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12 bppv final
This document discusses benign paroxysmal positional vertigo (BPPV). It begins with an overview of the anatomy and physiology of the vestibular system. It then defines BPPV and discusses its pathogenesis, symptoms, types, differential diagnosis, investigations and treatment modalities. The most common treatment is canalith repositioning procedures like the Epley maneuver which aims to move otoliths out of the semicircular canals.
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12 bppv final
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- 2. Topic is coveredunder following heads • Brief Anatomy and Physiology • Introduction • Aetio pathogenesis • Symptoms • Types and clinical features • Differential diagnosis • Investigations • Treatment modalities 2
- 4. Anatomy of thevestibular system 5
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- 6. Benign Paroxysmal PositionalVertigo (BPPV) • Benign: not a very serious or progressive condition • Paroxysmal: sudden and unpredictable in onset • Positional: comes with a change in head position • Vertigo: causing a sense of dizziness. 7
- 7. Introduction • BPPV –One of the commonest Vestibular End organ disorders • 17-25% of all vestibular disorders • Most common aural cause of vertigo • Chronic, Incapacitating, Affecting day to day functioning 8
- 8. Introduction • Hallmark ofthe disease is the onset of brief (seconds) spells of often severe vertigo that are experienced only with specific movements of the head with respect to gravity. • Typical Precipitating movements- – Turning in bed, – Getting In and Out of bed, – Bending and straightening – Extending the neck to look up and back • “TOP SHELF VERTIGO” 9
- 9. History • 1921 -First described by Barany • 1952 - Dix-Hallpike reported this entity in a large number of patients and described important features of nystagmus • 1962, Dr Harold Schuknecht proposed the cupulolithiasis (heavy cupula) theory. • 1980, Brandt and Daroff proposed positional exercises based on the canalolithiasis hypothesis even before the theory was described • 1980 – Hall, Ruby and McClure described the theory of canalolithiasis • 1991 - Free floating deposits demonstrated in Endolymph of PSSC–Parnes, McClure 10
- 10. Benign positional vertigo-epidemiology • Incidence: 1:20 in general practice 3:20 in ENT OPD • U.S. study – incidence 64 per 100,000. Av 10-64 / lakh • Incidence in general population is higher in persons older than 40 years. • Elderly patients – incidence approximately 8%. • 20% of all falls that result in hospitalization for serious injuries in the elderly are due to vertigo of end-organ origin (most often related to BPPV). • Average age of onset 51 years. M=F, some studies show a slight predilection for women. • Rarely seen in persons younger than 35 years without a history of antecedent head trauma. 11
- 11. • Idiopathic –48% • Head trauma • Viral neuronitis • Middle ear infection • Surgical damage to the labyrinth • Prolonged bed rest 12 BPPV- AETIOLOGY
- 12. PATHOPHYSIOLOGY OF BPPV • Vertigooriginates in Posterior Semi circular canal in majority of cases • Rarely in Lateral Semi circular Canal and still rarer in Superior semi circular Canal • “Cupulolithiasis” – Schucknect • “Canalithiasis” –Hal, Ruby, McClure, Parnes, Epley • Free Floating particles in endolymph of Posterior Semi circular Canal 13
- 13. Theories of BPPV 14 Cupulolithiasis •In 1962, Dr Harold Schuknecht proposed the cupulolithiasis (heavy cupula) theory. • Discovered basophilic particles or densities that were adherent to the cupula. • He postulated that the PSC was rendered sensitive to gravity by these abnormal dense particles attached to, or impinging on, the cupula. • This produces persistent nystagmus and also explains the dizziness when a patient tilts the head backward. • Cupulolithiasis – possible role in atypical BPPV
- 14. Theories of BPPV Canalolithiasis : – Hall, Ruby and McClure – 1980 – Free floating deposits demonstrated in Endolymph of PSSC–Parnes, McClure-1991 • The most widely accepted theory of the pathophysiology of BPV • Otoliths (calcium carbonate particles) are normally attached to a membrane inside the utricle and saccule • Otoliths may become displaced from the utricle to enter the posterior semicircular duct since this is the most dependent of the 3 ducts • Changing head position relative to gravity causes the free Otoliths to gravitate longitudinally through the canal. • The concurrent flow of endolymph stimulates the hair cells of the affected semicircular canal, causing vertigo. • Explains all features of typical nystagmus 15
