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Peripheral Vestibular Dysfunction

Peripheral Vestibular Dysfunction: Pathogenesis, mechanisms, & clinical findings Preceding viral illness or bacterial infection Vestibular structure pathologies Impaired resorption of endolymph (inner ear fluid involved in hearing & balance) in the membranous labyrinth (fluid-filled chambers & ducts in the inner ear) ↑ Humoral & cellular immune responses in the inner ear cause nerve inflammation Otoconia (calcium carbonate crystals in the inner ear) dislodge & migrate into the ear’s semicircular canals Direct entry of pathogens via oval or round window (membrane-covered openings between the middle & inner ear) Hematogenous (through blood) or subarachnoid space infection ↑ Accumulation of endolymph distends the membranous labyrinth & produces ↑ pressure on inner ear structures Dislodged otoconia cause differences in endolymph flow & subsequent asymmetric hair cell movement Ménière’s disease Endolymphatic hydrops (abnormal endolymph buildup in the inner ear) Vestibular hyperactivity & mismatched visual sensory input activates the histaminergic neuronal system in the hypothalamus Histaminergic neurons send activation signals to histamine H1 receptors in the brain’s vomiting centre Activation of H1 receptors stimulates the chemoreceptor trigger zone in the vomiting centre Nausea** Vomiting** Legend: ↑ Cytokines (immune chemical messengers) ICAM-1 & IL-1β recruit additional immune cells to the inner ear & further ↑ immune responses Activation of immune cells within inner ear Benign paroxysmal positional vertigo** Breakdown of the inner ear blood-labyrinth barrier Autoimmune inner ear disease (e.g., Cogan’s syndrome, granulomatosis with polyangiitis, systemic lupus erythematosus) Systemic manifestations of autoimmune disease (e.g., rash, joint pain, eye inflammation) Labyrinthitis (membranous labyrinth inflammation) Vestibular neuritis (inflammation of the vestibular nerve) Peripheral Vestibular Dysfunction Pathology of the inner ear & vestibular portion of the vestibulocochlear nerve Central nervous system receives dysregulated visual inputs, vestibular inputs, & proprioceptive (body positioning) inputs ↑ Damage to the hair cells (sensory receptors) in the inner ear ↑ Damage to the vestibulocochlear nerve Loss of nerve input from the vestibulocochlear nerve causes abnormal neuronal activity in the auditory cortex Asymmetric, mismatched, or contradictory sensory inputs cannot be properly interpreted by the brain Damaged hair cells cannot convert sound or movement into appropriate electrical signals for vestibulocochlear nerve transmission Brainstem & auditory cortex receive ↓ or no auditory signal input from the vestibulocochlear nerve Abnormal neuronal activity & nerve signals may be misinterpreted by the auditory cortex as sound Sensorineural hearing loss Dizziness Vertigo (abnormal sensation of spinning or movement) Subjective tinnitus** (continuous or intermittent perception of ringing or buzzing without an acoustic stimulus) Published November 23, 2025 on www.thecalgaryguide.com Vestibulocochlear nerve pathologies NF2 gene encodes for functional schwannomin (cell structure protein involved in suppressing tumour growth) Point mutations & loss of heterozygosity in the NF2 gene result in ↓ or absent schwannomin Schwann cells (cells protecting nerve fibres) form a protective myelin sheath on the vestibulocochlear nerve Schwann cells malfunction in the absence of schwannoma & the myelin sheath is compromised Vestibular schwannomas (benign tumours on the vestibulocochlear nerve) develop in the absence of functional schwannomin Asymmetric vestibular input disrupts the nerve inputs sent to the oculomotor nuclei (brainstem nerve cells responsible for muscles involved in eye movement) Triggers an abnormal vestibulo-ocular reflex (normal reflex keeps vision steady while the head moves) Authors: Nystagmus (repetitive & uncontrolled eye movements) Fariha Rahman Farah Ali Reviewers: Vaneeza Moosa Jessica Revington Gabrielle Juliet French* * MD at time of publication **See corresponding Calgary Guide slide Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications