Pathophysiology/Physiology

• What are the vestibular reflexes?

  Vestibulo-ocular

  Vestibulospinal

  Vestibulocollic
• What does the vestibulo-ocular reflex do?

  Keeps gazed fixed
• Pathway of vestibulo-ocular reflex?

  Vestibular information transmitted down vestibulocochlear nerve → to medial vestibular nucleus → communicates with nuclei of CN III, IV & VI → coordination of eye movement in order to counteract head movement (e.g. being able to focus on a single point whilst moving your head)
• What does the vestibulospinal reflex do?

  Stops you from falling over (innervates spinal cord LMNs)
• What does the vestibulocollic reflex do?

  Keeps your head up (innervates cervical LMNs)
• What is the pathway of vestibulocollic & vestibulospinal reflexes?

  Vestibular information is transmitted down VIII to the medial & lateral vestibular nuclei → project to & from cerebellum & down the spinal cord (through lateral & medial vestibulospinal tracts)

  Tracts mediate the vestibulocollic & vestibulospinal reflexes
• Vestibular sensation -> otolithic organs

  Tilt (linear) → otolithic membrane moves due to gravity → movement of stereocilia (within gelatinous cap) → opening of K+ channels → depolarisation → opening of voltage-gated Ca+2 channels → glutamate release → afferent neurons project to vestibular nuclei in the brainstem → vestibular nuclei project to multiple nuclei in the thalamus → project to distributed network of cortical areas involved in conscious vestibular sensation (lots of different areas which contribute to sense of self in space)
• What are the otolithic organs?

  Utricle & saccule
• Vestibular sensation -> semicircular canals

  Tilt (rotation) → endolymph moves due to gravity → moves gelatinous cupula → stereocilia detect displacement of endolymph → opening of K+ channels → depolarisation → opening of voltage-gated Ca+2 channels → glutamate release → afferent neurons project to vestibular nuclei in the brainstem → vestibular nuclei project to multiple nuclei in the thalamus → project to distributed network of cortical areas involved in conscious vestibular sensation (lots of different areas which contribute to sense of self in space)
• Phys hearing

  Sound waves in external acoustic meatus → TM vibrates → ossicles amplify waves → movement of oval window → sound waves through endolymph → basilar membrane vibrates → movement of stereocilia on hair cells → opens K+ channels → depolarisation → opens voltage-gated Ca+2 channels → glutamate release → projections to auditory branch on CN VIII → terminate on cochlear nuclei → cochlear neurons project to superior olive (ipsi- & contralateral) in pons → through lateral lemniscus to inferior colliculus (midbrain) → to medial geniculate nucleus (MGN) in thalamus → primary auditory cortex
• Define conductive hearing loss.

  Due to damage to the outer or middle ears, results in lack of conduction of sound to the cochlea
• Define sensorineural hearing loss.

  Due to defect in the sensory hair cell detection within the cochlea, or the neural coding detection by primary sensory neurons located in the spiral ganglion that project down the cochlear nerve
• What are the common causes of sensorineural hearing loss?

  Sudden sensorineural hearing loss (SSHL)

  Noise-induced hearing loss

  Presbycusis

  Vestibular schwannoma
• What are the common causes of conductive hearing loss?

  Any obstruction to ear canal (e.g. foreign body)

  Perforation of TM

  Fluid in the middle ear (e.g. otitis media, glue ear)

  Any disruption of ossicles (e.g. trauma)
• Pathophys of congenital cholesteatoma

  Rare

  Fragment of keratinized epithelial cells retained after birth → remnants form epithelial tissues (white & cyst-like) behind TM → cholesteatomas grow & invade the neighbouring bones & tissues (esp, air spaces in bone)
• What is cholesteatoma?

  An abnormal sac of keratinising squamous epithelium & accumulation of keratin within the middle ear or mastoid air cell spaces
• Pathophys of acquired cholesteatoma

  Eustachian tube dysfunction → negative pressure in middle ear → pocket of TM retracts into middle ear → squamous epithelial cells in pocket (only line the outer surface of TM) get pulled in → cells start hyperproliferating due to being in an abnormal environment → hyperproliferative cells secrete enzymes which can damage middle ear structures → can lead to permanent hearing loss
• Pathophys of otitis media with effusion

  Involves dysfunction of Eustachian tube (becoming obstructed or fails to function properly) → negative pressure relative to atmosphere → middle ear secretes fluid → fluid accumulates in middle ear space (may contain pathogens or leukocytes → further inflammation)
• What are the factors that can initiate Eustachian tube dysfunction?

  Allergies

  Chronic/recurrent infections of upper respiratory tract

  Exposure to cigarette smoke or other irritant

  Immune dysfunction
• What are the complications of otitis media with effusion?

  Conductive hearing loss

  Speech & language development issues & communication skills difficulties

  Chronic damage to TM
• What are the complications of cholesteatoma?

  Brain abscess

  Hearing loss

  Facial nerve damage

  Meningitis
• How does cholesteatoma affect the hearing pathway?

  Cholesteatoma has capacity to erode bone -> can lead to hearing loss by destroying ossicles
• What are the risk factors associated with cholesteatome recurrence?

  < 15 years old

  Cholesteatoma localised to mastoid

  Stapes erosion

  Incus erosion
• What are the 3 types of otitis media?

  Acute otitis media

  Chronic otitis media

  Otitis media with effusion
• How do we hear our own voice?

  Bone condution -> bypass eardrum, directly to cochlear
• Whre should the light reflex be on the TM?

  Should be a cone in the anterior inferior quadrant
• What are the 8 organs of speech?

  Lips

  Teeth

  Alveolar ridge

  Hard palate

  Soft palate

  Uvula

  Glottis

  Tongue
• How does cholesteatoma damage the tegmen?

  Cholesteatoma grows -> releases MMPs -> breakdown of ECM of tissues & bones

  Chronic inflammation associated with cholesteatoma -> production of ROS & activation of osteoclasts (via RANK-L)

  Inflammation & mechanial stress on the bone as the cholesteatoma grows, contributes to thinning of tegmen
• What happens if the tegmen is breached?

  Can cause number of problems…

  • CSF leaks
  • Meningitis
  • Brain infections
  • Hearing loss/tinnitus
• What are the 3 stages of speech production?

  Initiation

  Phonation

  Articulation