Neurotology/Audiology Flashcards
Match the terms: Most (efferent/afferent) neurons innervate (inner/outer) Hair Cells.
Efferent neurons predominantly innervate OHCs
Afferent neurons predominantly innervate IHCs
Which of the following have high Na/low K? Select all that apply: Scala tympani, scala vestibuli, cochlea, vestibule, endolymphatic sac
scala tympani, scala vestibuli, endolymphatic sac. (The trick is that endolymphatic sac has perilymph-like concentration despite being named “endolymphatic!”)
What type of OAE is used in neonatal hearing screens?
DPOAEs
How much is a maximal conductive hearing loss?
60dB
What would be the expected results for the following tests in auditory neuropathy: pattern of hearing loss, WRS on audiogram, ABR, acoustic reflexes, tympanometry, OAEs
SNHL, worse WRS than expected compared to PTA, absent ABR, absent ipsilateral and contralateral acoustic reflexes, present OAEs, normal tympanometry
Define: interaural attenuation, crossover, masking.
Interaural attenuation = the loss of sound energy from one side of the skull to another
Crossover = the amount of sound that is heard by the contralateral ear
Masking = sound played to the contralateral ear to account for crossover
Which end of the cochlea is sensitive to high frequencies?
Basal turn. The apex is sensitive to low frequencies.
When should masking be considered for air conduction using over the ear headphones, air conduction using insert earphones, and bone conduction?
10dB for bone (interaural attenuation = 0-10dB)
40dB for over ear
70dB for insert
How do dB HL values correspond to SPL vs SL and which one is used for reference in clinical audiometry?
HL is used in clinical audiometry. HL values are not uniformly/linearly corresponded to SPL values, as human hearing is not equally sensitive at all frequencies. SL is equal to HL but calibrated to the individual’s hearing.
What is the difference between hearing level, sound pressure level, and sensation level?
HL = threshold to hear 50% of stimuli in a “normal” ear. SPL = objective measure of sound intensity calibrated to micropascales. SL = individuals’s threshold
How do cochlear hearing losses impact the ABR at low, flat, or high frequencies?
Low frequency HL does not typically affect. Mild to moderate high frequency HL also does not impact so long as the signal/stimulus is adequate. Flat losses >75dB usually make ABR impossible. Everything in between affects waveform/latency/amplitude but not in a predictable way. (Note from Tiff – I included this because this topic came up in an actual question on the boards when I took them. Showed an audiogram with conductive hearing loss and an ABR with waveform latencies/altered audiogram, wanted to know if this is indicative of a retrocochlear lesion or normal for the audiogram. I don’t know if it was an experimental question).
Which level of ECOLI represents the first point of potential crossover to the contralateral side?
The superior olive.
What is auditory fatigue and how is it tested? What does it signify?
Inability to continuously perceive a note presented at a certain frequency at or slightly above db SL. Indicates VIII nerve lesion. May be tested with tone decay test, acoustic reflex delay, or supra threshold adaptation test.
What is the expected pattern of acoustic reflex responses in clinically significant left otosclerosis?
Absent left reflexes to bilateral stimuli. Present right reflexes to right stimulus. Possible present right reflex to left stimulus provided that degree of CHL < 65dB.
WRSs are usually presented at 30-40dB SL. How does that compare to db HL? (Eg if a person has a speech recognition threshold of 25 dB HL, at how many dB HL will a patient typically be presented with the word list for word/speech recognition?)
SRT in dB HL + 30-40 dB. In the given example, presentation will be at 55-65 dB HL.
Explain the pneumonic ECOLI.
Eighth nerve, cochlear nucleus, olivary complex, lateral lemniscus, inferior colliculus
What are the four sources of impedance matching in the middle ear, and how much is added by that source?
1) area effect of the TM (17:1 size difference TM to oval window)
2) lever action of the ossicular chain (additional 1.3:1)
3) natural resonance and frequency of the middle ear/EAC
4) phase difference between the round and oval windows
What is recruitment? What is its significance?
