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Subjective Tinnitus - Pathophysiology and clinical findings

Vestibular Neuritis

Vestibular Neuritis: Pathogenesis and Clinical Findings Authors: Ryan Chan Jonathan Wong Reviewers: Mehul Gupta Davis Maclean Saud Sunba Yan Yu* Euna Hwang* * MD at time of publication Recent viral illness or upper respiratory tract infection Virus spreads along upper respiratory mucosa and into the inner ear structures Vestibular Neuritis Presumed idiopathic viral-induced inflammation of the vestibular nerve; typically unilateral Reactivation of Herpes Simplex Virus-1 in vestibular (Scarpa’s) ganglion Inflammatory cell infiltration leads to degeneration and atrophy of the vestibular nerve Superior Vestibular Neuritis (40-48%) Inflammatory cells traverse through only one long bony canal, easier for inflammatory cell infiltration Loss of afferent innervation from the superior and horizontal semicircular canal (SCC), utricle, and parts of the saccule Combined Superior Vestibular Neuritis and Inferior Vestibular Neuritis (34-56%) Inferior Vestibular Neuritis (1.3-18%) Inflammatory cells must pass through two separate bony canals, making inflammatory cell infiltration more difficult Loss of afferent innervation from the posterior semicircular canal (SCC) and saccule Utricular degeneration Displacement of otoliths/ otoconia (commonly into the posterior SCC) BPPV (can occur several months after onset of neuritis) Loss of horizontal SCC afferent neuron signaling to the brain Unilateral Loss or ↓ of normal nystagmus response to Caloric Testing (insertion of cold and warm water/air into the ear canal while supine) Loss of utricular afferent neuron signaling to the brain ↓ or absent Ocular Vestibular- Evoked Myogenic Potentials (VEMPs) and Normal Cervical VEMPs ↓ unilateral vestibular input to the brain leads to acute phase symptoms (over time, brain can compensate which allows for some symptom improvement) Loss of posterior SCC and saccular afferent neuron signaling to the brain ↓ or absent Cervical VEMPs, but Ocular VEMPs are normal ↓ or absent input to the ipsilateral vestibular nuclei elicits a vestibular nucleus response similar to contralateral SCC excitation Acute-Phase Spontaneous Nystagmus Fast phase beats away from the affected side (3- 10 days) And Loss of ocular fixation on Head Impulse Test ↓ or absent saccular input to the lateral vestibular nuclei (e.g., lateral vestibulospinal tract) results in the loss of lower limb postural adjustability Postural Instability (e.g., abnormal Romberg/sharpened Romberg, Fukuda step test) Bilateral mismatch of vestibular information to the brain Peripheral Vertigo (lasts several hours to days; rapid onset, severe, constant) Nausea and Vomiting Only the vestibular part of the vestibulo- cochlear nerve is affected, not the cochlear nerve No Hearing Loss or Tinnitus Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 19, 2021 on www.thecalgaryguide.com

BPPV

Benign Paroxysmal Positional Vertigo (BPPV): Pathogenesis and Clinical Findings Authors: Ryan Chan, Jonathan Wong, Mehul Gupta, Yan Yu* Reviewers: Davis Maclean, Saud Sunba, Euna Hwang* * MD at time of publication Up-beating, torsional geotropic (towards the ground) fast-phase nystagmus (towards affected side) Down-beating +/-torsional fast-phase nystagmus (towards opposite side) Idiopathic Older Age Head trauma Recent Ear Surgery Underlying Vestibular Disorders/Infections: Meniere’s Disease, Vestibular Neuritis, Labyrinthitis Risk Factors of Labyrinth Ischemia: Hypertension, Hyperlipidemia, Migraines Dislodged otoliths/otoconia from the macula of the utricle Posterior Canal BPPV (~95-99%) Superior Canal BPPV (~1%) Horizontal Canal BPPV (~5-20%) Ocular muscles are stimulated to generate a downward, torsional slow-phase movement Ocular muscles are stimulated to generate an upward, torsional slow-phase movement Cupulolithiasis Theory: Otolith adheres to cupula of the semicircular canal (SCC) Otolith displaces the cupula during head position changes resulting in prolonged sense of head rotation along the semicircular canal axis OR Canalithiasis Theory: Free-floating otolith in the semicircular canal (SCC) Otolith induces inertial drag of the endolymph fluid during motion, displacing the cupula, resulting in prolonged sense of head rotation Dix-Hallpike Maneuver: Sitting with head rotated laterally (45°), moving quickly to supine with head extended 30° off table. Observe for any nystagmus. Direction of nystagmus indicates which of the three semicircular canals is affected. Ocular muscles are stimulated to generate a horizontal slow-phase movement away from affected side Horizontal Nystagmus: Fast phase beats toward the affected side Supine Head Roll Test: lying supine, roll head laterally to each side to move otoliths along horizontal SCC axis BPPV: Episodic, positional bouts of vertigo and nystagmus not due to an underlying neurological or insidious reason If the otolith is free-floating in the SCC, movement of the affected ear towards the table generates a net stimulatory endolymph flow in the affected horizontal SCC The stimulatory signal is carried to brainstem nuclei, generating a reflexive slow movement of the eyes away from the affected ear, and quick horizontal movements back towards the affected ear Geotrophic Horizontal Nystagmus: fast-phase nystagmus beats horizontally towards the table If the otolith is adherent to the SCC cupula, movement of the affected ear towards the table generates a net inhibitory deflection of the horizontal SCC cupula The inhibitory signal is carried to brainstem nuclei, generating a reflexive slow movement of the eyes towards the affected ear, and quick horizontal movements away from the affected ear Apogeotropic Horizontal Nystagmus: fast-phase nystagmus beats horizontally towards the ceiling Otoconia & otoliths only affect the semicircular canal (SCC), not the cochlea No tinnitus or hearing loss Otoconia tend to settle quite quickly (<1 min) when body is still, resolving the mismatch of body movement & semicircular canal (SCC) excitation Vertigo and nystagmus is transient (lasting ~1min or less) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 9, 2022 on www.thecalgaryguide.com