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Flashcards in Hearing, Vertigo, ETC... Deck (55):

Sections of Normal Ear



Transduction of Sound

-sound waves propagate in air, enter external auditory canal & bounce off tympanic membrane
-membrane moves malleus, incus, & stapes
-stapes mov. changes the pressure in the fluid filled inner ear and that triggers wave in the basilar membrane of the cochlea
-hearing by bone conduction: bone transmits vibration


Transduction of Sound: at Cochlea

-hair cells with stereocilia are found in the organ of Corti, which rests on the basilar membrane
-hair cells are in contact with the tectorial membrane and are deformed by the traveling wave of sound
-high frequency tones maximally displace the basilar membrane near the base of the cochlea
-as freq. of sound dec., the point of maximal membrane displacement moves toward the cochlear apex
-distortion of the stereocilia on the hair cells causes depolarization of the cell & that results in inc. electrical activity along the auditory nerve


Hearing Loss

-Very common
-all ages
-1/1000 children: sig. hearing loss
-10% of population has some hearing loss
-will inc. as population ages


Causes of Conductive Hearing Loss

-transmission of sound through air is blocked
-may diff. causes: ear wax, foreign object in ear canal, otitis externa, tympanic membrane perforation, otitis media with effusion, otosclerosis


Sensorineuroal Hearing Loss

-Disorders of the cochlear nerve, central pathways
-prebyacusis - age related
-viral - mumps, measles, rubella, CMV, HIV
-ototoxicity: drugs
-meniere's disease
-vestibular Schwannomas (acoustic neuroma)


Mixed Hearing Loss

-Otosclerosis involving the ossicles & the cochlea
-transverse & longitudinal temporal bone fx
-head trauma
-chronic otitis media
-cholesteatoma & middle ear tumors
-some inner ear malformations


Meniere's Disease

-dilated membranous labyrinth (hydrops)
-produces vertigo, fluctuating sensorineural hearing loss & tinntius
-dec. resorption of endolymaphatic fluid causes build-up or hydrops with high pressure, bowing & subsequent rupture in the membranse separating the endolymph from the perilymph
-30min to several hrs until equilibrium is reestablished
-hearing loss persists & gradually worsens
-Treatment: low salt dies & diuretics can be helpful


Clinical Assessment of Hearing Loss

-constant, progressive, fluctuating
-ear discharge
-tinnitus, vertigo
-family history - otosclerosis


Hearing Loss Examination

-pinna (deformity)
-external auditory canal (obstruction)
-tympanic membrane
-middle ear space (aerated)
-pneumatic otoscopy
-Weber & Rinne


Rinne Test

-tell whether air conduction is greater than bone conduction
-normal: patient should hear sound in air after bone stops


Weber Test

place on patients forehead
-if conductive hearing loss: sound will lateralize to that ear


TM Perforation

-common & usually a consequence of infection
-trauma, including barotrauma, can perforate the membrane wall
-deg. of hearing loss depends on the size of hole



-growth of abnormal bone around the otic capsule leads to fixation of the stapes resulting in a conductive hearing loss
-often accompanied by progressive sensorineural component
-starts in 20s to 30s and is bilateral
-family history +
-treatment is observation, hearing aid, or stapedectomy


Vestibular Schwannomas

-Schwann cells, former designation of the tummor is preferable
-Meningiomas also occur in this spot
-present with sensorineural hearing loss & not with vertigo
-compression of the eight cranial nerve is so slow & gradual that the brain has adequate time for central compensation when the vestibular input dec. on one side
-by blocking visual fixation & provoking the semicircular canals, still detect the vestibular abnormality but that is a topic covered in a separate module on vertigo



-20% elderly patients experience is once a year that restricts activity & prompts physician visit
-Presyncope (faintness, lightheadedness)
-loss of balance, unsteadiness of gait
-Vertigo (spinning, swaying, illusion of movement)
-double vision, psychological dissociative feelings, vague sensations (hypoglycemia; drug intox. giddiness)


Dizziness from Orthostatic Hypotension?

-lower body venous pooling (prolonged squatting)
-IV volume depletion
-medication effect
-autonomic neuropathy

-vasovagal reaction (neurocardiogenic syncope)


Dizziness from Heart Diseases?