Disproportionate increase in subjective loudness for a given increase in dB stimulus. Indicates cochlear pathology.
What is the transformer ratio of the middle ear? How many dB does that equal?
22:1 (17 area effect x1.3 lever action); 25 dB
What is meant by the “cochlear amplifier”?
Active feedback mechanism causes OHCs to stiffen/relax the basilar membrane so that a narrow band of IHCs will receive maximal stimulation for a given frequency
When might one see a Type Ad tympanogram? (Try to provide at least 1 example).
Decreased compliance/loose compliance - partial ossicular discontinuity/disarticulation, flaccid TM.
Why is the term “sensorineural” favored over “nerve loss” in SNHL?
Because majority of SNHL is cochlear rather than retrocochlear.
What is rollover and what does it signify?
Decrease in word recognition score with increase in presentation volume. Marked rollover suggests retrocochlear lesion; slight may be seen in SNHL or cochlear lesions.
Which of the following does not impact latencies on ABR: Age, Gender, Temperature, Medications, State of Arousal, Hearing Loss.
Trick question! They all impact ABR latencies. However, note that it is generally accepted that they are not acutely affected by most sedative anesthesia, drugs, or state of arousal (hence why a sedated ABR is still accepted as reliable)
When might one see a Type As tympanogram? (Try to provide at least 2 examples).
Restricted compliance - stiff TM (tympanosclerosis), otosclerosis, malleolar fixation.
Which of the following would not be helpful in the evaluation of pseudohypoacusis: Stenger test, Lombard test, OAE, Bekesy audiometry, acoustic reflexes.
Trick question! All would be helpful. Presence of TOAEs ensures there is no significant hearing loss >40dB. Stenger is helpful for identifying malingerers (play tone in both ears, louder in the affected ear - malingerer will say they hear nothing). Lombard increases background noise and monitors patient for increasing the volume of their speech. A continuous stimulus line trending above a interrupted stimulus line on Bekesy audiometry suggests pseudohypoacusis. Acoustic reflex present at 5dB above voluntary audiometric threshold suggests pseudohypoacusis.
In what type of hearing loss affecting either the stimulus ear or recording/reflex ear might the stapedial reflex be absent?
Stimulated ear: significant hearing loss > 65dB (conductive or SNHL)
Recording/reflex ear: significant conductive pathology or hearing loss
What are the three types of audiometric testing appropriate for children prior to PAE? At what age is each test appropriate?
Behavioral Response Audiometry up to 6 months. Visual Reinforcement Audiometry from 6 to 30 months. Conditioned play from ~30-36 months of age.
What type of OAE can provide frequency-specific information?
DPOAEs; but DPOAEs may be recorded even in a moderate to severe hearing loss
How is significant ototoxic change defined?
threshold shift of 20dB at a single frequency, threshold shift of 10dB in two adjacent frequencies, loss of response at 3 consecutive frequencies where previous responses were recorded
What are the 3 classifications of noise-induced hearing loss?
Transient threshold shift, permanent threshold shift, or acoustic trauma
Based on OSHA guidelines, how many hours can a person be exposed to 90dB SPL? 95dB SPL? 105 dB SPL?
8 hours; 4 hours; 1 hour
What are the commonly accepted anatomical origins for waves I, III, and V of an ABR?
I. distal eighth nerve
III. caudal brainstem near trapezoid body and superior olivary complex
V. lateral lemniscus as it enters the inferior colliculus
(This always confused me that it doesn’t quite line up perfectly with ECOLI. Just important to realize that it doesn’t – ECOLI is meant to be a mneumonic for the general propagation of auditory signal)
What 3 electric potentials occurring with sound stimuli are measured by ECOG?
Summating potential
Action potential
Cochlear microphonic
(There is also a resting potential, but this is without stimulus)
Is the cochlear microphonic, summating potential, and action potential AC or DC?