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- 16. Symptoms • Discrete episodesof vertigo induced by specific head motions of duration less than 1 min. • Single bouts clustered in time with remissions lasting months or more. • Dizziness with rapid head movements. (Cupulolithiasis) • Disequilibrium worse in the morning or after day time naps. • Nausea and vomiting 17
- 17. NYSTAGMUS IN BPPV… • Nystagmus : characterization and types – Rt / Lt , vertical / horizontal , changing – Tortional = Rotational – clockwise / counterclockwise – Geotropic- toward the earth – Ageotropic – opposite
- 18. DIRECTION OF NYSTAGMUS Destructivelesion of the vestibular end organ or the vestibular nerve will produce transient horizontal nystagmus with its quicker phase towards the opposite side. Unilateral cerebellar lesion will produce vertigo with its quicker phase to the same side Paretic lesion of labyrinth the nystagmus is towards healthy side 19
- 19. Nystagmus 20 Appearance LatencyDuration Fatigability Localisation Central Pure vertical, usually downbeat Unusual Persistent Unusual Brainstem or cerebellum Peripheral Postr SCC Torsional towards the downward eye, vertical upbeat, geotropic Usual (seconds) Brief(<1 min) Usual Posterior semi- circular canal Peripheral Lat SCC Horizontal, geotropic or ageotropic Usual (seconds) Brief (<1 min) Less susceptible than PSCC Horizontal semi- circular canal
- 20. I. Classic BPPV •Involves the Posterior SCC – Canalilithiasis of Posterior SCC – most frequent cause – Reversal upon return to upright position – Response decline upon repetitive provocation Types of BPPV
- 21. II. Lat. SCCBPPV • Most common atypical BPPV • 3-9% of cases • Paroxysmal horizontal direction changing nystagmus –beats towards ground (geotropic) when head turned to side while patient lies supine - Canalilithiasis • Ageotropic – Nystagmus away from the dependent affected ear - Cupulolithiasis • Nystagmus lasts 1 minute, minimal latency and no fatigability. • Occurs with head to either side but stronger on one side. 22
- 22. III. Ant. SCCBPPV • Rare – 2% • Down-beating /torsional NG for the opposite ear on Dix-Hallpike maneuver • Torsional downbeating nystagmus during Hallpike test induced when the abnormal anterior canal (which lies at right angles to posterior) is uppermost. • Repositioning maneuver starts with abnormal ear uppermost moving across to opposite head hanging position. 24
- 23. BPPV - D.D •Meniere’s disease • Vestibular migraine • Recurrent vestibulopathy • Vestibular Labyrinthitis – Lasting days • Inner ear fistula • Inner ear trauma • Superior SCC dehiscence syndrome • Central origin : Stroke , MS , cerebellar degeneration • Vertebral artery insufficiency • Cervical vertigo 25 Minutes to hours Variable duration
- 24. HISTORY: Confirmation of dizziness Associatedsymptoms •Otalgia, otorrhoea, Tinnitus, headache, •Aural fullness, head injury, acoustic trauma, ototoxic drug intake, DM, HTN, •TB, CVA, IHD •H/o Ear surgery •Difficulty in speaking/walking •Diplopia/dysarthria, loss of consciousness points to brain stem dysfunction 26 EVALUATION AND DIAGNOSIS
- 25. Pattern Of Vertigo Onset,duration, continuous/ paroxysmal Period of complete relief Postural Preliminary tests Of Balance Degree Of Vertigo – Is there nausea/vomiting (I) Finger Pointing (II) Rapid Alternate Movements Of Hand (III)Gait (IV)Tandem Walk (V) Rhombergs test (VI)Unterbergers test 27
- 26. Ears-EAC-FB/WAX -TM for perforation,AOM/OME -Cholesteatoma Hearing tests -TFT -PTA -FFH -Impedance Audiometry Otological examination Detailed clinical examination General Systemic 28
- 27. Ocular Examination Ptosis Pupillaryreactivity Ocular alignment Eye movements Convergence 29
- 28. Labyrinthine Function tests (I)Caloric tests to look for nystagmus (II) Dix Hallpike tests for positional vertigo (III) ENG (IV) VNG DIX-HALL PIKE TESTS 30
- 29. RECENT ADVANCES INEVALUATION VIDEO NYSTAGMOGRAPHY (VNG) •VNG– Video images of the eyes are obtained without direct contact using high resolution cameras with infrared illumination. Setup is fast & as easy using Frenzel glasses. The eyes are visualized, enabling simultaneous subjective evaluation while eye movements are analyzed by digital image processing to obtain vertical and horizontal eye position. Can be used for teaching purpose. 31
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- 31. Laboratory tests Routine hemogram,urine examination Blood sugar T3, T4 ,TSH Serological tests to rule out Syphilis Radiological investigations X-Ray Skull-Per orbital view X-Ray mastoids X-Ray Cervical spine CT- Temporal bone and Brain SPECIAL TESTS EEG BERA Psychological Evaluation 34 To rule out other pathologies
