Final Exam Study Guide (Prev. Material) Flashcards
Failure of canalization
Associated w/ microtia & ME anomalies
-More common in males
congenital aural atresia
what is seen in herpes zoster oticus
aka ramsay hunt syndrome / shingles
painful rash in ear canal, concha or below/behind auricle
HL & vertigo w/ CN VIII n involvement
what is seen in cerumen impaction
-Tymps →volume < .2 = complete obstruction & flat tymp
→volume >.2 = hole somewhere and might get pure tones
-Pure tones→mild CHL (up to 30dB)
-Otalgia
-Vertigo/Dizziness
-Coughing→arnold’s reflex (branch of CN X in EAC)
what is seen in otitis externa
Severe pain →swelling due to edema that causes the pain
-CHL
-Whitish, watery otorrhea
-Acute swelling that can close canal
acute: bacterial, swimmers ear, pain
chronic: seborrheic dermatitis, itchy, watery, swelling causing stenosis
what is seen in collapsing canals
Normal tymps
-CHL present @ or worse in HF w/ supras
-Thresholds become better w/ inserts or soundfield
Problem for younger children→ cartilage is not fully developed
-Older adults → cartilage is deteriorating
what is seen in otomycosis
-HL or a wet feeling
-Blue-black, green, yellow or white colored
-Debris visible
what is seen in necrotizing external otitis
-Immunocompromised PT w/ ear pain
what is seen in exostosis
Pain/discomfort
-Tinnitus
-Associated OE
-If large enough, can cause CHL
Bony growth that starts unilateral but ends usually bilaterally
irregular and multiple
what is seen in osteomasas
same as exostosis
smooth and regular
what is seen in osteoradionecrosis (ORN)
-Ear fullness
-Otalgia
-Foul odor
-CHL/SNHL
-Bloody otorrhea
-Tinnitus
-Microscopy→debris & granulation tissue, yellowish colored bone
what can be seen in otitis media
-Otoscopy →pneumatic otoscopy*, discolered ™, partial/complete bulging or retracted, perf, discharge, fluid lines/bubbles
-Immittance→ flat type b w/ HV = perf, flat type b NV = effusion, negative type c pressure = ET dysfunction
-ARTs→ abn/abs, unilateral OM = only ispi of unaffected present, bilateral oM = ipsi & contra bilaterally abn/abs
-Pure tones→WNL, CHL, mixed, SNHL, can fluctuate, could have ABG
-Speech→ normal supra threshold test, srt/pta in agreement
what can be seen in cholesteatomas
-Presents w/ HL first
-Otoscopy→ normal or perf present
-Tymps→any type depending on size, location & what is damaged
No damage to ™ or ossicles = normal
ME stiffness = As
Ossicular disarticulation=Ad
™ perf/ME full = B w/ LV
™ perf/ME not full = B w/ HV
-Audio→ depends based on where it is & stage it is picked up (norma→ just perf no ODl, CHL→ ossicular disartic, mixed
can recur even after surgery
what can be seen in OTSC
Otoscopy→normal or schwarze sign (reddish glow)
Tymps→type A or AS, only ME condition w/ normal tymps
-ARTs→ abn in most due to reduced mobility of stapes
-Audio→early =normal/mild CHL w/ rising, middle =CHL/Mixed w/ rising or flat, late=flattening of rising CHL/Mixed
(CHL doesn’t exceed 60-65 dB
Max CHL)
BC→Carhart’s notch (poor @ 2 by 15-20dB & narrows ABG), also associated w/
D/D for OTSC
Meniere’s (vertigo, tinnitus, LF SNHL)
Osteogenesis imperfecta (blue sclera, noise notch, fragile bones, collagen gene)
SSCD (3rd window, LF CHL but ARTs normal)
Normal ARTs with CHL
SSCD not OTSC
What is seen in ossicular disarticulation
-Otoscopy→perf, bleeding, rarely normal canal or ™, ME filled w/ blood or CSF
-Immittance→ Ad, ARTs abn
-pure tones→acute/delayed CHL or mixed
-Vestib→ BPPV, perilymphatic fistula/leak
Ice cream cone sign is abnormal on CT
what are s/s of paragangliomas
-Otoscopy→red mass in ME
-Immittance→ As or B & pulsating w/ jagged edges
-Audio→CHL & sometimes mixed
what is a type a tymp
normal
intact tm
normal ME fxnw
what is a type Ad and when is it seen
high admittance
compliant system
ossicular disarticulation or loss of elastic fibers in TM
what is type As tymp and when would you see it
reduced admittance
stiff system from thick (scarred) tm or OTSC
what is type b tymp and when would you see it
reduced admittance/flat
ME fluid (OM)
TM perf
debris in EAC
when would you see type c tymp and what is it
intact TM w/ negative ME pressure
ETD
ME fluid
type b high volume
perf or pe tube
in type b tymp will you see any other parameters?