CM = AC AP = AC SP = DC
With respect to ECOG, what is the summating potential a reflection of?
It reflects the time-displacement pattern of the cochlear partition in response to the stimulus envelope
What type of SP is expected in endolymphatic hydrops? (Large or small)
Enlarged
On what site is a transtympanic electrode placed?
Cochlear promontory
With respect to ABRs as a screening tool, what type of ABR is better for detection of small tumors?
Stacked ABR
What type of ABR is used for pediatrics, difficult-to-test, and possible non-organic hearing loss?
Threshold ABR
You are performing a threshold ABR in an individual suspected of non-organic hearing loss. At 2000Hz, wave V disappears with a 15 dB HL stimulus. What does this indicate?
You are near the patient’s hearing threshold
What is the generally accepted difference between ABR thresholds and behavioral thresholds?
ABR thresholds are 10-20dB higher than behavioral
What is the clinical implication/significance of the following findings on ABR: [a] delayed wave I latency; [b] small or absent wave I with delayed absolute latencies of other waves; [c] normal wave I with delay of all other absolute latencies; [d] wave I-III interpeak latency; [e] inter-aural (between ears) wave V latency >0.4ms?
a. CHL
b. SNHL
c. neural hearing loss
d. best descriptor of eighth nerve tumor
e. suspicious for unilateral retrocochlear lesion; sensitive for eighth nerve tumor
What electrical neural monitoring test can be used to assess frequency-specific profound hearing loss?
Auditory Steady State Response (Click and tone burst ABR cannot do this, as masking dilemma cannot be overcome). Difficult to do ASSR with bone conduction as well due to masking dilemma.
AKA 40Hz response, envelope-follow, frequency-following, amplitude-modulating-following response
What is Heschl’s gyrus?
The supratemporal plane of the auditory cortex
What does a cVEMP test? Is this ipsilateral or bilateral?
cVEMP is a reflection of the saccule, posterior SCC, inferior vestibular nerve, and central connections. Ipsilateral response.
What are the expected findings on cVEMP in a patient with [a] SNHL [b] CHL [c] clinically significant SSCD [d] severe otosclerosis?
a. no impact
b. increased thresholds or low amplitudes
c. Increased amplitudes and decreased thresholds/ability to detect despite an ABG
d. expected to be absent
What is Alexander’s Law? Keeping that in mind, if you are speaking to a patient with postoperative vertigo following resection of a right acoustic neuroma, which side should you stand on to reduce/minimize their nystagmus? Which direction will the slow phase of nystagmus be after a left labyrinthectomy?
Alexander’s law states that in a unilateral peripheral vestibular loss, eye movement in the direction of the stronger labyrinth will exacerbate the nystagmus. Hence, you should stand on the right side of a right acoustic neuroma patient with postop vertigo. The slow phase of nystagmus after a left labyrinthectomy will be towards the left.
Gaze-stabilizing reflexes include smooth pursuit, optokinetic nystagmus, and VOR. Which one(s) dominate in slow head movement? Which one(s) for fast movement?
Smooth pursuit +OKN dominate in slow. VOR for fast.
What is the function of the cupula?
The cupula is the gelatinous part within the ampulla of the canal and contains hair cells. Its job (in part) is to block fluid flow by nature of its gelatinous consistency, allowing endolymph from the affected SCC to deflect the cupula (instead of freely floating into the vestibule) and excite the stereocilia of the hair cells causing sensation of head rotation.
How are the SCCs paired in canal planes?
The two horizonal canals are paired. Then LARP (left anterior/right posterior) and RALP (right anterior/left posterior).
Note: The extraocular muscles are also paired. Medial/Lateral recti correspond with horizontal canals, superior/inferior with anterior canals, and obliques with posterior canals.
Contrast the following between the utricle and the saccule: innervation? directionality of sensation for linear acceleration?
Utricle (“Up”) - innervated by the superior VN. Senses horizontal movement. Saccule (ball sack hangs down; lol sorry) - innervated by inferior VN. Senses vertical movement.
