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![INTRODUCTION
Disorder in which there is sudden, spontaneous, isolated,
total or subtotal loss of afferent vestibular input from one
labyrinth resulting in severe vertigo
[ Scott brown otorhinolaryngology, 7th edition,vol
3]
2nd most common cause of vertigo of peripheral origin
[Cummings otolaryngology Head & Neck Surgery,](https://image.slidesharecdn.com/zlflytsnrrkkey4tdbkz-vestibular-neuronitis-bppv-240404125037-6bc407ef/85/VESTIBULAR_NEURONITIS__bppv-ent-hns-pptx-5-320.jpg)
![ Synonyms:
INTRODUCTION
Vestibular neuritis
Acute unilateral peripheral
neuropathy
Labyrinthitis
Neurolabyrinthitis
[ Scott brown otorhinolaryngology, 7th
edition,vol 3]
No gender bias
Middle aged people](https://image.slidesharecdn.com/zlflytsnrrkkey4tdbkz-vestibular-neuronitis-bppv-240404125037-6bc407ef/85/VESTIBULAR_NEURONITIS__bppv-ent-hns-pptx-6-320.jpg)
![C. HEARING LOSS
TINNITUS
Typically
absent
b. Nystagmus
Spontaneous, horizontal-torsional
Strictly unidirectional
Quick phase towards unaffected side
Magnifying frenzel lenses may be reqd
CLINICAL MANIFESTATIONS
[ Scott brown otorhinolaryngology, 7th
edition,vol 3]](https://image.slidesharecdn.com/zlflytsnrrkkey4tdbkz-vestibular-neuronitis-bppv-240404125037-6bc407ef/85/VESTIBULAR_NEURONITIS__bppv-ent-hns-pptx-9-320.jpg)
![D. Head impulse test
CLINICAL MANIFESTATIONS
[ Scott brown otorhinolaryngology, 7th
edition,vol 3]](https://image.slidesharecdn.com/zlflytsnrrkkey4tdbkz-vestibular-neuronitis-bppv-240404125037-6bc407ef/85/VESTIBULAR_NEURONITIS__bppv-ent-hns-pptx-10-320.jpg)
![DIFFERENTIAL DIAGNOSIS
1. Cerebellar infarction
Head impulse test –ve
Nystagmus: Bidirectional
Not suppressed by visual fixation
Can’t stand without support even with eyes open
[ Scott brown otorhinolaryngology, 7th
edition,vol 3]](https://image.slidesharecdn.com/zlflytsnrrkkey4tdbkz-vestibular-neuronitis-bppv-240404125037-6bc407ef/85/VESTIBULAR_NEURONITIS__bppv-ent-hns-pptx-13-320.jpg)
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VESTIBULAR_NEURONITIS__bppv ent & hns.pptx
- 1. VESTIBULAR NEURONITIS & BPPV DR. INDIRAACHARYA 2ND YEAR, MS (ORL-HNS) GMSMA OF ENT-HN STUDIES MMC-TUTH,IOM
- 2.
- 3. CLASSIFICATION Disturbanc es Of Vestibular Function Periphera l Centr al Vestibular neuronitis BPPV Meniere’s disease Brain ischaemia Posteriorfossa tumors Basilar Migraine Scott Brown Otorhinolaryngology, 7th
- 4.
