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BPPV: Pathophysiology, Diagnosis, and Facts

Learn about the pathophysiology of Benign Paroxysmal Positional Vertigo (BPPV) and how it is diagnosed. Discover important facts and diagnostic considerations from a Board-certified audiologist.

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BPPV: Pathophysiology, Diagnosis, and Facts

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  1. BPPVPathophysiology and Diagnosis. Dr.MohammadShafique Asghar Au.D, (USA). American Board of Audiology, (Board certified audiologist). M.Sc Audiological Medicine,(UK). MCPS (ENT), M,B.B,S (Pb).

  2. BPPV Facts • BPPV is the # 1 cause of vertigo, • Requires 4.5 physician visits before correctly diagnosed. • May indicate a more serious inner ear or disease process. • Can lead to falls or drop like attacks. • Has a 95% or greater success rate.

  3. BPPV (facts) • # 1 cause of dizziness in individuals over 60 Years of age. • May be seen in any age group, post mild head trauma. • Greater incidence in women than in men. • May trouble the patient for years.

  4. BPPV (Facts).. • 1000 patients with vertigo. • 50->75% will have a single, treatable diagnosis: BPPV. • You must ask for H/O position exacerbation, even if “dizzy all the time”. • Must repeated search for BPPN • Only 50% +ve in office exam.

  5. BPPV (facts)… • When is BPPV really bad. • Average # of physician visited : 4.5 • Average time to diagnosis : 2.5 years. • Patient may be totally disabled. • Longest duration 50 years. • Failure of diagnosis : Poor Hx & Exam.

  6. Pathophysiology. • Barany was the first to describe the condition (1921) • Dix and Hallpike (1952) were the first to describe the provocative positioning techniques and the clinical indicators of BPPV.

  7. Pathophysiology.(cont…) • It was Harold Schuknecht (1969) who after studying the temporal bones indicated that there was a residue of otoconia imbedded within or adhering to the cupola of posterior canal. • He thought that the heavily weighted cupula was the cause of transient vertigo and it was termed as Cupulolithiasis.

  8. Pathophysiology.(cont…) • Parns (1992) revealed that the debris may not be adhere Cupula but rather was free floating within the long process of the posterior canal. • This led to the development of Canalilithiasis theory.

  9. Pathophysiology.(cont…) • At one time it was believed that the symptoms were caused by the dysfunction within the otolith mechanism and in particular Utricle. • But in actual fact: The otolith debris degenerate in the Utricle and it is their migration into the posterior canal that causes the manifestation of the symptoms.

  10. Pathophysiology.(cont…) • Like in Lindsay Hemenway syndrome, there is ischemia of the anterior vestibular artery. • This causes degeneration of the otolith within the Utricle as well as loss of sensitivity within the horizontal canal. • The debris however migrate in to the posterior canal which is an “innocent bystander” .

  11. Pathophysiology.(cont…) • There is no pathology within the posterior canal. However the gravity dependent material which either adheres to Cupola (Cupulolithiasis) or lies within the long process Canal (Canalilithiasis) causes a deflection of the cupula with change in head position.

  12. Pathophysiology (cont..)

  13. Predisposing conditions to BPPV. • Vestibular neuritis, • Labyrinthitis, • Meniere’s disease, • Head trauma, • Vertibulobasilar ischemia, • Prolonged bed rest, • Idiopathic.

  14. BPPV – History. • Antecedent head injury. • Worse in AM. • “Dizzy all the time” ask for aggravating factors. • Occurs in 60-75% of all individuals ages 60-80 years.

  15. BPPV-History • Activities: Taking a shower, backing a vehicle, turning over in bed. • Intermittent, short (30”) duration. • Multiple attacks (4-100) attacks/day. • My doctor did not find anything. • Tests are all negative, including vestibular tests.

  16. Diagnostic Considerations. • History: • Brief attacks of vertigo and concomitant rotational nystagmus, precipitated by rapid head extension as well as lateral head tilt towards the affected ear. • May be accompanied by nausea, vomiting and diarrhea.

  17. History (cont…) • Episodes lasts for less than a minute and usually 30 seconds. There may not be any H/O an ear related disease.

  18. Diagnostic Considerations. • Most of the patients recover spontaneously (70%). • 20-30% present with recurrent symptoms.

  19. Gold Standard for diagnoses. • Dix Hallpike Maneuver and • The Roll test for lateral SSC.

  20. Important. • Before performing Dix Hallpike test one should perform the vertebral artery test to rule out the possibility of a patient experiencing a basilar artery stroke.(Gans 2001)

  21. Vertebral artery test. • Put the patient in sitting position. • Ask him to push his head forward, • Turn the head to one side, • Pitch the head back.