Discuss ampullopetal vs ampullofugal. Which SCCs are excited by ampullofugal flow vs ampullopetal flow?
Ampullopetal = toward ampulla Ampullofugal = away from ampulla (like centriFUGAL forsces)
Horizontal is excited by ampullopetal. Anterior/Posterior by ampullofugal.
On what principle with respect to excitatory vs inhibitory responses in the VOR is the head thrust test based?
Excitatory forces at HIGH velocity dominate the VOR. Hence, unilateral vestibular loss/weakness will cause a saccade during head thrust test because the weaker/inhibitory side cannot keep up with the excitatory forces. This asymmetry is masked in normal subjects by reciprocal wiring in the brainstem, but is brought out when only one labyrinth/one peripheral vestibular system is working.
Why doesn’t whole-labyrinth irritative nystagmus (excitatory stimulation of all 3 canals) have a vertical component?
The upward component of the anterior canal cancels out the downward component of the ipsilateral posterior canal. However, both the anterior and posterior canals have the same torsional direction, which is doubled in an pathologic excitatory stimulus.
What nerve is most often affected in vestibular neuritis?
Superior vestibular nerve
Name 2-3 potential vertiginous syndrome diagnoses based on length of episode (more than three accepted): seconds to minutes; minutes to hours; hours to days; constant
seconds to minutes: BPPV, PLF, VBI
minutes to hours: Meniere’s, migraine
hours to days: migraine, vestibular neuronitis
constant: mal de debarquement, uncompensated vestibular hypofunction, psych
What is the likely vertiginous syndrome based on positional triggers:rolling over to side in bed; with neck extension while standing upright; with rapid head movements
rolling: BPPV
neck extension: VBI
rapid head movements: vestibular hypofunction
What is the purpose of Fresnel glasses during bedside examination? What is expected directionality of post-headshake nystagmus evaluation using Fresnel glasses in a patient with left peripheral vestibular hypofunction?
Purpose is to suppress ocular fixation/compensation for underlying vestibular dysfunction. With left peripheral hypofunction, expect drift to left and beat to right.
What is the bedside maneuver for evaluating for lateral/horizontal canal BPPV?
Supine with head slightly extended past level, roll to affected side (affected ear down) and assess for nystagmus. Fix with “Log roll” - roll away from affected ear
What is hennebert’s sign? What is Tullio’s phenomenon? Name 3-5 syndromes that can cause them.
Hennebert’s sign - vertigo with pneumatic otoscopy or tragal pumping. Tullio’s - vertigo with loud noises. Can be caused by SSCD, enlarged vestibular aqueduct, otic syphilis, PLF, lateral/horizontal canal fistula (cholesteatoma)
What syndromes can cause post-hyperventilation nystagmus?
Demyelinating lesions - MS, vestibular schwannoma, compression by a blood vessel (vascular loop- AICA)
What is the purpose of Jongkees formulas? What is the upper limit of normal?
Calculate unilateral weakness or directional prepondarance in caloric testing. Cutoff is 25% for both.
Which of the following treatments has been demonstrated to yield a clear benefit lasting 3 weeks if initiated promptly for vestibular neuronitis (within first few days)? Prednisone, antiviral medications, hyperbaric oxygen, Epley maneuver
Prednisone
Name 3 non-ablative (hearing preservation) treatments for Meniere’s disease.
low salt diet, diuretics, IT dexamethasone, endolymphatic sac surgery (controversial), vestibular nerve section
Name 3 ablative (non-hearing preservation) treatments for Meniere’s disease.
IT gentamicin*, labyrinthectomy
*titrated IT gent injection based on lateral canal caloric responses has been shown to have reasonable hearing preservation but hearing loss must still be discussed with the patient
What is Wallenberg syndrome? Which artery is infarcted?