- 5. INTRODUCTION Disorder in whichthere is sudden, spontaneous, isolated, total or subtotal loss of afferent vestibular input from one labyrinth resulting in severe vertigo [ Scott brown otorhinolaryngology, 7th edition,vol 3] 2nd most common cause of vertigo of peripheral origin [Cummings otolaryngology Head & Neck Surgery,
- 6. Synonyms: INTRODUCTION Vestibularneuritis Acute unilateral peripheral neuropathy Labyrinthitis Neurolabyrinthitis [ Scott brown otorhinolaryngology, 7th edition,vol 3] No gender bias Middle aged people
- 7. Single episode ofcontinuous rotatory vertigo A/w nausea, vomiting & postural imbalance Increase in intensity over hrs Aggravated by head movement CLINICAL MANIFESTATIONS a. Vertigo
- 8. Minimized bykeeping head still & eyes shut Subsides over 24- 48 hrs May persist upto 2-6 months Commonly unilateral Relapsing episodes ( few cases) Less intense Shorter CLINICAL MANIFESTATIONS
- 9. C. HEARING LOSS TINNITUS Typically absent b.Nystagmus Spontaneous, horizontal-torsional Strictly unidirectional Quick phase towards unaffected side Magnifying frenzel lenses may be reqd CLINICAL MANIFESTATIONS [ Scott brown otorhinolaryngology, 7th edition,vol 3]
- 10. D. Head impulsetest CLINICAL MANIFESTATIONS [ Scott brown otorhinolaryngology, 7th edition,vol 3]
- 11. DIAGNOSIS 1. Clinical Diagnosis 2.Subjective visual horizontal test (SVH) Asked to adjust a light bar with gravitational horizontal Normal subj : within 2-3° Acute vestibular dz : deviate by >=20°
- 12. 3. Electronystagmography 4. Calorictesting 5. MRI of brain DIAGNOSIS
- 13. DIFFERENTIAL DIAGNOSIS 1. Cerebellarinfarction Head impulse test –ve Nystagmus: Bidirectional Not suppressed by visual fixation Can’t stand without support even with eyes open [ Scott brown otorhinolaryngology, 7th edition,vol 3]
- 14. 2. Labyrinthine infarction Acute U/L vestibulopathy Hearing loss 3. Autoimmune inner ear disease B/l, asymmetric cochlear hearing loss Sometimes vestibular involvement DIFFERENTIAL DIAGNOSIS
- 15. 4. 1st Attackof Menieres dz Tinnitus & deafness may not be evident in early stage Peripheral vestibular function recovers between attacks DIFFERENTIAL DIAGNOSIS
- 16. THEORIES 1. Idiopathic 2. Viralorigin= schuknecht & kitamura Based on : a. Epidemiological evidence – incidence during epidemics of viral infection b. Clinical evidence- upper resp. viral disorder precedes vestibular syndrome Ballengers otorhinolaryngology, Head and Neck surgery,16th ed
- 17. Most commonlyIdentified virus: Herpes simplex virus type I Some instances: Borrelia infection Superior div of vestibular nerve is commonly affected THEORIES Vertigo coincident with recurrence of cutaneous Zooster Bony canal: - Longer - Narrower
- 18. Findings in affectedvestibular nerve: Viral inclusions Signs of vasculitis THEORIES Not identified Diffuse lymphocytic infiltration with areas of gliosis Decreased no. of fibres Signs of degeneration in remaining fibres
- 19. THEORIES 3. As afeature of generalized polyneuritis Based on: - finding of hearing loss in higher frequencies - ABR results suggesting CNS involvement 4. Vascular Cause No evidence of vascular occlusion affecting vestibular system 5. Immune mechanism Ballengers otorhinolaryngology, head and neck surgery,16th edition Cummings otolaryngology Head & Neck Surgery, 4th ed
- 20. 1. Acute form Single prolonged vestibular disorder Doesnot recur after resolution 2. Chronic form Recurrent vestibular attacks following initial episode TYPES
- 21. MANAGEMENT 1. Recent prospectiverandomized trial Placebo Methylprednisolo ne Valcyclovir Methylprednisolo ne + Valcyclovir Vestibular neuronitis t/t with • Caloric irrigation : measure extent of U/L canal paresis within 3 days after onset of symptoms and 12 months afterward • Methylprednisolone grp: mean improvement in vestibular funcn
- 22. • Vestibular rehabilitationtherapy MANAGEMENT
- 23. OUTCOMES AND COMPLICATIONS Invariablysubsides over following days Acute Peripheral vestibulopathy on opp side – b/l sequential vestibular neuritis (some cases) Repeated attacks on same side- r/o Meniere’s dz 20 % of pt develop: post- SCC type Bppv
- 25. Disorder characterized bybrief attack of vertigo, with associated nystagmus,Precipitated by certain changes in head position with respect to gravity Most common cause of pripherally induced vertigo (20 % – 40 % ) 1st described by Barany in 1921 INTRODUCTION Cummings otolaryngology Head & Neck Surgery, 4th edition Scott brown otorhinolaryngology, 7th edition
- 26. Mean age ofonset: 4th & 5th decade F > M = 1.6 : 1 to 2:1 C/F: 1. Rotational vertigo Induced with shift of body position INTRODUCTION
- 27. Position Change Shortlatency of 8 sec Vertigo Lasts for 5 – 10 secs Gradually disappears INTRODUCTION
- 28. • May persistsfor few weeks & months 2. No concomitant hearing loss &/or tinnitus INTRODUCTION
- 29. CAUSES 1. Idiopathic- 48%(Baloh and colleagues) 2. Closed head injury (Most common known cause) 3. Vestibular neuritis (15%) 4. Predisposing factors: Infections surgical procedures- stapedectomy insertion of a cochlear implant Prolonged bed rest Meniere’s disease Cummings otolaryngology Head & Neck Surgery, 4th edition
- 30. THEORIES 1. Barany (1921) Recognised several manifestations of bppv Didn’t correlate nystagmus with positioning manoeuvre Concluded: abnormality in encoding of head posn by otolith 2. Dix & Hallpike (1952) Correctly identified offending labyrinth Scott brown otorhinolaryngology, 7th edition,vol 3
- 31.