-ones that dec. cardiac output

-cardiac arrythmia
-congestive heart failure
-obstructed cardiac outflow (aortic valvular stenosis, cardiac tamponade, idiopathic hypertrophic subarotic stenosis (IHSS))
-pulmonary embolism


Gait Imbalance in the Elderly

-neuronal loss due to aging or disease in networks that sub serve:
cerebellar function (stroke, alcoholism)
vestibular function (prior head trauma)
visual orientation (cataracts)
peripheral nerve function (position sense in legs)


Elderly "Dizzy when I walk"

-neuronal loss due to aging or disease in networks that subserve: motor strength (stroke, cervical spondylosis), frontal lobe apraxia, basal ganglia (Parkinson's, Lewy body dis, PSP, MSA), Arthritis & pain (hip & knees), inactivity & fear of falls

-drug toxicity & dehydration


Psychiatric "Disassociation"

-feels distant from the real world
-home stressors
-past/current depression, panic attacks, anxiety, neurosis, psychosomatic personality
-family history of psychiatric disease
-hyperventilation for 3 min to reproduce symptoms (may activate seizure focus)
-neuropsych eval. Minnesota Multiphasic Personality Inventory (MMPI) detects somatization tendencies
-consult psychiatry


"True" Vertigo

-Disease of vestibular system (central & peripheral)
-illusion of movement (whirling, spinning, swaying)
-often accompanied by nausea & vomiting
-Nystagmus (clinical sign): fast & slow components, defined by fast component (saccade), brain suppresses visual blur during saccade, vision possible only during slow phase of eye movement, room spinning to right to slow phase to left



-spin around the z-axis


Specialized Vestibular "organs" act as motion transducers for?

-Translational motion (linear around x, y, z)
-Rotational motion (angular around x, y, z)


How does the vestibular system monitor position?

-detecting angular (rotational), static & linear acceleration with specialized motion detectors



-coplaner with the vertical axis
-detect static head positions & linear accelerations in plane



-coplaner with the horizontal axis
-detect static head positions & linear accelerations in plane


What does the ampulla detect?

-rotational acceleration or deceleration within the plane of the canal



-located inside ampulla transduce this information for each semicircular canal



-tallest cilia in ear
-depending on how it's bent, potassium channels in the tips of other cilia either open or close
-cilia project into endolymph that is rich in potassium, K influx depolarizes the cell membrane which then activates Ca channels that open only when the membrane is depolarized
-Ca influx activates Ca dep. K pumps that extrude the K into the K poor perilymph
-allows for electrical resonance of the membrane to shift up or down in frequency & to modulate the conc. of Ca at the hair cell base
-a rise in local Ca conc. triggers release of neurotransmitter


Hair Cells in Utricle

-highly organized so that the kinocilium faces a midline valley called the stroila
-mirror like arrangement
-orientation curves by 90 deg. so that every movement in a 2D plane will be covered
-head in neutral position, utricle is coplanar with ground


Utricle Kinocilia Orientation

-toward the striola


Saccule Kinocilia Orientation

-away from the striola


Vestibular System & Eye Movements

-net inc. in firing from the left vestibular apparatus via Scarpa's ganglion causes the eyes to move to the right
-acts as "pushing" muscle directing the eyes to the center, if one side is weak, the normal side will push the eyes toward the weaker side

-if head suddenly turned left, the left horizontal semicircular canal will be stimulated & the right canal will be inhibited (reflex movement of eyes to right so that point of visual fixation is maintained: vestibulo-ocular reflex)


Movement of Endolymph in the Canal

-cause either stimulatory or inhibitory response


"True" Vertigo

-disease of one vestibular apparatus, 8th cranial nerve, vestibular nuclei, & associated pathways
-uneven vestibular tone on eyes
-ocular drift toward side of lesion (slow phase nystagmus)
-mismatch with other sensory info. reaching cortex
-corrective saccade from frontal eye fields (fast component of nystagmus)
-Repetitive cycles (Nystgums - sign of vergigo)
-Illusion of movement (whirling or spinning)
-often accompanied by nausea & vomiting


Gaze-Evoked Horizontal Nystagmus

-with extreme lateral gaze, normal people may show a few beats of nystagmus or even sustained nystagmus
-induced with alcohol, sedatives, & anticonvulsant meds
-direction change
-no vertigo


