Vestibular System and Vertigo Flashcards
Anatomical substrate for the transduction of sound
External ear carries the sound in to the tympanic membrane. It vibrates, transfers sound to the ossicles which vibrate against the oval window. Moves the fluid in the cochlea which vibrates the basilar membrane (base [high F]–>apex [low F]) and bends the stereocilia on the hair cells in the organ of corti. Influx of K causes depolarization, translates this to a Ca influx on the basilar side of the cell, which is sensed by the auditory nerve.
Conductive vs. Sensorineural hearing loss
Conductive - [external/middle ear problem] something’s blocking the external ear, like wax or foreign object
Sensorineural - [internal ear problem] something that’s affecting the hair cells or the auditory nerve
Can also be mixed - involves pathology affecting middle and inner ear simultaneously like trauma, otosclerosis, congenital malformation, infection and tumors
Signs and symptoms of hearing loss
- complaints of hearing difficulty
- check for structural abnormalities, discharge, pain, etc.
- Weber and Rinne tests reveal conduction issues
- audiogram can quantify frequency of sound that’s impaired
Causes of hearing loss - conductive
- infection, inflammation, perforation of tympanic membrane, otosclerosis (which is bony overgrowth of stapes, ossicles to stiffen, failure to transmit vibrations to cochlea)
- try plugging one ear and see what it sounds like - Weber lateralizes here and BC>AC in Rinne test
Causes of hearing loss - sensorineural
- damage to hair cells in organ of corti from very loud noise, infection, ototoxic meds, temporal bone fracture, or Meniere’s disease
- age-related hearing loss is progressive and called presbycusis
- vestibular schwannoma, and tumors of cerebellopontine angle that compresses CN8
Why do you not really see hearing loss in strokes or patients who suffer other structural damage (like demyelinating disorder)?
- CAN occur but there’s so much crossover of tracts between CN8 and the MGN, and ultimately Heschl’s gyrus
- this redundancy protects against unilateral hearing loss (not the case with other sensory modalities like vision as we know)
Meniere’s disease
- disorder of decreased fluid resorption in the labyrinth, resulting in hydrops/increased pressure and rupture of membranes that would otherwise separate the endolymph and perilymph
- mixture of the 2 fluids (of diff concentrations) produces a sudden change in the VC pressure and electrical firing properties
- produces vertigo, fluctuating sensorineural hearing loss which is progressive; sx remit and relapse
- tx with low-salt diet, diuretics, and vestibular sedatives (anti-ACh, BZDs, anti-histamines) may help during attack
Audiogram for:
- conductive hearing loss
- sensorineural hearing loss
- Meniere’s disease
- otosclerosis
- middle ear effusion
- conductive: uniform increase in threshold for hearing all frequencies
- sensorineural*: higher threshold on higher frequencies
- but noice-induced HL is selective for 4000Hz compared to all other frequencies
- otosclerosis: higher threshold for lower frequencies (early on) because of stapes fixation
- Meniere’s disease: higher threshold for lower frequencies (early on)
- effusion: higher threshold for higher frequency
Tumors of the cerebellopontine angle
- Vestibular schwannoma (contrast-enhancing)
- meningiomas also occur here
These typically present as typically present as hearing loss and not vertigo because it compresses the nerve slowly enough that the brain can compensate for the unilateral decrease in vestibular input. They also can cause obstructive hydrocephalus if they compress the 4th ventricle, or ispilateral cerebellar dysfunction from compression of cerebellar peduncles.
Vertigo vs. dizziness
Vertigo = spinning, swaying, illusion of movement; 'true' vertigo will include N/V/nystagmus Dizziness = can encompass pre-syncope, loss of balance, unsteadiness, double vision, psych dissociative feelings, vague sensations
Central vs. peripheral vertigo
- peripheral has 5-20s delay (upon reclining) to onset of vertigo/nystagmus; improves in 1-2min, with visual fixation, and on repetition
- central: no latency of onset; no improvement with fixation or repetition
Benign Paroxysmal Positional Vertigo (BPPV)
- otoconia break free from the gelatinous membrane (with trauma or age) in utricle
- usually land in the posterior SCC (because of position during sleep)
- the otoconia forms a plug and, upon stimulation of the affected SCC, creates sump-like pressure which increases the signal from the ampulla
- this makes the pt feel like the head has rotated faster and to a greater extent than it actually has
- usually benign and self-limited
- can be cured by Epley maneuver
Common causes of peripheral and central vertigo
Periph > Central
- Peripheral: BPPV (MCC), neuronitis, Meniere’s disease
- Central: vestibular neuritis, MS, stroke, migraines, tumor, injury, infection, TIAs
Nystagmus
Fast phase (defines directionality) = corrective saccades from FEF; cortex ignores this visual information Slow phase = drift from the stronger vestibular system pushing toward midline; this information is seen and this is the 'direction' they see the world spin **A right beating nystagmus means the world is seen spinning to the right
4 possibilities when a patient says “I am dizzy”
- vertigo: sensation of motion; vestibular
- presyncope: sensation of impending faint; cardiovascular
- disequilibrium: neurologic
- ill-defined giddiness: psychiatric disorder