no because ™ is not moving in order to measure them
all you see is volume
type b low volume
obstruction - cerumen, debris, cholesteatoma
type b normal volume
fluid behind ear, cholesteatoma - something not allowing movement of ™ but volume is good
what if there is abn gradient/width
cannot include as jerger type
sensory portion of ART
afferent
VIII CN
interneurons of ARTs
ventral cochlear nucleus & SOC
motor portion of ART
efferent
CN VII
Acoustic reflexes are elicited between about
60 to 90 dB SL
what is SL in ARTs
is referenced to threshold level
if 1000 Hz is 30 dB you can elicit a reflex 60-90 above this and result is dB HL
Normal ARTs occur between ~ ______for pure tones
85 to 100 dB HL
Reflexes are above the level of cognitive control; they are involuntary/automatic
false
below
If the ART is measured on the same side to which a loud sound is presented, then it is
ipsi art
If the ART is measured on the opposite side to that to which the loud sound is presented, then it is
contra art
If tone is presented on the probe side, then it is
ispi
If tone is presented on the earphone side
contra
A normal ear should yield present ARTs from 500 to 2000 Hz at normal levels
4000 Hz, & occasionally 2000 Hz can normally be absent in older ears
true
how will a ME pathology affect art
even with 15 dB ABG can decrease intensity of signal going in
ART is abn/abs on same side and opposite equal to amount of ABG
a right-sided ME pathology will have
abnormal right ipsilateral and contralateral as well as left contralateral ARTs
what will bilateral ME pathology show in ARTs
all four ART patterns are abn
For a right cochlear pathology ARTs will show what
pattern of elevated/absent responses on the right side (both ipsilateral and contralateral) and present/normal responses on the left side (both ipsilateral and contralateral)
The signal will affect the ARTs once the cochlear hearing loss shows AC thresholds >
50 to 60 dB HL
ARTs occur for cochlear loss
at lower SLs (30 to 40 dB SL)
probably due to recruitment, a hallmark of cochlear impairment
R Cochlear path
AC thresholds below 50 to 60 dB HL; reflexes at lower SLs
all normal
R Cochlear path
AC thresholds above 50 to 60 dB HL
R ipsi & contra abn
L both normal
R Cochlear path
Bilateral Cochlear pathology – AC thresholds above 60 dB HL
all abn
Elevated/absent ARTs, which do not agree with the cochlear hearing loss are cause for suspicion of
retrocochlear pathology
where is reflex decay done
contralateral at 500 & 1000 Hz because this is the most sensitive for vestib schwannomas
what will ARTs show for CN VIII pathology
he side affected (wherever stimuli is delivered) will show abnormal ARTs, like a cochlear loss, only the ARTs will be abnormal at lower thresholds (sound effect)
what would a R CN VIII path show for ART
right ipsi and r contra are abn
L are normal
What is congenital aural atresia? What is a condition associated with it? What is the FDA approved device for it and at what age?
failure of canalization results in this
associated with microtia & ME anomalies
spontaneous, can occur with Treacher collins, trisomy 22, crouzon’s & hemifacial microsomia
FDA approves surgical BAHA for kids with bilateral or unilateral atresia after 5 yrs old
under 5 can use BC HA coupled to soft/hard headband
Man with bilateral mixed HL from 500-4000 in the high frequencies. What could be the cause?
Collapsing canals
What is the external canal condition caused by radiation to the head and neck?