- 32. Scukneccht &ruby (1973) Histology of deposits on cupula of post SCC THEORIES o Granular, amorphous mass o Distinguishable in light microscope o No internal str. Or organisation Assumption: Diff specific wt of cupular deposit to that of cupula itself Changes in gravitational forces
- 33. Scukneccht’s theorymodification BPPV was d/t deposition of otoconia on cupula of post canal K/A Cupulolithiasis Drawbacks: poorly explained- THEORIES Brief duration of nystagmus Reversal of nystagmus Paroxysmal nature
- 34. 4. Moriarty etal. Investigated incidental distribution of cupular deposits 1/5th cases all 3 SCC None experienced BPPV previously THEORIES
- 35. 5. Parnes &Mc clure : Described new surgcal technique for t/t Opening &occluding post SCC instant relief from vertigo Found: Free floating & mobile particles in endolymph influence cupula in post SCC THEORIES
- 36. 6. Reformulated theoryof Hall, Ruby & McClure Consistent with 5 features of Post. canal BPPV A. Canalithiasis mechanism Explains Latency of nystagmus Time for motion of material within post. canal to be initiated by gravity THEORIES Cummings otolaryngology Head & Neck Surgery, 4th edition
- 37. B. Nystagmus duration Timerequired for dense material to reach lowest part of canal C. Vertical & torsional nystagmus Consistent with eye movt evoked by stimulation of post. canal nerve Ampullofugal stimulation of post Scc. THEORIES Contrn of - ipsilateral Sup Oblique C/L Inf Rectus
- 38. D. Reversal ofnystagmus Retrograde movement of material in lumen Back toward ampulla Ampullopetal deflection of cupula E. Fatigueability of nystagmus Explained by dispersion of material within canal THEORIES
- 40. 1. POST SCCBPPV Most common variant Torsional (rotatory) nystagmus Beating clock-wise Canalolithasis Characteristics: a. Latency b. Adaptation c. Fatigueability
- 41. 2. LAT. SCCPPV Most common atypical BPPV 12% of cases Mainly Induced by repositioning maneuver for posterior canal BPPV Nystagmus: purely horizontal Cummings otolaryngology Head & Neck Surgery, 4th edition
- 42. Nystagmus and vertigo:- when head turned both to side of lesion & to opp ( geotropic/ageotropic) - Stronger in dirn of abnormal side Less susceptible to fatigue with repetitive testing 2. LAT. SCC PPV
- 43. 3. ANT. SCCBPPV Rare – 2% Nystagmus: torsional + down-beating
- 44.
