Test 2: Auditory & Vestibular CC (these go together in my brain) Flashcards
Conductive deafness
- What is it
- **What causes it? **
- Deafness from obstruction–sound doesnt reach the tympanic membrane or cross the middle ear properly
- Causes: occlusion, middle/outer ear infection, OTOSCLEROSIS, temporal bone fracture (damage to ossicles)
Sensorineural deafness
- deafness from nerve damage
- Caused by: lesion to cocheal, cochlear portion of CN VIII, prolonged noise exposure, some antibiotics, infections or tumors, inner ear infection or labyrinithitis
What kind of deafness is caused by
- Otitis externa
- otitis media
- otitise interna
- Conductive deafness
- Conductive deafness
- sensoorineural deafness
Otosclerosis
- What is it (how does it happen?)
- **What kind of deafness does it cause? **
- tissue overgrowth that causes fixation of the stapes in the oval window
- **CONDUCTIVE **hearing loss 50% of the time.
What would happen if a bug got into your ear and ate up all you hair cells?
You’re screwed. hair cells DO NOT REGENERATE.
- What is the Rinne Test?
- What does it test?
- What is the normal response? what is a positive Rinne test?
- Negative Rinne test?
- Vibrating tuning fork is placed on mastoid process and then it is moved to the air in front of the ear
- Compares air vs bone conduction
- Normal: Air conduction should be greater than bone conduction. AC>BC= positive rinne test= normal
- Negative: Bone conduction>Air conduction **indicating conduction deafness on that side. **
- **What is the Weber’s test? **
- What does it test
- Normal response?
- Abnormal?
- Vibrating tuning fork is placed on the vertex of the head.
- Nerve or conduction deafness
- Normal: patient hears equally on both sides
- If the sound is louder on one side, that is indicative of ipsilateral conduction deafness OR contralateral nerve deafness.
You do a Rinne test and Weber test on a patient and find
- Weber: Right ear lateralization
- **Rinne: **BC>AC on Right, AC>BC on left
DDx?
Weber test tells us either: Conduction deafness in right ear OR nerve deafness in left ear
**Rinne test: **Conduction deafness on Right
_Diagnosis: conduction deafness in right ear _
You do a Rinne test and Weber test on a patient and find
- Weber: Left ear lateralization
- **Rinne: **BC>AC on Left; AC>BC on right
DDx?
Weber test tells us either: Conduction deafness in left ear OR nerve deafness in right ear
**Rinne test: **Conduction deafness on left.
Diagnosis: conduction deafness in left ear
You do a Rinne test and Weber test on a patient and find
- Weber: Right ear lateralization
- **Rinne: **Positive in both ears
DDx?
Weber test tells us either: Conduction deafness in right ear OR nerve deafness in left ear
Rinne test: (positive= AC>BC= normal) No conduction hearing loss
_Diagnosis: nerve deafness in left ear _
You do a Rinne test and Weber test on a patient and find
- Weber: Left ear lateralization
- **Rinne: **AC>BC both ears
DDx?
Weber test tells us either: Conduction deafness in left ear OR nerve deafness in right ear
**Rinne test: **No conduction hearing loss
_Diagnosis: nerve deafness in right ear _
Stria vascularis-
- what is it?
- Damage causes?
- Stria vascularis changes the endolymphatic potential via selective absorption and secretion of ions.
- Loss of endolymphatic potential = failure of mechanoelectrical transduction
How can you monitor cochlear function?
**Cochlear microphonic= **Recording stimulus-related changes in electrical potential between the perilymph and haircells
Treatment for **sensorineural hearing loss? **How does it work?
Cochlear implants- wire electrodes are tuned to specific frequencies and implanted so that each wire stimulates the appropriate nerve terminal in the cochlear spiral.
Cochlear damage causes ________ hearing loss and may cause ______.
Cochlear damage = sensorineural deafness and may cause tinnitus.
Monaural Deafness- What is it? Where’s the lesion?
- Deafness in ONE ear only
- Lesion of cochlear nerve or cochlear nucleus
**Why won’t you get monaural deafness if you damage the inferior colliculus? What are the sx of damaging CENTRAL pathway? **
- Inferior colliculus recieves input from BOTH ears (due to trapezoid body) so you won’t have complete hearing loss from one ear
- Inattention to stimuli on contralateral side OR inability to follow conversation in a noisy room.
What is the cocktail effect?
- Something I am lacking completely.
- The ability to focus your attention on ONE conversation in a noisy room.