ORN
what are the signs of impacted cerumen?
Mild CHL
tymps <.02 ml
Coughing
Dizziness
all
What is not the sign of impacted cerumen?
Otalgia
Tymps >.03 ml?
Complaints of fullness
Mild CHL
Dizziness
Tymps >.03 ml?
List 2 surgical complications of otosclerosis & discuss one of them
OTSC surgery can result in a perilymphatic fistula and a decrease in WRS. Regarding PLF, if implanted prosthesis gets misplaced after surgery it can puncture a hole into the inner ear space allowing perilymph to escape into the ME cavity
Another complication is
Cholesteatomas are pseudotumors. Justify this. What are tymps findings of one that caused ossicular chain disarticulation? What is preferred treatment.
they are this because they are not considered tumors but they have same mannerisms like bone erosion, growth, and vasculature. They will take over and invade all structures that they contact, similarly to a tumor. In the R ear, tymps would show a type Ad with high static admittance. Surgery is the preferred treatment and antibiotics can be given beforehand to reduce inflammation and bleeding for surgery.
What demographic group is most prone to otosclerosis
white women bw 20-40 yrs
What is correct for ossicular disarticulation?
only caused by temporal bone fractures
typically self correcting condition
hemotympanum is never reported with this
can be caused by a single exposure to very high intensity sound
ARTs are normal if tympanic membrane is intact
can be caused by a single exposure to very high intensity sound
Otosclerosis is a focal disease of
otic capsule
SSCD is differential diagnosis for otosclerosis. Clinically, they are differentiated by
normal ARTs
Jerger type Ad can be clinical finding in which disorders
ossicular disarticulation
Jerger type b HV can be clinical finding in which disorders
cholesteatoma
Glomus jugulare tumor can present with
unilateral CHL
unilateral mixed HL
tymp with jagged edges corresponding to PT pulse
intact but inflamed looking ™
FN weakness/paralysis potential complication for what conditions
glomus tympanicum
chronic suppurative OM
cholesteatoma
gunshot wound to temporal bone
what is a contraindication for surgery for OTSC
OTSC involvement of endolymphatic duct with meniere’s disease like s/s
which infectious disease affect mother that results in congenital HL in fetus
CMV infection
rubella (german measles)
AIDS
17 yr old female has chronic bilateral OM since 6 mos old. Has had plenty of PE tubes but none for the last 3 years. Has significant allergies and frequency neg ME pressure (type c) bilaterally. Last ME infection was reported 3 yrs ago. She noticed hearing in right ear is worse for the last year. Copious foul smelling discharge noted on otoscopy in R ear. Pure tones show mild - moderate CHL in R and normal in L. Type b HV in R and type A tymp in left.
She most likely developed which condition due to chronic OM and/or negative ME pressure in R ear
what is the best treatment for this?
cholesteatoma
surgery
incorrect for glomus tumors
can arise from paraganglia cells on dome of internal jugular vein, arnold & jacobsons
glomus tympanicum can commonly grow to large size and cause hoarseness and dysphagia
several genes are associated with thee but most are sporadic
involvement of XII N indicates extensive growth of jugulare tumor
glomus tympanicum can commonly grow to large size and cause hoarseness and dysphagi
causes profound permanent SNHL visual problems and neurological and motor deficits in affected babies
CMV
HL secondary to ____ can result in cochlear ossification
meningitis
an incudomalleolar disarticulation appears as an ______ sign on CT scans
broken ice cream cone
one pathology/condition that could result in tymp with type b high ECV?
cholesteatoma
what do we see with rubella virus
german measles
Congenital HL cataracts, cardiovascular cataracts, possibly ID
what do we see with CMV
Progressive & profound SNHL by age 3-5 (CI candidates)
-Decreased life expectancy, larger spleen & liver, “blueberry muffin” rash, & decreased immunity
Neurological deficits, blindness, ID, cardiovascular problems
what do we see with AIDS
n all cases of sudden bilateral or unilateral HL→populations at risk should be considered for HIV
-OME, otalgia, vertigo, tinnitus, fullness, reduced OAEs, delayed ABR interwaves (from HIV or the drugs), recurrent/chronic OME
what do we see with meningitis
high fever, stiff neck, malaise, nausea, vomiting
-Untreated→ blindness, paralysis, HL/deafness (acquired SNHL) & vertigo
what do we see with perilymphatic fistual
Vertigo w/out HL
-HL w/out vertigo
-Symptoms not determined from Meneries (SNHL, vertigo, tinnitus, aural fullness)
-Audio: presentation of complex symptoms→ case hx, symptoms they present with; dix hallpike to see nystagmus
Which nerve is involved in eye movements assessed during vestibular testing?