- 32. BPPV - Treatment •Watchful waiting • Pharmacotherapy • Canalith repositioning procedure • Vestibular rehabilitation • Surgery care – Singular neurectomy – Post. Canal occlusion – Vestibular nerve section
- 33. Pharmacotherapy • Directed principallyat suppressing vestibular response. • Alleviating nausea associated with vertigo. • Does not treat underlying cause. – Low dose diazepam – used prior to CRP – Antiemetics like phenergan – Longer acting vestibular suppressants like clonazepam for chronic disequilibrium 36
- 34. Canalith Repositioning Procedure( CRP ) • The treatment of choice for BPPV (Epley maneuver) • The patient positioned in a series of steps so as to slowly move the otoconia particles from the Posterior SCC into the utricle. • Takes approximately 5 minutes. • The patient is instructed to wear a neck brace for 24 hours and to not bend down or lay flat for 24 hours after the procedure. • Dix-Hallpike test is repeated soon after the CRP and after 1 week. • If the patient does experience vertigo and nystagmus, then the CRP is repeated with a vibrator placed on the skull in order to dislodge the otoconia. 37
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- 42. CRP – Semontmaneuver 45
- 43. Brandt-Daroff Exercises • Methodof treating BPPV, usually used when the office treatment fails. • These exercises should be performed – For one week, three times per day – For three weeks, twice per day. • In each time, one performs the maneuver as shown five times. • 1 repetition = maneuver done to each side in turn (takes 2 minutes) 46
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- 45. Lampert maneuver- Lat.SCC BPPV 48
- 46. Complications of CRP •Failure – 25% (12%-56) • Recurrence – 13% in 6 months • Side effects – Nausea ,Vomiting, Fainting, Sweating • Worse vertigo – Lateral SCC BPPV • “Canalith jam” • Conversion to another canal 49
- 47. Vestibular Rehabilitation Exercises(VRE) • Reduces symptoms, Promotes Spontaneous resolution • Safe and effective • Cawthorne-Cooksey Exercises • Need to be carried out regularly – Over 12-16 Weeks before improvement is noticed 50
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- 49. Surgery • Singular neurectomy •Posterior Canal Plugging Procedure • Vestibular Nerve Section 52 Role of Surgery • Very limited, < 2% may need Surgery which is rarely offered • Highly responsive to physical therapy interventions • Only in intractable cases affecting the life style of the patient
- 50. Singular neurectomy • Evolvedby Gacek • Section the posterior ampullary nerve that transmits information from the posterior semicircular canal ampulla toward the brain. • Highly rational • Technically difficult • Can cause hearing loss in 7-17% of patients and fails in 8-12%. • Anatomical abnormalities of singular canal 53
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- 52. Posterior Canal PluggingProcedure • Parnes and McLure introduced this concept. • Prevent movement of debris towards ampulla. • Technically simpler and safer. • Replaced the singular neurectomy. • Less than 20% hearing loss. 55
- 53. Posterior Canal PluggingProcedure 56
- 54. Vestibular Nerve Section •Done when the attacks of vertigo cannot be controlled with medication. Seems unreasonably aggressive for BPPV • Approaches – Middle fossa, retrolabyrinthine, retrosigmoid • The vestibular part of the nerve is cut. • The operation is done with a neurosurgeon and takes about two hours. • The success rate (no vertigo attacks) is over 90%. • The hearing is slightly affected. 57
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- 56. Bibliography • Scott BrownOtorhinolaryngology, Head and Neck surgery, 7th edition • Otorhinolaryngology Head & Neck Surgery, Ballenger (17th edition) • Galsscock – Shambaugh Surgery of the Ear 5th edition • Cumming’s otolaryngology, head and neck surgery 4th edition 59
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Editor's Notes
- #18 first noticed in bed, when waking from sleep. Any turn of the head bring on dizziness. Patients often describe the occurrence of vertigo with tilting of the head, looking up or down (top-shelf vertigo) rolling over in bed. nausea and vomiting. There is no new hearing loss or tinnitus.
- #26 Vascular loop syndrome Post. Fossa lesions : acustic neuroma , meningioma
- #56 A mastoidectomy is performed through an post aural incision. The vestibular system is then uncovered The posterior semicircular canal is opened, exposing the delicate membranous channel in which the crystalline debris is floating. The canal is then gently, but firmly packed off with tissue so the debris can no longer move within the canal and strike against the nerve endings. The canal is then sealed and the incision closed. One-night hospital stay is advised. The patient returns in one week for suture removal.