I’m super jealous of all the people that have an intact cocktail effect. I’m going to destroy ______ so that everyone is like me!MWAHAHAHAHHAH
Damaging the central hearing pathway. Ie: superior olive –> inferior colliculus –> MGN –> cortex
I want to damage the ________ in order to sneak past the guard’s LEFT side and steal the gold.
RIGHT side central lesion
(central lesion causes inattention on CONTRAlateral side)
Blood supply to internal ear (and what that a. is a branch of)
labyrinthine a (internal auditory a.) <==AICA <==basilar a.
**SX: **
- Monaural hearing loss
- ipsilateral facial paralysis
- inability to look toward side of lesion
DIAGNOSE! (what would cause this?)
**Occlusion to AICA. **
Inner ear is ischemic (loss of labyrinthine a), facial nerve damage, pontine gaze center damaged.
What vessel would I occlude to kill:
- Cochlear n
- superior olive/lateral lemniscus
- Inferior colliculus
- MGN
- primary auditory cortex
- association cortex
- Cochlear n= labyrinthine a (from AICA)
- superior olive/lateral lemniscus= short circumferential of basilar
- Inferior colliculus=**superior cerebellar, quadrigeminal **
- MGN= **thalamogeniculate a. **
- primary auditory cortex=** M2 ** of MCA
- association cortex= M2 of MCA
**Central deafness (this is different than central LESIONS). **
Deafness cause by damage to cochlear nuclei or central pathways that move information to the auditory cortex.
Since it can be cochlear nerve or central lesion, then the symptoms for **central deafness are not always the same. **
Youre alone in your aparment and you start hearing an out of tune orchestra, buzzing of insects of strands of music.
- What’s going on?
- What are some other things that might be going wrong?
- Pontine auditory hallucinations.
- cranial nerve deficits and long tract signs.
Music still sounds the same (to patient), but everytime someone (not patient) “talks” it’s nonsense (to patient).
- Where’s the lesion
- What might cause this?
- Wernickes aphasia= Area 22 damaged
- MCA occlusion
Reading and writing are an important job for?
Area 39 (angular gyrus) and 40 (supramarginal gyrus)
the _______ connects broca’s area to primary and association auditory cortex.
**arcuate fasciculus **
Patient can understand everything, but everytime he/she tries to talk, it’s nonsense.
- Lesion?
- What can cause it?
- Broca’s (expressive) aphasia= area 44/45 (pars opercularis and pars triangularis)
- MCA branches
**Middle ear reflex= ___ muscles **
- What is it (pathway)
- What’s the purpose/function
- Is this more effective for LONG or SHORT stimuli?
2 Muscles= tensor tympani (CN V) and stapedius (CN VII)
**BILATERAL PATHWAY (afferent activates both efferents) **
- Loud sound ==> activate ear hair cellls==> sprial ganglion cells==> cochlear nucleus ==> superior olive (caudal) ==> facial nucleus==> stapedius to DAMPEN sounds (sound of your own voice)
- ==> superior olive (rostral)==> CN V ==> tensor tympani (chewing)
- More effective for LONG stimuli because it takes a while.
Rapid startle reflex pathway (to sound)
Lateral lemniscus ==> reticulospinal neurons
Pathway for turning head towards sound
Sound==> spiral ganglion==> cochlear nucleus==> superior olive==> central nucleus of inferior colliculus==> (interneuron) external nucleus of inferior colliculus)==> Deep superior colliculus ==> **tectobulbospinal **fibers to PPRF, RF and spinal cord
What is the nerve that innervates it, the function, and how it does it’s function?
- tensor tympani
- Stapedius
- **Tensor tympani= **CN V= malleus pulls on TYMPANIC MEMBRANE TO TENSE IT.
- Stapedius= CN VII= inhibits movement of **STAPEs **by pulling on it’s neck.
Perilymph vs endolymph
- Perilymph= between membranous labyrinth and bony labyrinth. **HIGH SODIUM **
- **Endolymph= **in membranous labyrinth. **HIGHT POTASSIUM. **
**Blood supply to labyrinth, consequences of occluding it. **
- labyrinthine a. from AICA
- Sx:
- Vestibular function is compromised= vertigo, oscillopsia (looks like stuff in visual field is oscillating) , nystagmus, unstable gain
- Cochlear function is also compromised=monaural hearing loss
**Meniere Disease **
- How is it caused
- Sx
- increased endolymph volume= endolymphatic hydrops= distention of mebranous labyrinth
- Vertigo, postitional nystagmus and nausea (vomitting), tinnitus
- 1oTreatment: with diuretics and Na restriction, 2o treatment= shunt to remove excess fluid; 3o=vestibulotoxic agent into perilymph (gentamicin)
**Tullio Phenomenon **
- What is it
- **What causes it? **
- **Sx **
- **treatment **
- vertigo and oscilllopsia in response to loud sounds
- Temporal bone thins exposing bony labyrinth to the extradulra space
- vertigo, ascillopsia
- Surgery to fix crappy bone
- What are some ototoxic drugs?