  22. Vertebral artery test (cont…) • Positive findings: • Persistent dizziness, • Diplopia, • Slurred speech.

  23. Dix Hallpike Maneuver. • Patient is seated at the end of the examination table, • Hold the head, turn it to 45 degrees to the affected side (Rt or Lt) • . The patient is laid down with the head hanging over the edge of the table.

  24. Dix Hallpike Maneuver (cont…) • The briskness of the maneuver is not important • The eyes are observed for nystagmus preferably with Frenzal’s glasses.

  25. Dix Hallpike Maneuver

  26. BPPV Exam

  27. ENG in BPPV

  28. Roll test. • The head is suddenly rolled to RT or Lt sides with the head kept in 30 degree position. • There will be geotropic nystagmus, i.e nystagmus beating toward the down most ear. • If Ageotropic it indicates debris in the opposite ear.

  29. Diagnostic Indicators. • Latency of onset (1-10 sec). • Subjective vertigo, • Posterior canal: Rotary torsional nystagmus beats towards the undermost ear with an upwards bounce or beat. • Anterior canal: Rotary torsional nystagmus beats towards the undermost ear with a downward bounce or beat.

  30. Diagnostic indicators. • Horizontal canal: Geotropic (linear) nystagmus towards the undermost ear. • If the head is kept in the critical position the nystagmus adopts.

  31. Fatigue with repetition. • Canalilithiasis : Yes • Cupulolithiasis : No

  32. BPPV canal involvement. • Posterior Canal 1% • Anterior Canal .1% • Horizontal Canal .01%

  33. Feature of three common BPPV varieties.

  34. Caloric test results. • Normal in most of the cases, but • 30-50% patients may have vestibulopathy. This is indicated by reduced labyrinthine reactivity to caloric irrigation.

  35. Summary of Diagnostic criteria. • History, • Clinical observation of the cardinal symptoms, • Only require Frenzal’s glasses • You may use Infrared video oculography for monitoring the eyes.

  36. Dx: BPPV. (summary) • Hx/Sx: Room spins when rolling on one side (Lt or Rt). Has fallen in drop like attacks. No other complaints. • Dx: SOP –NORM, Audio- NORM, • VAT- NORM, Immittance –NORM, • ENG- Dix Hallpike ABN, ABR- NORM, • Rx/Tx: Liberatory or repositioning Maneuver, • VRT if With vestibulopathy.

  37. Treatment. • Nearly 70% will recover spontaneously and the rest will need some kind of treatment. • Rest of the patients (30%) can be treated with some kind of repositioning or libratory maneuver, depending upon diagnosis (Canalilithiasis or Cupulolithiasis) canal involved and the ear involved.

  38. Pre-treatment evaluation. • Ear Involved • Unilateral • bilateral. • Which canal • Canalilithiasis or Cupulolithiasis.

  39. Pre-treatment evaluation. • Majority of the patients unilateral BPPV. • 90% of the patients have posterior canal involvement. • 90% of the patients will present predominantly with Canalilithiasis.

  40. Treatment (BPPV).. • Pharmacological : BPPV does not respond to anti motion medications. • Surgical: • Singular neurectomy, • Sup.SCC blockade.

  41. Treatment (cont).. • Non surgical: • Habituation – (Brandt & Daroff, 1980). • Liberatory (Semont, 1988). • Epley’s repositioning- (Epley, 1992).

  42. Treatment. • Canalilithiasis is treated mostly by Epley’s Canalilith repositioning maneuver • Cupulolithiasis is treated by Semont' s libratory maneuver. • Gan’s Suggests that all the patients be treated with Epley’s maneuver and only patients who do not respond can be treated with Semont’s maneuver.

  43. Epley’s maneuver

  44. Semont Maneuver

  45. Patient instructions after treatment. • No special instructions are needed except for avoiding tipping of head for an hr.

  46. Brandet Daroff exercise.

  47. Brandet Daroff exercise.

  48. DX/Tx Precautions • History: Cervical injury. • Lower back injury. • Hiatal hernia. • Obesity. • Vertebrobasilar insufficiency. • Select diagnostic & treatment strategy accordingly. • Anxious patients may need TLC and or/medication.

  49. Treatment outcomes: • Goal: Extinguish positional vertigo. • 95% + success with all types of treatments. • 50% also present with vestibulopathy. • Vestibular rehabilitation therapy resolves residual symptoms. • Patients are not told “Learn to live with it”.

  50. Treatment efficacy.

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