- 45. History Positional manoeuvres Imaging ofpost. Fossa reqd when: - Nystagmus - atypical for any of BPPV syndromes - Brainstem or cerebellar signs - Positional vertigo not resolving with repeated therapeutic
- 46. Electro-oculography Videonystagmography devices Do notrecord torsional eye movements a/w BPPV
- 47. POSITIONAL MANOEUVRES Whento conduct ? In all pts with episodic vertigo, provoked by head, neck movt or posns No excuses for not conducting it Purpose ? To attempt to illicit vertigo
- 48. Pt counselling Only way to make dx of BPPV Should look straight at one point on examiner’s face Requirements In any position Frenzel’s glasses not reqd POSITIONAL MANOEUVRES Suppression of torsional nystagmus by visual fixation < nystagmus in other planes
- 49. Conducted onboth sides : if no nystagmus on 1st side BPPV diagnosed & treated on one side If symptoms persist Manoeuvre Carried out on separate session on both sides POSITIONAL MANOEUVRES
- 50. POSITIONAL MANOEUVRES (POSTSCC BPPV)
- 51. POSITIONAL MANOEUVRES (LATERALSCC BPPV) Cummings otolaryngology Head & Neck Surgery, 4th edition
- 52. Standard Dix-hallpiketesting Rt. Post. Canal lt superior canal POSITIONAL MANOEUVRES (ANTERIOR SCC BPPV) lies in same plane & viceversa
- 53. TREATMENT Repositioning manoeuvres Surgical treatment Brandt Daroff positional exercises Semont's liberatory manoeuvre Epley’s repositioning manoeuvre
- 54. BRANDT DAROFF POSITIONALEXERCISES
- 55.
- 56.
- 57.
- 58.
- 59. MECHANISMS UNDERLYING BPPV Copyright©2003 CMA Media Inc. or its licensors Parnes, L. S. et al. CMAJ 2003;169:681-693 Fig. 4: Left inner ear CANALITHIASIS VS. CUPULOLITHIASIS
- 60. MECHANISMS UNDERLYING BPPV CANALITHIASIS DELAYEDONSET SHORT DURATION SYMPTOMS COINCIDE WITH NYSTAGMUS Herdman & Tusa, 2004
- 61. MECHANISMS UNDERLYING BPPV CUPULOLITHIASIS TYPICALLYNOT DELAYED ONSET LONG DURATION SYMPTOMS MAY STOP Herdman & Tusa, 2004
- 62. POSTERIOR CANAL BPPV •CHARACTERIZED BY BRIEF ATTACKS OF ROTARY NYSTAGMUS CAUSED BY HEAD MOVEMENTS • ROLLING OVER IN BED • LOOKING UP/DOWN • BENDING FORWARD • SITTING UP • LYING DOWN • TURNING QUICKLY
- 63. POSTERIOR CANAL BPPV •MOST COMMON VARIANT • POSITION RELATIVE TO VESTIBULE • CANALITHIASIS MORE PREDOMINANT • DIAGNOSED USING THE DIX-HALLPIKE MANEUVER • BEST SEEN WITH FRENZEL LENSES OR VIDEONYSTAGMOGRAPHY
- 64. POSTERIOR CANAL BPPV •TYPICALLY, THE NYSTAGMUS BEATS TOWARD THE UNDERMOST (AFFECTED) EAR • AS SEEN BY THE INVESTIGATOR • ABNORMAL DIX-HALLPIKE MANEUVER TO THE RIGHT WILL RESULT IN NYSTAGMUS WITH A COUNTER-CLOCKWISE FAST PHASE • ABNORMAL DIX-HALLPIKE MANEUVER TO THE LEFT WILL RESULT IN NYSTAGMUS WITH A CLOCKWISE FAST PHASE