- Why are they ototoxic?
- Aminoglycoside antibiotics (gentamicin, streptomycin)
- the may reduce transudction currents of hair cells
- What would happen if on one side the afferents of the vestibular nerve were diminished/cut?
- What could cause this?
- reduced impulse frequency on affected side= comparative higher frequency on INTACT side= Interpretation of **TURN HEAD AWAY FROM LESION. **
- Glomus tumor or vestibular shwannoma
If I want you to look RIGHT, what should I do?
Stimulate right horizontal fibers (vestibular afferents) and and inhibit left side afferents of vestibular n.
**You turn towards vestibular activation (if they’re unequal) **
**How can vestibular issues cause orthostatic hypotension or tachycardia? **
Medial and inferior vestibular nuclei project to solitary tract to influence **respiration and circulation ** in response to **postural changes. **
What is an example of suppressing the vestibuloocular reflex?
Turning head while focusing on moving object.
**Ex: watching airplane or bird or baseball or anything that’s moving. **
- Nystagmus is the ______ phase.
- If you are turning to the RIGHT, tell me about the eye movements
- direction of the fast [return] phase
- If you’re turning to the right, your eyes slowly turn to the **OPPOSITE SIDE (left) **to keep focus on the hot guy that just walked by. Eventually, the eyes can’t turn anymore and they “reset”. This is the nystagmus= ie the fast phase and occurs in the SAME direction you’re movint. ** **
Linear movements cause the vestibuloocular reflex. They depend on receptors from _________.
**Otolith organ receptors. **
Patient comes in complaining of diziness or vertigo. What do you do?
Caloric test.
**Caloric test **
- Normal outcome
- **Unilateral lesion causes? **
**NORMAL: **
- cold water= nystagmus beating away
- Warm water= nystagmus beating towards
- **remember that nystagmus refers to the fast “reset” phase!**
**LESION= weakened/reduced/absent nystagmus on SAME side of lesion. **
As a joke, you tripped your friend and for some reason she didn’t react and fell flat on her face.
- What went wrong?
- What should normally happen?
- no vestibulocolic response
- Normally neurons in the medial vestibular nucleus get input about direction and activate NECK muscles. In this case, they would **excite dorsal neck flexors ( splenius) ** and inhibit anterior extensors so that the head gets pulled away from falling direction.
What is the primary vestibular cortex?
TRICK QUESTION (pulled a Mimi). There is no primary cortex, but there are FOUR main **CORTICAL areas. **
- Primary somatosensory cortex, area 2v and 3a
- Parietal cortex area 7 (VIP, MIP and MST)
- Parietoinsular vestibular cortex (PIVC)
- Frontal eye field= Area 6 & 8
- 2v function and location
- 3a function and location
- 2v= body motion when stimualted. Location: Posterior to hand and mouth area of postcentral gyrus at base of intraparietal sulcus.
- 3a recieves input from VPL and VPM and projects to area 4 of motor cortex. 3a= integration of neck and body movement. Location: base of central sulcus adjacent to motor cortex
Area 7
- Where is it
- parts and functions
- Area 7 = parietal cortex
- VIP= spatial coding, MIP and MST= body motion in space (spatial awareness)
Parietoinsular vestibarl cortex- function
integration of body motion, somatosensory, proprioceptive and visual motion.
Prefrontal area 6 &8 (aka?) function
Area 6 + 8= frontal eye field
Fx: saccades and smooth pursiot
Patient is confused about spatial awareness- Lesion location?
**parietal cortical area 7 **
Patient has episodes of vertigo, unsteadiness and loss of percetion for visual motion
**PIVC- parietoinsular vestibular cortex **
**Dizziness-associated sx and potential cause? **
general term for spatial disortientaion that may or may not involve feelings of movement. Might also have **nausea or postural instability. **
**NOT ALWAYS VESTIBULAR ORIGIN **
**Vertigo- **associated sx and cause
Types of vertigo?
**specific **perception of body motion= spinning or turning without any real motion.
**Subjective= **patient feels like he/she is spinning, environment is stable
**Objective= **patient feels stable, but environment is spinning.
How can you elicit nystagmus? What direction is it?
Spinning around and around (to the right), and then stopping
World spins in OPPOSITE direction (left)=Left Nystagmus
What happens if you sit but everything around you spins?