CN III - Occulomotor
Which branch of the FN innervates the outer ⅔ of the tongue & can be sacrificed during ME surgery such as removal of cholesteatoma?
chorda tympani
a left FN schwannoma will show an abnormal left ispilateral response and an abnormal _____ contralateral response
right
what do we see in NIHL
Both TTS & PTS accompanied by tinnitus
-symmetrical
-profound SNHL is rare
-LF thresholds better than 40 dB HF thresholds rarely better than 75 dB
-Presbycusis can flatten noise notch
-Noise notch noted from 3-4 sometimes 6 kHz
what do we see in acoustic trauma
-Otoscopy→TM perf or hemorrhage
-Audio→ similar to NIHL, noise notch at 3-6, HF sloping or flat (more common) configuration, mixed HL (OD)
-Tymps→Ad w/ OD
-ART→abs w/ OD
™ perf, OD, tinnitus, otalgia, HL and/or vertigo
Osteopetrosis (bony dysplasia) is a disorder of aging that results in hardening of the cranial bones
false
______ syndrome is a rare congenital disorder with possible multifactorial inheritance resulting in hypoplasia of CNs VI & CN VII
mobius
what do we see in osteopetrosis
bony displasia
Congenital facial paralysis
-Vision & HL
what do we see in mobius
congenital hypoplasia of 6 & 7 n
-Bilateral facial paralysis
-CN VI uni or bilateral paralysis (cross eyed)
-ID, deformities of extremities, musculoskeletal deformities
In the case of Bell’s palsy, MEAR will be present if the lesion is ______ to the stapedius nerve
distal
In the case of Bell’s palsy, MEAR will be present if the lesion is ______ to the stapedius nerve
distal
what will we see in bell’s palsy
-partial/total unilateral facial paralysis → onset with 48 hr period,
fever & stiff neck @ onset, no hl/vertigo, no other cranial neuropathy, eye drying (due to lack of eye closure & lacrimation
-W/in 3-6 mos of onset→normal otoscopy, HL rare for pure tones, normal tymps, abnormal ARTs (proximal lesion to stapedius nerve), present ARTs (distal lesion to stapedius nerve)
what is D/D for bells palsy
-CPA/skull based tumors
-vestib schwannoma
-OM
-Parotid gland tumors
who is most at risk for bells palsy
-Most common cause of acute unilateral facial paralysis
-affects both sexes & right more
-Pregnancy increases risk 3 fold
what would we see with facial neuromas
-Immittance→normal tymps, ARTs abn w/ lesion PROXIMAL to stapedius n & ARTs present w/ lesion DISTAL to stapedius n
-Pure tones→ SNHL
-ABR→ shows whether its acoustic or facial neuroma
- Facial weakness usually gradual (⅔ of all cases), HL (~ 50%, SNHL, CHL, or mixed depending on tumor location - CHL occurs if lesion is on mastoid segment of FN invading ME cavity/ear canal/tympanic portion
-Others→tinnitus, otorrhea, ear canal mass, otalgia, vestibular symptoms
what are D/D for facial neuromas
-OM w/ CHL (w/ or w/out cholesteatoma),
cholesteatoma paragangliomas, meningiomas,
acoustic neuroma (vestib schwannoma →because of SNHL that can be present in facial neuroma
when should you refer for vestib schwannomas
unexplained unilateral or asymmetric HL
15 dB thresh difference bw ears @ 2 adjacent frequencies for unilateral HL and 20 dB thresh difference bw ears @ 2 adjacent frequencies for bilateral HL
unexplained unilateral or asymmetric tinnitus or vertizo/dizziness
aural fullness
facial paralysis/weakness
asymmetric WRS w/ NU-6 lists
> 15%?