- 65. ANTERIOR CANAL BPPV •LEAST COMMON VARIANT – 1-2% • DIAGNOSED USING DIX-HALLPIKE MANEUVER • CHARACTERIZED BY DOWNBEAT ROTARY NYSTAGMUS • CAN BE PROVOKED FROM THE OPPOSITE EAR TO THE SIDE OF THE DIX-HALLPIKE MANEUVER • CAN BE PROVOKED FROM THE DIX-HALLPIKE MANEUVER FROM EITHER SIDE OR HEAD-HANGING BACK POSITION • DUE TO ORIENTATION OF ANTERIOR LIMB OF THE ANTERIOR CANAL (NEAR SAGGITAL PLANE)
- 66. HORIZONTAL CANAL BPPV •APPROXIMATELY 3-12% OF INDIVIDUALS WITH PAROXYSMAL POSITIONING VERTIGO • DIAGNOSED BY POSITIONAL TEST OR ROLL TEST
- 67. HORIZONTAL CANAL BPPV •CHARACTERIZED BY SHORT LATENCY HORIZONTAL NYSTAGMUS THAT IS PROVOKED BY BILATERAL HEAD TURNS • PROLONGED DURATION AND POOR FATIGABILITY • NYSTAGMUS CAN BE SEEN IN BOTH LATERAL RIGHT AND LATERAL LEFT POSITIONS • GEOTROPIC NYSTAGMUS - “BAD” EAR TYPICALLY HAS THE STRONGEST RESPONSE • AGEOTROPIC NYSTAGMUS – “BAD” EAR TYPICALLY HAS THE WEAKER RESPONSE (INHIBITORY RESPONSE)
- 68. HORIZONTAL CANAL BPPV NYSTAGMUSCAN BE GEOTROPIC OR AGEOTROPIC • GEOTROPIC – CANALITHIASIS • OTOCONIA MOVE FREELY IN THE CANAL TO THE LOWEST POSITION (TOWARD THE AMPULLA) CAUSING AN EXCITATORY RESPONSE WITH THE AFFECTED EAR DOWN
- 69. HORIZONTAL CANAL BPPV •AGEOTROPIC – CUPULOLITHIASIS • OTOCONIA ARE ADHERENT TO THE CUPULA CAUSING GRAVITY SENSITIVITY AND AN INHIBITORY RESPONSE WITH THE AFFECTED EAR DOWN • NYSTAGMUS WILL BEAT TOWARD THE UPPERMOST EAR
- 70. MIXED CANAL BPPV BPPVCAN AFFECT MORE THAN ONE SEMICIRCULAR CANAL RESULTING IN VARYING PATTERNS OF NYSTAGMUS • POSTERIOR AND HORIZONTAL CANALS MOST COMMON • SIMULTANEOUS POSTERIOR AND HORIZONTAL CANAL BPPV
- 72. REFERENCES Scott brown otorhinolaryngology,7th edition,vol 3,pg 3748 to 3782 Cummings otolaryngology Head & Neck Surgery, 4th edition, pg 3329-3247 Ballengers otorhinolaryngology, head and neck surgery,17th edition,pg 408- 437
- 73. Scott brown otorhinolaryngology,7th edition,vol 3 REFERENCES
Editor's Notes
- #6 One of the most common cause of vertigo of peripheral origin 2nd only to BPPV.but acc to Ballengers otolaryngology it is 3rd most common after BPPV N MENIERES
- #7 There r no. of synonyms used in literature to describe this disorder like Vestibular neuritis, Labyrinthitis ,Neurolabyrinthitis , Acute unilateral peripheral neuropathy.But since there is absence of auditory symptoms uniformly, a more accurate clinical term is vestibular neuronitis WHICH WAS coined by Hallpike in 1949.It has no gender bias n typically affects middle aged people
- #8 Subsides over 24- 48 hrs ie it’s the tym for central compensation to occur
- #9 few cases experience relapsing episodes .