**Optokinetically induced nystagmus **
You flip over in bed and suddenly have brief episode of vertigo.
- What is this called
- cause?
- **Benign paroxysmal positional vertigo **
- otoconial crystals in utricle separate from otolith and get stuck in cupula OR semicircular canal
Pt Hx: severe vertigo. Patient has nausea and vomitting. No hearing loss or other CNS issues. URT infection a few weeks ago
- **Diagnose!-whats the pathophysiology? **
- **Treatment? **
- Vestibular neuritis- edema of vestibular nerve/ganglion from acute viral infection (ex HSV).
- **Treatment: **antemetics, vestibular suppressants, corticosteroids (reduce inflammation), antiviral agents.
Cupulolithiasis
Otoconial crystals get lodged in cupula and increase the density of the cupula= abnormal defelctions.
**compared the canalithaisis, episodes last LONGER and harder to treat (50% success) **
Canalithiasis
The otoconial crystals get stuck in the semicircular canals. Episodes have a latency and are shorter than cupulothiasis BPPV.
Causes of BPPV?
Cerebellar infarct, cerebellar disorders, intracranial tumors, CN VIII compression, migraines, MS, chiari malformation, drugs (ototoxicity?)
What two tests do you do on people with BPPV? What does each test do?
- Dix-Hallpike= manipulate head to generate nystagmus by rolling otoliths into semicircular canal (+ test= DPPV?)
- Epley maneuver= rotating head to remove otoliths from semicircular canal
Dix hallpike= DICK MOVE- you’re making them dizzy
Epley= ‘ELP ME! = help me get rid of these damn otoliths!
What is a **cholesteatoma? **
A skin cyst that may form on the ossicles (according to his pp picture). I’m pretty sure it’s a conduction hearing loss.
What sound would you lose if I destroyed the **BASE ** of the basilar membrane? The apex?
Base=stiff= high frequency
Apex= lower frequency
What’s the “low” road of the auditory system?
MGN==> Amygdala basolateral nucleus==> amygdala central nucleus==> emotional response control systems
How can you differentiate between nystagmus caused by
- central lesion
- **peripheral lesion **
- Central- can cause vertical nystagmus, the direction can change, and nystagmus can occur without vertigo
- Peripheral- CANNOT BE VERTICAL! NO CHANGE IN DIRECTION! ALWAYS ASSOCIATED WITH VERTIGO!
Most common cause of vertigo?
_Migraines! _
- 60-80% of vertigo patients without heraing loss have migraines!
- 35% of people that have migraines get vertigo
- 88% of patients (tested) thought their migraines were “sinus headaches”
- What happens if you lean to the right?
- What happens if I steal your right utricle?
- Right lean= stimualtion of right utricle==> medial and lateral vestibulospinal tract cause right leg to stiffen and realign the person
- Removal or right utricle= leaning to the right
**How do you test the vestibulospinal system? **
VEMP=vestibular evoked myogenic potential.
sound==> saccule==> medial vestibulospinal tract==> gamma motor neuron==> SCM muscle spindle = Turned neck
HX: 65 year old main, diziness. Disequilibrium without vertigo. occured daily with head movement. Especially bad when he walked. His gait veered to teh right and left.
Large acoustic neuroma
- PT: 55 year old male. Acute onset disequilibrium (felt like he was being pushed to the ground from the left. Vertigo, nausea, blurred vision. No hearing loss of tinnitus.
- Fm Hx: hypertension in patient, cerebral vascular disease runs in the fam.
- Physical: distracted, undershoot dysmetria when looking right to left, overshoot on left to right. Asymmetrical impairement in ocular pursuit (had trouble following objects that moved to the left). Nystagmus switched sides. Paresthesia of right face, diminished gag reflex, pain/temp diminshed on left side. Wide gait.
PICA syndrome (wallenberg syndrome)= lesion in lateral medulla.
HX: 68 yr old woman. Diziness, unsteadiness for months. Symptoms started after stereotactic irradiation of treatment of small acoustic neuroma. Sx got wrose with fatigue and esertion. Veering to the left when walking, especially in dim light. Store ilses and sidewalks bother her. Meclizine didn’t help
Damage to her LEFT vestibular nerve from her stereotactic irradiation.
HX: 41 year old woman. Diziness and progressive hearing loss in left ear.
**Physical: **Decreased hearing in left ear, AC>BC. Mild diziness. Left facial pain and decrased left corneal reflex. Decrased tast on left side of tongue.
Left acoustic neuroma/Vestibular shwannoma