Lateral medullary syndrome. Ipsilateral Horner’s, ataxia, vertigo, hearing loss + DYSPHAGIA. PICA. “Pikachu - PICA can’t chew” (to differentiate from AICA, which has fACIAl involvement)
What symptoms would be expected in AICA infarction?
Lateral pontomedullary syndrome. Same as Wallenberg (Horner’s, ataxia, vertigo, hearing loss) except facial nerve involvement instead of dysphagia. AICA has fACIAl involvement; pikachu (PICA can’t chew).
Type 1 vs Type 2 Hair Cells: Shape, Excitatory vs Inhibitory, # of nerve terminals per cell
Type 1: flask, excitatory, 1 nerve terminal per cell
Type 2: cylinder, inhibitory, multiple terminals per cell
What is Ewald’s law?
States that eye and head movements occur in the plane of the stimulated SCC and direction of endolymphatic flow
Name 1-2 findings on ENG suggestive of central pathology.
Spontaneous nystagmus with normal calorics. Direction changing nystagmus. Bilateral reduced or absent calorics without history of ototoxicity/ear disease. Abnormal saccades/pursuits. Hyperactive calorics.
Name 1-2 findings on ENG suggestive of peripheral pathology.
Unilateral caloric weakness. Bilateral reduced calorics with history of ototoxicity/ear disease. Fatiguing positional nystagmus. Intact fixation suppression response. Direction fixed nystagmus.
What three factors are measured during rotational chair testing?
phase, gain, symmetry
Define certain, definite, probable, and possible Meniere’s.
Certain - Definite + histopathologic confirmation.
Definite - 2 or more vertiginous episodes lasting 20min or more with associated ipsilateral tinnitus with documented audiologic confirmation of hearing loss on at least one occasion and other causes excluded.
Probable - one episode of vertigo + other criteria fulfilled.
Possible - one episode of vertigo without documented hearing loss
What findings, if present, would be consistent with Meniere’s on audiogram, ENG/VNG, and ECoG?
Audio = fluctuating low frequency SNHL. ENG/VNG - unilateral hypofunction on calorics.
ECoG - SP/AP Ratio > 0.3
Test of choice for otic syphilis?
FTA-ABS (treponemal antibody); VDRL is less sensitive
Two conditions that can cause audiovestibular dysfunction and interstitial keratitis?
Cogan Syndrome (bilateral, rapidly progressive deterioration; autoimmune) Otic Syphilis (fluctuating SNHL, vertigo)
Schwartze sign?
reddish discoloration of the cochlear promontory seen during active/otospongiotic phase of otosclerosis
What are the four types of hearing aids? Which one is provides the most amplification?
BTE, ITE, ITC, CIC. BTE provides the most amplification
Two best predictors of success with hearing aids?
WRS and dynamic range
CROS vs BiCROS hearing aid?
CROS - contralateral routing of signal, wear microphone in bad ear and receiver in good ear. BiCROS adds amplification to good ear
Special considerations for stapes in osteogenesis imperfecta?
Don’t fracture the tympanic ring
Don’t fracture the incus with over crimping
2-3 conditions in which hearing aid should be considered instead of stapedectomy in otosclerosis?
Meniere’s, contralateral vestibulopathy, blindness, significant mixed hearing loss
2 options for management of floating stapes footplate?
laser a fenestration or abort and let heal
How to manage a dehiscence facial nerve with significant overhang?
Abort. If minor overhang, bend the prosthesis wire
How to manage a vestigial persistent stapedial artery?
Proceed. Anything more than vestigial should abort.
At what age is a child considered post lingually deafened?
5 years
What is the one situation in which a full hearing aid trial is not required for CI candidacy?
meningitis
Boundaries of the facial recess?
fossa incudis (incus buttress), chorda tympani, facial nerve
Distance from the oval window to the round window?