- #10 Quick phase of nystagmus beating towards unaffected side therefore dx is excluded if nystagmus changes in dirn when diff posn of gaze r adopted.since nystagmus is suppressed by visual fixation it may not be detected on a standard neurologic examn.Removal of visual fixation using an opthalmoscope or magnifying frenzel lenses may be reqd to detect nystagmus .Auditory symptoms like hearing loss n tinnitus r typically absent
- #11 The pics a-c represents responses of normal healthy subj n d-f represents responses of pt with rt sided vestibular loss.In both cases subj’s head is rotated toward rt.Before head rotation subj is instructed to look at examiner’s nose without blinking.During head rotation, eyes of healthy subj stay fixed(b) n remains so at the end of head rotation(c) so no refixation is reqd.In pt with u/l vestibular loss,during rotation of head towards affected sideVOR is deficient n cannot move eye to compensate for head rotation so eyes move in same dirn as head ie to rt.at end of head rotation eyes have been dragged off target n so a corrective saccade is reqd to refixate examiner’s nose(f arrowhead)
- #12 Althouch vestibular neuritis is a Clinical Diagnosis several investigations r helpful in assessing pt during acute phase of illness.Subjective visual horizontal test ..pt is seated with their head fixed erect asked to adjust a light bar until it looks to be aligned with gravitational horizontal .Done with a push button controller.Normal subject can consistently set light bar to within 2-3 degree of true gravitational horizontal.Pt with acute u/l vestibular dz set the bar towards side of lesion n SVMAY deviate from true gravitational horizontal by 20 degree or more
- #13 3. Electronystagmography..Is also useful but doesnot create permanent record of nystagmus. Caloric testing is more useful for demonstrating a canal paresis 3-4 days after onset of symptoms.MRI of brain generally not reqd unless central cause for pt’s symptoms is suspected.MRI with gadolium contreast may show Enhancement of vestibular nerve on lesioned side of vestibular neuritis
- #14 Cerebellar infarction is the main differential dx in a pt presented with acute spontaneous vertigo. If Head impulse test –ve pt doesnot have vestibular neuritis and cerebellar infarction needs to be considered as a possibility. Nystagmus: Bidirectional n Not suppressed by visual fixation ie it will be obvious even without Frenzel lenses.Pt with cerebellar infarction Can’t stand without support even with eyes open whereas those with vestibular neuritis can.Whenever cerebellar infarction is suspected MRI should be performed..as it develop edema severe enough to to cause lethal compression of post fossa str.
- #15 It is caused by occlusion of internal auditory artery , branch of ant inf cerebellar artery that supplies entire inner ear.results in Acute U/L vestibulopathy N Hearing loss making it clinically distinct from vestibular neuritis.But those without hearing loss were also reported who were thought to have occlusion of internal auditory artery. Autoimmune inner ear disease results in obscure sases of B/l, asymmetric cochlear hearing loss usually without but Sometimes with Vestibular involvement.
- #16 1st Attack of Menieres dz may mimic vestibular neuritis .Tinnitus n deafness characteristically seen in Menieres may not be evident in early stage.But peripheral vestibular funcn typically recovers between attacks of acute spontaneous vertigo, thereby helps to distinguish this condition from vestibular neuritis.
- #17 1. Idiopathic..unknown origin. Also based on studies of human temporal bone from pts with known hx of vestibular neuronitis.Similarity betn temporal bone pathology induced by Zoster n that of vestibular neuronitis has been noted
- #18 Most commonly Identified virus IS Herpes simplex virusType I it was demonstrated using PCRT.It is a neurotropic virus n thought to exist in latent form in human vestibular ganglion. Vertigo coincident with recurrence of cutaneous Zooster has been reported. Borrelia infection has also been noted in some instances In most cases only superior div of vestibular nerve is affected. Bony canal through which superior div of vestibular nerve travels is longer n narrower than that of inf div n thuis renders sup div of nerve more vulnerable to entrapment when it is inflamed .
- #19 However , viral inclusions in vestibular neurons n signs of vasculitis not identified
- #20 3. As a feature of generalized polyneuritis .Based on: - finding of hearing loss in higher frequencies,: subjectively hearing remains Nornmal.However in a study of such pts with normal conventional audiogram hearing loss was found in higher freq.ABR results suggesting CNS involvement .so these suggest vestibular neuronityis to be a feature of a more generalized polyneuritis.But such findings havenot been uniformly confirmed Other proposed causes are vascular cause n immune mechanism.But there is No evidence of vascular occlusion affecting vestibular system in any of temporal; bone studied. Similarly there is no evidence to support immune mechanism
- #22 As vestibular neuronitis is thought to be d/t selective viral infection,Recent prospective randomized trial was reported . pts with acute vestibular neuronitis were randomly assigned to t/t with placebo,methylprednisoloine,valcyclovir or methylprednisolone with valcyclovir.Vestibular funcn was determined by caloric irrigation to measure extent of unilateral canal paresis within 3 days after onset of symptoms and 12 months afterward.Mean improvement in vestibular funcn was in methylprednisolone grp .There was no beneficial effect of valcyclovir when used alone n combn of methylpred n valcyclovir did not lead to additional improvement over that seen in methylpred alone.