other tests: rollover, ARTs, RDs, ABRs
when should you refer for SSNHL
IMMEDIATE referral
pure tones → sudden decrease or asymmetry in hearing of at least 30 dB w/ at least 3 consecutive test frequencies
onset for over no more than 72 hrs
corticosteroid treatment is most effect given w/in 2 wks of onset
when should you refer for OM
flat (wide width) w/ normal ECV
cloudy ™ and/or air bubbles or air-fluid line or bulging ™
repeat tymp in 6-8 wks to monitor and refer if needed
when to refer for PE tubes
flat w/ large ECV → patent tubes (open)
asymptomatic PTs w/ patent → follow managing physicians advice on care & f/u
symptomatic PTs w/ patent → refer to managing physician
symptoms → blood, otorrhea, otalgia, significant CHL
flat w/ normal ECV → obstructed tubes, possible O
when to refer for perf
flat tymp w/ large ECV → ™ perf
can be visualized on otoscopy
asymptomatic & undiagnosed PT → follow dry ear precautions and refer to otolaryngologist
asymptomatic & diagnosed previously → follow managing physicians treatment
symptomatic PTs, whether diagnosed or not → refer to managing physician
symptoms→ otorrhea, blood, otalgia, significant CHL
when to refer for ossicular discontinuity
Ad, narrow width, high admittance, hyper flaccid
significant CHL across audiogram
refer for medical eval
when to refer for OTSC
A or As, narrow width, normal compliance, unremarkable otoscopy
refer for medical eval w/ CHL & BC notch @ 2kHz
when to refer for tinnitus
somatic tinnitus→ pulsatile tinnitus, refer
mood disorder suicidal ideation w/ it → refer to mental health provider
symptoms associated w/ head or neck movement including tinnitus modulation
otalgia, otorrhea, dizziness, vertigo
when to refer for dizziness
PT w/ atypical findings to BPPV → symptoms not provoked by head position & negative Dix-Hallpike
PT w/ BPPV w/ no improvement after 2-3 canalith reposition treatments
what does ME path look like on ARTs for L
abn L ispi & contra and abn right contra
what does me path for bilateral look like on ARTs
all abn reflexes
what is seen in ANSD
disruption of neural synchrony
-ECochG & ARTs absent → 8th n involvement
-Present OAEs until blood supply compromised
-Abs ABR w/ present CM(OHC produced)→no wave 5 latency increase, response reverses based on stim polarity
-Poor WRS in noise
-Audio can have varying severity & configurations
-Contralateral suppression w/ OAEs abs
who is at risk for ANSD
-Premature & very low birth weight
-Prolonged NICU stay
-Anoxia/hypoxia
-Hyperbilirubinemia
how is ANSD diagnosed
-Present OAEs & reversal ABR, abs ART→anything involving 8th n is abnormal
-Actual hearing thresh typically ~10 to 15 dB HL better than ABR thresh
what is management of ANSD
*question is not how severe HL is but how severe dys-synchrony is
-CI can be either success or not→ neural integrity compromised will not be
what is seen in HHL/cochlear synaptopathy
-Loss of connection bw auditory n fibers & hair cells
-Adversely affects fine speech structure decoding & speech perception especially seen in noise
-Not seen on an audiogram
Classic complaint→ “I can hear but I cannot understand what people say”
what is seen in presbycusis
Formula→genetics / (age + noise + ototoxic drugs)
-Slow, progressive HF sloping SNHL
-speech perception especially w/ noise & reverberation
-Recruitment
what is seen in ABR w/ CHL
absolute latencies are pushed out but relative interwave latencies were retained within normal limits
what is seen in ABR w/ SNHL
wave 1 is prolonged (~ 2 ms)
wave 5 has normal latency (~ 6 ms)
Latency-intensity function shows a wave V not repeatable at 45 dB nHL – a higher hearing threshold
whatdoes BS show in ABR
only wave 1 present
what does vestib schwan show in ABR
diminished wave I and absent wave III & V
