruction 2. Cupulolithiasis 3. based on the fatigability of the nystagmus
  69. 69.  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)
  70. 70.  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
  71. 71.  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.

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