- #23 Vestibular rehabilitation therapy..it has shown to facilitate compensation and improve both postural and visual stability
- #24 Acute unilateral vestibular syndrome that occurs with vestibular neuritis invariably subsides over following days d/t central vestibular compensation. In small proportion of cases there will be attack of acute peripheral vestibulopathy on the opposite side – a condition called bilateral sequential vestibular neuritisIf repeated attacks on same side Meniere’s dz needs to be considered esp if there is recovery of lateral scc fun on caloric testing betwn attacks. Following an attack of vestibular neuronitis,20 per of pt develop Post. SCC type bppv on affected side .
- #26 Most common cause of pripherally induced vertigo REPRESENTING 20 % – 40 % OF PTS with vestibular dz
- #27 Rotational vertigo induced when pt shift body position particularly posn of head. most frequently cited occurrence of this symptom follows rolling over or getting into bed and assuming a supine posn. Frequently a specific side is identified as being associated with symptom onset
- #30 In a large survey by Baloh and colleagues, no cause was identified in 48% of cases. most common known cause is closed head injury, followed by vestibular neuritis. BPPV will eventually develop in nearly 15% of patients suffering from vestibular neuritis. predisposing factors include infections and certain surgical procedures like stapedectomy & insertion of a cochlear implant. Prolonged bed rest & Meniere’s disease also are predisposing factors
- #31 Barany (1921) recognised several manifestations of bppv like nystagmus n vertigo but didn’t correlate onset of nystagmus with positioning manoeuvre Concluded: abnormality in encoding of head posn by otolith were responsible for signs n symptoms he noted. 2. Dix & Hallpike (1952) described Dix hallpike manoeuvre for eliciting pattern of nystagmus n its associated symptoms.Correctly identified offending labyrinth.Incorrectly concluded : BPPV results from otolithic disturbance
- #32 Detachment of otoconia,probably from utricle..floats freely in endolymph.upon rotatory movement,displace cupula overlying sensory epithelium of ampulla of post. Scc.
- #33 Schuknect presented Histology of deposits on cupula of post SCC.It appears finely amorphous mass which is basophilic,clearly Distinguishable in light microscope With no any distinguishable internal str. Or organisation
- #34 Scukneccht’s modified HIS theory.Rather than d/t movt of loose otoconia in post canal, BPPV was d/t deposition of otoconia on cupula of post canal k/a cupulolithiasis. Drawbacks of this cupulolithiasis mechanism r..it poorly explains Brief duration of nystagmus ,Reversal of nystagmus upon return to siutting posn n Paroxysmal nature of disorder
- #35 Moriarty et al.Investigated incidental distribution of cupular deposits in labyrinth.granular deposits were identified in 1/5th cases. Deposits were present in all 3 SCC. Inspite of this relatively high incidence of cupular deposits ,none of subjs experienced BPPV previously
- #37 consistent with 5 typical features of post canal BPPV.canalithiasis mechanism explains latency of nystagmus that occurs as a result of time needed for motion of material within posterior canal to be initiated by gravity
- #38 nystagmus duration is correlated with length of time required for dense material to reach lowest part of the canal. vertical (up-beating) and torsional (top of the eyes beating toward the lowermost ear) components of the nystagmus are consistent with eye movt evoked by stimulation of posterior canal nerve.Ampullofugal stimulation of post Scc.cause Contrn of ipsilateral Sup Oblique n C/L Inf Rectus
- #39 reversal of nystagmus when the patient returns to sitting upright position is due to retrograde movement of material in lumen of post canal back toward ampulla, with resulting ampullopetal deflection of cupula. fatigability of nystagmus evoked by repeated Dix-Hallpike testing is explained by dispersion of material within canal.
- #41 POST SCC bppv: Most common variant with Torsional (rotatory) nystagmus beating clock-wise from observer point of view.It means During a left-ear-down head hanging position , left posterior canal is triggered n upper pole of pt's eye beats towards pt's left shoulder.occurs Due to canalolithasis ie free Floating particles in the lumen of canal. characteristics r presence of latency, adaptation & fatigability. Adaptation refers to decline & eventual disappearance of nystagmus within a min. Fatigability means ,on repeated positionings ,nystagmus &vertigo are less with time.