2mm
Where should a cochleostomy be placed relative to RW?
anterior and inferior
From what structure are CSF leak/gushers during CI surgery thought to originate?
lateral IAC
How to manage a pediatric ear tube preoperatively for CI?
remove, allow to heal before proceeding
How to manage acute otitis media / bulging red TM preoperatively for CI?
give antibiotics and delay the case
How to manage serous effusion preoperatively for CI?
proceed normally if no signs of infection
When is a split electrode used? Where do the two electrodes get inserted?
cochlea ossificans; one through a basal turn drill out and the second anterior to the oval window
describe the course of the ICA from entry to petrous temporal bone up to cavernous sinus
ICA -> fibrous ring -> enter temporal bone at inferior face in hypotympanum-> 90 deg turn anteriorly (horiz petrous), then 90 deg turn superiorly anterior to middle ear structures (vertical petrous) -> pass/abut posterior wall of eustachian tube -> foramen lacerum -> cavernous portion
name the structure that crosses each of the following: foramen rotundum, foramen ovale, foramen spinosum, foramen lacerum
rotundum = V2, ovale = V3, spinosum = mid mening artery, lacerum = carotid
what is the role of angiogram, BTO, or SPECT in skull base malignancy?
evaluate patency of arterial structures that may be invaded; BTO + SPECT useful when considering carotid sacrifice.
what are the pedicle arteries for a pericranial flap?
supraorbital + supratrochlear
With respect to malignant invasion of the orbit, at which of the following boundaries should exenteration be considered? orbital base, periorbita, orbital fat, muscle
orbital fat
What is Hitselberger’s sign? What diagnosis does it suggest?
Numbness/hypoesthesia in posterior EAC / concha; suggests acoustic
Describe characteristic MRI findings for the following petrous apex/CPA lesions: vestibular schwannoma, meningioma, cholesteatoma, arachnoid cyst, lipoma, cholesterol granuloma, paraganglioma, hemangioma
vestib scwhannoma: enhances on T1+C, no dural tail, hypointense on T2. Mening = same as acoustic but + dural tail. Cholesteatoma = isointense/hypointense on T1, hyperintense T2, bright on DWI; arachnoid cyst = same as chole but not bright on DWI and usually hypointense on T1; cholesterol granuloma = bright on T1+T2 and doesn’t enhance; lipoma = like cholesterol granuloma but disappears with fat suppresion; paraganglioma + hemangioma both have salt and pepper voids
What is gradenigo syndrome? What diagnosis does it suggest?
retroorbital pain, otorrhea, lateral abducens palsy. suggests petrous apicitis
What regions are accessed by each of the Fisch infratemporal fossa approaches?
Fisch A = temporal bone/infralabyrinthine (most common for glomus). Fisch B = clivus. Fisch C = nasopharynx
From what cells do glomus tumors arise?
Glomus - neuroectocrine cells from jugular bulb adventitia, jacobsen’s, or arnolds nerve.
Are men or women more likely to get glomus?
women (5:1)
Muscles innervated by the facial nerve?
stapedius, stylohyoid, posterior belly of the digastric, muscles of facial expression
Parasympathetic glands innervated by branches of the facial nerve? which branches?
Lacrimal gland via GSPN
Salivary glands via chorda tympani
Afferent functions of the facial nerve?
Taste from anterior 2/3 of tongue
Sensation from multiple locations - including concha, parts of EAC, TM
5 intratemporal segments of the facial nerve? Which segment is most narrow?
Pontine/cerebellar; meatal; labyrinthine (most narrow); tympanic/horizontal; mastoid/vertical
5 extratemporal branches of the facial nerve?
Temporal, zygomatic, buccal, marginal mandibular, cervical.
3 landmarks for the extratemporal facial nerve (parotid surgery)?
Tragal pointer (1cm ant/inf/deep), 6-8mm inferior to tympanomastoid suture line, level of the posterior belly of the digastric.
3 Landmarks for the intratemporal facial nerve (middle ear/ mastoid surgery)?
Cochleariform process, superior to the oval window, inferior to the lateral canal at the level of the lateral canal.