Ice Water Calorics

-ice water in external auditory canal causes a drop in the tonic vestibular firing rate
-other ear continues to fire at baseline rate (2 sides are unequal now)
-normal side pushes the eyes toward the side of ice water irrigation


Motion Sickness

-mismatch b/w what eyes report to brain & the vestibular feedback
-induces vertigo, nausea, & vomiting
-visual fixation suppresses vertigo due to vestibular-visual imbalance or mismatch


Frenzel Lenses

-20 diopter lenses eliminate visual fixation
-magnify & illuminate the eyes


History for Dizziness

-time course
-effect of position, triggers?
-History & Review of Systems: otologic, cardiac, psychiatric, neurological
-Drug toxicity:
anti-HTNs, dopamine agonist - orthostasis
sedatives & anticonvulsants - gait dysequilibrium
amninglycosides - otoxocity


Physical Exam for Dizziness

-Cardiac Murmurs & Arrhythmias
-Visual loss
-peripheral sensory loss
-gait disturbance
-brainstem/cranial nerve deficits associated with central vertigo


Neuro-otoogic Exam

-inspect tympanic membranes
-check hearing, Weber & Rinne tests
-Extra-ocular eye movements: nystagmus
-Thwart visual fixation (Frenzel lenses, cover the visually fixating eye during funduscopy)
-Maneuvers that provoke & detect vestibular imbalance: head thrust maneuver, head shaking nystagmus, Dix-Hallpike maneuver


How to see subtle nystagmus without Frenzel lenses?

-close other eye during funduscopy, to eliminate visual fixation and watch the optic disc jiggle


Head Thrust Maneuver

-tests for dec. in the vestibulo-ocular reflex or VOR
-sudden turn of the head stimulates one horizontal semi-circular canal while inhibiting the other
-this causes a reflex compensatory movement of the eyes in the opposite direction via the pathways shown eariler


How to stimulate the horizontal semi-circular canals?

-tilt head forward 30deg. to make the canals coplaner with the floor
-start continuous side to side shaking for 20 sec. then stop


Semicircular Canals

-Posterior, Anterior, Horizontal (right & left)


Dix-Hallpike Maneuver

-to maximally stimulate the left posterior canal & inhibit the right anterior canal, the head is turned to the left by about 45 deg. and the patient lies down backwards from a sitting to a lying position


Peripheral Vertigo with Nystagmus: Dix-Hallpike

-5-20 sec. latency of onset
-subsides over 1-2min (improves w/visual fixation)
-Nystagmus inc. with gaze away from lesion
-Usually mixed horizontal (torsional (horizontal predominating))
-Habituates with repetition


Central Vertigo with Nystagmus: Dix-Hallpike

-no latency of onset
-Sustained with position (does not improve with visual fixation)
-no inc. but may change direction with change of gaze
-usually single plane nystagmus (horizontal, vertical or torsional)
-does not habituate
-other brainstem deficits


Benign Paroxysmal Positional Vertigo (BPPV)

-Dix-Hallpike makes diagnosis
-otoconia embedded in utricle break free of the gelatinous membrane with age or trauma, the post. semicircular canals are the most dependent during sleep these displaced particles (Ca carbonate) collect in these canals (1 or both), forms sludge that can plug up canal lumen so when head movement involves affected post. canal there is a slump-like action that produces greater pressure than normal
-causes greater distortion of the cupula in the ampulla & the canal signals the brain that the head has rotated posteriorly faster & more than it has

-vertigo starts 5-10 sec. after head movement and lasts for 30-45 seconds


How is Benign Paroxysmal Positional Vertigo Cured?

-canalith reposition (Epley) maneuver



-less common cause of BPPV
-particles can reach the cupula & cause distortion there


Vestibular Neuritis

-Postulated viral infection (HSV1 viral reactivation)
-Severe Vertigo, nausea, vomiting
-Gait: veers toward affected ear early-on
-Positional changes not tolerated
-Ice-water in normal ear provides immediate (temporary) relief
-Labyrinthitis is the term used if hearing is also affected


Vestibular Neuritis Symptomatic Relief

-benzodiazepines, meclizine, scopalamine patch, antiemetics
-IV Methylprednisolone speeds recovery
-central compensation over 1-2 weeks