- #42 lateral semicircular canal has been identified as affected structure in approximately 12% of cases, with a significant fraction of these being induced by repositioning maneuver for posterior canal BPPV.it is usually due to canalolithasis and occasionally D/T cupulolithiasis ie particles become adhesive to cupula.
- #43 produces intense nystagmus & vertigo when head is turned both to: side of lesion and to opp dirn.ie may beat toward (geotropic) or away from the downward ear ie (ageotropic). intensity of nystagmus is stronger in dirn of abnormal side, i.e. stronger rt beating nystagmus with right ear down suggests right horizontal canal BPPV. less susceptible to fatigue with repetitive testing than the vertical torsional nystagmus of posterior canal BPPV It is a much more self-limiting condn than other canal BPPV & can disappear spontaneously in a few days
- #44 superior scc is affected in only 2% of cases of BPPV.Nystagmus: torsional component added to vertical nystagmus of down-beating type. down beating nystagmus, is considered to be of central origin.so besides ant scc bppv it’s also +nt in neurological disease
- #46 Typical sign ie nystagmus n symptoms like vertigo n nausea provoked by specific positional test are the basis of diagnosis….. Cases with central positional vertigo but normal imaging may be due to migrainous vertigo or drug effects such as amiodarone
- #47 electro-oculography and many videonystagmography devices do not record torsional eye movts associated with BPPV.THEY reflect solely associated vertical and horizontal components of eye movts..therefore they r of less imp.
- #48 LIKE Dix hallpike manoeuvre is Vital component of examn in balance disordered pts mainly BPPVWhen to conduct ? In all pts with episodic vertigo PARTICULARLY IF Provoked by head, neck movt or posns No excuses for not conducting POSITIONAL MANOEUVRE but 2 most commonly heard excuses r- couch in my room is placed awkwardly to do hallpike or we have not got Frenzel glasses in our clinic
- #49 Pt should b made aware that despite modern technology, this is only way to make dx of BPPV.Pt should Be warned that even if they feel vertiginous, they should Look straight ahead at one point on examiner’s face As if eyes r wandering around, obsv of nystagmus is difficult. Requirements :can be done with couchIn any position n Frenzel’s glasses not reqd. rationale for using Frenzel's glasses is when pt is able to fixate, nystagmus can be potentially suppressed. In BPPV nystagmus is extremely strong and so pt is unable to suppress it with visual fixation. most common form of BPPV, posterior canal BPPV in which there is torsional (rotatory) nystagmus. ability to suppress torsional nystagmus by visual fixation is less than nystagmus in other planes
- #50 should be conducted on both sides particularly if no nystagmus is observed on first side. If BPPV has been Diagnosed and treated on one side. If symptoms persist, Hallpike manoeuvre will have to be carried out on a separate session on both sides. This is because of fears that a new Hallpike after an Epley or Semont manoeuvre could undo benefits of t/t
- #51 Pt is positioned on examn table such that when he/she is in supine ,head extends over edge.Pt is lowered with head supported.Turned 45 degree to one side .Eyes r crfully observed N One should wait for 10-20 secs as most cases of BPPV have latencies of 5-6 secs.If no abnormal movt seen pt is returned to upright posn.n manoeuvr is repeated with head in opp dirn.Finally head extended supine.
- #52 Lateral canal BPPV can be detected by variation of Dix-Hallpike maneuver: pt is 1ST brought to supine position with the head resting on examining table ie not hyperextended below. head is then turned rapidly to right so that pt’s right ear rests on table. Eye movements are monitored for 30 seconds. pt is then returned to supine position & head is turned rapidly to left so that left ear rests on table. Eye movements are again monitored.
- #53 elicited by standard Dix-Hallpike positioning testing. rt post canal lies in roughly same plane as that of lt sup canal, and viceversa. Placement of head into rt Dix-Hallpike position will therefore bring lt superior and rt posterior canals into plane of gravity. A nystagmus resulting from lt superior canal BPPV in this position, be expected to be downbeat, with a torsional component directed such that superior part of each eye beats toward upward ear.