Most common site of facial nerve dehiscence?
tympanic segment
Most common site of iatrogenic facial nerve injury during middle ear surgery?
tympanic segment above oval window
Most common site of facial nerve injury during mastoid surgery?
second genu near lateral canal
If recovery of function is not observed, at what point after onset of paralysis should MRI of the facial nerve be considered? Name 2-3 additional indications for imaging.
4-6 months of no recovery. Also consider imaging with: 3 weeks progressively worsening, recurrent ipsilateral, facial twitching, other cranial neuropathies.
Define/describe: neuropraxia, axonotmesis, neurotmesis.
neuropraxia - compression injury, recovers with no electrical abnormality.
axonotmesis - damage to axonal structure without damage to endoneurium, will see Wallerian degeneration followed by subsequent recovery.
Neurotmesis - damage to axon and endoneurium. Wallerian degeneration and uncertain recovery.
What is Bogorad syndrome?
innervation of the lacrimal gland instead of submaxillary, causes crocodile tears during eating.
When should ENoG be offered after acute facial paralysis?
Between 3 days and 14 days (after Wallerian degeneration allowed to occur).
When should surgical decompression be considered based on results of ENoG after acute facial paralysis?
> 90% degeneration on the affected side + confirmation with electrical silence on EMG -> surgical decompression offered.
What type of EMG potentials would be expected with degeneration and at what time point after facial nerve injury would that be seen? What type of potentials with evidence of nerve recovery and at what time point after injury would that be seen?
Expect electrical silence at acute injury with degeneration and then spontaneous fibrillation potentials after 14-21 days. With nerve recovery, see polyphasic action potentials after 6 weeks.
Regarding TB fractures (longitudinal vs transverse, though this terminology increasingly outdated): ____ are the most common type. ___ carry a higher risk/percentage of facial nerve injury.
Longitudinal most common. Transverse = higher %age facial nerve injury.
Regarding extratemporal facial nerve injury: injuries distal to the ____ should be left to recover spontaneously.
lateral canthus
How should a box cutter injury lateral to the lateral canthus be managed in the presence of gross wound contamination?
Debride/wash out wound. Tag the ends of the severed nerve and return within 30 days for reanastomosis
Possible causes of facial paralysis at birth?
CULLP, mobius, birth trauma (esp forceps delivery)
Possible causes of bilateral simultaneous facial paralysis?
Lyme, sarcoidosis (Heerfordts/uveoparotitis), Guillan Barre (most common for simultaneous bilateral), Mobius, Melkersson-Rosenthal (recurrent; may be unilateral, a/w chronic/recurrent facial edema and tongue fissuring).
Surgical approach for facial nerve decompression for a hearing ear? Non-hearing ear?
Hearing ear = MCF +/- transmastoid decompression. Non-hearing = translab
Prognosis in Ramsay Hunt for facial nerve recovery?
Worse than Bell’s; depends what you read but anywhere from 40-60% will recover complete function
MOE is thought to invade bone through which structure in the lateral canal? Is this structure normal or a developmental abnormality? What is an analogous structure in the medial canal? Is this structure normal or a developmental abnormality?
Fissures of Santorini; normal structure. Foramen of Huschke; developmental abnormality/failed to obliterate.
First line therapy for MOE?
Ciprofloxacin PO
Name 3-5 risk factors for AOM?
smoker in the home, daycare, siblings, cleft palate, non-breast fed, supine bottle feed, and so on
Mechanism of pneumococcal penicillin resistance?
penicillin binding proteins
When should treatment be initiated in an 18mo with mild AOM and with what antibiotic/dose for what duration?
Immediate initiation for <2 years old; start with amox 90mg/kg/day divided TID for 10 days.
When should treatment be initiated in an 7yo with mild AOM and with what antibiotic/dose for what duration? What if patient is pen allergic? What if patient has severe disease with fever >39C?
