This document provides an overview of benign paroxysmal positional vertigo (BPPV), including its causes, symptoms, diagnosis, and treatment. It describes the anatomy and physiology of the peripheral and central vestibular systems. BPPV is caused by loose calcium carbonate crystals, called canaliths, becoming trapped in the semicircular canals. It is diagnosed using the Hallpike-Dix maneuver to provoke nystagmus. Treatment involves repositioning maneuvers like the Epley maneuver to dislodge the canaliths.

1. Benign Paroxysmal Positional Vertigo (BPPV) Amy Flory PT NAUPT 04/20/09

2. Peripheral vestibular anatomy Semi-circular canals 3 SSC, oriented at right angles to each other. Membranous, filled with endolymph, surrounded by perilymph. The ampulla contains sensory cells projecting into the gelatinous cupula.

4. Peripheral vestibular anatomy Otolith organ anatomy Utricle and saccule are oriented at right angles to each other. Sensory hair cells contained within the macula project into the otolithic membrane. The otolithic membrane is embedded with calcium carbonate crystals, called otoconia, or otoliths.

5. Peripheral vestibular anatomy The vestibular nerve is composed of the superior and inferior nerves exiting the vestibular apparatus. The superior nerve carries information from anterior and lateral SSCs and the otolith organs. The inferior nerve carries information from the posterior SSC and the saccule.

6. Periph. Vest. afferent physiology The sensory receptors of the vestibular nerve are directionally oriented. The six SSCs are paired such that each pair is sensitive to motion within one plane of 3D space. Matched pairs respond to angular acceleration in an “equal-opposite” fashion.

7. Periph. Vest. afferent physiology Vestibulo-ocular reflex (VOR) Vestibular apparatus afferents synapse in vestibular nuclei, then through MLF to Abducens and Oculomotor nuclei, resulting in gaze direction same as endolymph movement. Enables gaze stabilization on a stationary target during head movement (image stabilizer)

8. Central vestibular anatomy The vestibular nuclear complex: 4 “major” nuclei and >7 “minor” nuclei. The nuclei are connected with cerebellum, reticular formation, spinal cord, and eye movement systems.

9. Central vestibular efferent anatomy Medial vestibulospinal tract: originates from medial, superior, descending vest. nuclei and descends bilaterally to the cervical spinal cord in the MLF Mediates postural change in response to SSC input (stabilizes head position)

10. Central vestibular anatomy Lateral vestibulospinal tract: originates from lateral vest. nucleus and descends to the anterior horn cells in the spinal cord Mediates postural changes in response to cerebellar and otolithic input (compensates for head tilts and body movements)

11. Central vestibular anatomy Cervical spinal proprioceptive input Mostly from facet joints and capsules Less so from deep paraspinal muscles None from superficial muscles and skin Luxon, LM. Vertigo: new approaches to diagnosis and management. British Journal of Hospital Medicine. 1996;56(10):519-520.

12. Central vestibular physiology Varied and widespread vestibular nuc. connections enable postural corrections in different situations (e.g. the postural correction used when the otolithic organs are stimulated is different when the head is forward vs. when it’s turned to the side)

13. Central vestibular physiology Vestibulo-spinal reflex Actually many different reflexes, depending on state of system (static, tonic, dynamic). Example: head tilt to one side results in extensor activity ipsilaterally and flexor activity contralaterally while in stance.

14. Central vestibular physiology Smooth pursuit Maintains gaze on a moving target Subject follows one finger in 30-40° arc for 2-3 seconds in each direction Saccades Ballistic eye movements to bring a periph. visual object to the fovea in shortest possible time Subject fixates on target 40° from center on command;3-10 seconds before repeating

15. Central vestibular physiology Nystagmus Slow phase (peripheral component) is in opposite direction of perceived head-on-body rotation. Fast phase (central component) is in same direction of perceived head-on-body rotation. Spontaneous nystagmus usually a central finding, unless <1 week since onset

16. Benign Paroxysmal Positional Vertigo (BPPV) Cause of 40% of peripheral vestibular cases Diagnostic criteria Nystagmus is predictably produced Paroxysmal nystagmus (immediate to <10 sec onset with provoking position) Symptoms experienced while nystagmus is present Fatiguing symptoms and nystagmus Latency of several seconds Positionally provoked

17. BPPV: Etiology & Presentation Cupulolithiasis Canaliths adhered to the cupula Immediate onset of symptoms in provoking position May continue >1 minute Eases with return to upright

18. BPPV: Etiology & Presentation Canalithiasis Canaliths floating freely in the SSC endolymph Latent onset of symptoms in provoking position Usually fatigues within 1 minute Repeats (and reverses) on return to upright

19. BPPV: Hallpike-Dix test Patient in long-sitting Head turned to testing side “Lie back as quickly as you can” End position: supine, head 30° below horizon Hold position up to a minute without symptoms

20. BPPV: Variants Posterior canal Most common form Nystagmus is torsional and geotropic toward involved ear in Hallpike-Dix test Horizontal/lateral canal 10% of BPPV cases Nystagmus is horizontal; may not be provoked with H-D test (use supine head turns)

21. BPPV: Treatment Canalith repositioning Maneuvers by the therapist in the clinic; inc. Epley, Modified Liberatory, Semont, BBQ roll, etc.. Exercises done by the patient at home, TID; inc. Brandt-Daroff exercises, BBQ roll and variants

22. BPPV: Treatment Cupulolithiasis Semont maneuver Other repositioning maneuver with mastoid vibration or oscillation Brandt-Daroff exercises Canalithiasis Canalith repositioning maneuver Brandt-Daroff exercises

23. Canalith repositioning maneuvers Goal is to float debris from SSCs and cupula back into utricle Timing strategy applied to positioning sequence to approximate migration rate of debris All are based on the Epley maneuver

24. Modified Liberatory Maneuver (modification of Epley Maneuver) Patient is quickly moved into H-D position, affected side down; supported there for 4 minutes. Turn head slowly (30-45 sec) to opposite H-D position. Hold 4 minutes. Patient rolls onto unaffected side, nose pointed to floor, for 30 seconds. Return slowly to sitting, then rotate head to face forward, chin slightly tucked.

25. Post-maneuver instructions For 48 hours following maneuver Avoid looking up or down Avoid lying below 30 degrees above horizontal For 7 days following maneuver Avoid lying on affected side Avoid turning head toward affected side while supine

26. Thank you! Amy Flory PT CoreBalance Therapy LLC www.corebalancetherapy.com 928-556-9935