If 7 years, wait 72h for resolution, then amox same dose for 5 days if uncomplicated. If pen allergic, azithromycin first line. If severe disease, augmentin
Definition of recurrent AOM?
3 in 6 months or 4 in 12 months
Most common organism for: otitis externa, AOM, COM
OE = pseudomonas, AOM = strep pneumoniae; COM = nontypeable H flu
Painless otorrhea, multiple perfs in a single TM — what diagnosis is suggested by these findings? 2-3 options for diagnosis? Management?
MTB. Can diagnose with PPD, biopsy, CXR. Management is RIPE
Management of AOM with facial paralysis? COM with facial paralysis?
IV antibiotics and tube. COM with facial paralysis = surgery with tympmastoid
Most common intracranial complication of AOM/COM?
meningitis
What is otic hydrocephalus and with which complication of AOM is it associated?
hydrocephalus from propagation of clot to transverse sinus; a/w lateral sinus thrombosis. Check eyes for papilledema; avoid LP to prevent herniation
Through what structure does labyrinthitis progress to meningitis?
cochlear aqueduct
Diagnosis and management for otic syphilis?
treponemal antibody has highest sensitivity and can capture tertiary. VDRL RPR also reasonable sensitivity but only for primary/secondary and can be false positive. Management is Penicillin G
Responsible organism and implicated deer tick in Lyme disease?
Borrelia bergdorferi, Ixodes deer tick
Treatment for CMV symptomatic infections in neonates? asymptomatic infections?
Ganciclovir (shown to reduce HL). No recommendation for asymptomatic
Pittsburgh TNM staging for ear SCC? (2000)
T1= no bony erosion, T2= limited bony erosion, T3= full thickness bony erosion or middle ear/mastoid involvement, T4= facial paresis, >0.5cm soft tissue invasion, or into bad things (carotid artery, petrous apex, jugular foramen, dura). N1 = any node. Automatically Stage IV disease. M1= any met. Automatically Stage IV disease.
Keratosis obturans vs cholesteatoma of EAC: Bony erosion? Bony expansion? Pain?
Both erode bone. Keratosis obturans expands it. Keratosis painless, cholesteatoma = pain.
Osteoma vs Exostosis: Sessile/pendunculated? vascular channels? involved in suture lines? cold water exposure?
Osteoma pedunculated, exostosis sessile. Osteoma with vascular channels and involved in suture lines. Exostosis a/w cold water exposure
Longitudinal vs Transverse TBone Fractures: more common? higher risk of facial nerve injury?
Longitudinal more common. Transverse higher risk of facial nerve injury
What virus has been associated with otosclerotic foci?
Measlesvirus
What is paracussis willi and what does it suggest?
Better hearing in noisy environments, suggests otosclerosis
1 and #2 cause of revision stapes surgery?
1 prosthesis displacement, #2 incus erosion
Describe Jaersdoerfer criteria and scoring system. What is the “cutoff” for surgery?
10 points total: 2 points for stapes. 1 point each for external ear appearance, tympanic membrane, round window, oval window, malleo-incudal complex, incudostapedial joint, facial nerve, mastoid air cells, middle ear space. >6 = candidate for surgery. <6 do not operate
Where in the inner ear is the immunogenic response located?
endolymphatic sac
MOA(site) for ototoxicity with each of the following drugs: aminoglycosides, macrolides, diuretics, salicylates, cisplatin, carboplatin
aminoglycosides = outer hair cells. Macrolides/diuretics/salicylates = stria vascularis. Cisplatin = outer hair cells, carboplatin = inner hair cells
Which ototoxic hearing losses are reversible with drug cessation?
Macrolides, diuretics, salicylates
Which ototoxic drugs affect select frequencies (eg HF SNHL or high to mid SNHL) rather than a a b/l flat SNHL?
aminoglycosides, cisplatin
Name 2-3 malignancies that can metastasize to the temporal bone
renal cell carcinoma, lymphoma, breast cancer, prostate cancer
