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Disorders > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the two types of noise induced hearing loss (NIHL)

A

Noise induced permanent threshold shift (NIPTS) and acoustic trauma

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2
Q

Noise induced permanent threshold shift

A

Repeated exposures to SPLs lower than those that produce acoustic trauma
Long term exposure
Occupational ONIHL

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3
Q

Acoustic trauma

A

Permanent cochlear damage after one exposure to very high SPLs
Signs and symptoms- otalgia, drainage, perf, hemotympanum, vertigo, muffled hearing, tinnitus

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4
Q

Other effects of noise exposure (7)

A

Fatigue
Annoyance/irritation
Reduced processing capacity
Physical effects
Tinnitus, hyperacusis
Vestibular
Low and ultra high frequency effects

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5
Q

What fraction of Americans with hearing loss have noise exposure?

A

1/3

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6
Q

Risk factors for NIHL

A

White/hispanic older males
Education is at most high school
Smoking
Diabetes
Ear canal
Genetics
Cerumen
Frequency temperature
Response to sound

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7
Q

What is the most common cause of noise exposure

A

Occupational

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8
Q

What federal administration regulated occupational safest

A

OSHA (Occupational Safety and Health Act)

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9
Q

Complications in NIHL

A

Dehydration, heart disease, smoking, alcohol, diabetes

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10
Q

OSHA hearing standards

A

8 hours at 85 dBA

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11
Q

For every 5 dB increase, what happens to the time

A

It cuts exposure time in half ex. 4 hours at 90 dBA

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12
Q

Contributing factors when considering how much noise is too much noise

A

Duration of exposure
Level of exposure
Frequency spectrum of the noise
Distance from the source

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13
Q

Equal energy hypothesis

A

Equal amounts of sound energy will produce equal amounts of hearing impairment regardless of how the sound energy is distributed in time
Biologically this does not make sense

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14
Q

Temporary threshold shift (TTS)

A

Exposure to loud sound for a few hours
May seem like buzzy ears, muffled hearing
Thresholds decline but recover within hours or days

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15
Q

Can a TTS cause long term effects?

A

Yes, but the permanent consequences may not be apparent for many years

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16
Q

Metabolic exhaustion

A

Auditory fatigue
Physiologic processes cannot keep up
Ex. change in oxygen tension in endolymph, glycogen depletion, free radical breakdown
Could lead to cell death if unrelieved
Known that taking breaks away from noise during prolonged noise can avoid TTS

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17
Q

Preconditioning/otoprotection

A

Exposure to conditions that turn up innate protective pathways including HSP heat shock proteins and anti-oxidant enzymes

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18
Q

What can permanent damage due to the ear?

A

OHC and IHC damage
Supporting cell damage
Tectorial membrane damage
Changes in structure
Changes in ion levels in levels or outside of cells
Mixing of fluids
Ganglion cells and connections, channel regulation
Generation of potentials
Efferents
Central connections

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19
Q

General rules of NIHL PTS

A

SNHL, bilateral, initially a history of TTS
High-frequency losses rarely exceed 75 dB and low frequency losses rarely exceed 40 dB
Dose related

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20
Q

NIHL prevention

A

Information about what sounds can cause damage
Wear hearing protection
Be alert to hazardous noise in the workplace
Protect children
Baseline audiogram
Public awareness- educate, provide tools

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21
Q

Sensory hearing loss (according to Schuknecht)

A

From the cochlea
Degeneration of hair cells and supporting cells at the base of the cochlea
Atrophy of the organ of corti which then affects the auditory nerve
Abruptly sloping, high frequency loss
Starts at middle age and progresses slowly
Speech discrimination abilities should match audiogram

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22
Q

Neural hearing loss (according to Schuknecht)

A

Loss of dendrites and then cochlear neurons
High frequency, often mild HL
Poor speech discrimination scores (often worse than what would expect from audiogram)
Progresses rapidly with aging
Two types- primary (affects spiral ganglion cell directly, less common) and secondary (hair cells die, no input, nerve cells die)
Can cut half the nerve without changing thresholds
Can lose up to 90% without threshold change
Relevant to ANSD, central functions, hidden hearing loss

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23
Q

Can spiral ganglion cells survive a long time without hair cells?

A

Yes, there is evidence in hearing aid users

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24
Q

Summary of neural temporal bone studies

A

Number of ribbon synapses per IHC decreased with increasing age
Peripheral axon counts decreased linearly with age
Axon loss 3x greater than IHC degeneration
SGN count decrease linearly with age

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25
Q

Metabolic presbycusis (according to Schuknecht)

A

Flat SNHL with good preservation of speech understanding

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26
Q

Mechanical (cochlear conductive) presbycusis (according to Schuknecht)

A

Changes to cochlear mechanics due to mass/stiffness changes or atrophy of spiral ligament
Sloping hearing loss, including low frequencies
Speech understanding is generally good

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27
Q

Central presbycusis

A

Neuronal loss
Synaptic
Chemistry
Connectivity
Speech of processing
Physiology

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28
Q

Incidence/prevalence of presbycusis (for 65-75, 75+, 90+)

A

65-75- 30-35%
75+- 40-50%
90+- greater than 90%

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29
Q

General age related hearing loss (ARHL) clinical characteristics

A

Bilateral, symmetric SNHL (high frequencies most affected)
Progressive hearing loss with age
Initially word recognition scores consistent with PTA, but progressively poorer
Gradual onset
Negative history for noise
exposure
Normal otologic exam
DPOAEs decline independently of thresholds
SRT will increase with age
Tymps usually normal with some decreased compliance in age

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30
Q

ARHL trends for male/female

A

In U.S. females do better than males but there are ethnic differences
Female: 10-16kHz by 40s, 6-8kHz by 50s, speech frequencies by 60s
Male: 10-16kHz by 30s, 6-8kHz by 40s, speech frequencies by 60s

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31
Q

Does noise exposure accelerate aging of the auditory system?

A

Yes, will see effect on ABR

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32
Q

Physical effects of aging for the outer and middle ear (5)

A

Loss of tissue elasticity of pinna and ear canal
Stiffening of tympanic membrane
Degeneration of middle ear muscles
Calcification of ligaments
Ossification of ossicles

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33
Q

Clinical effects of aging for the outer and middle ear

A

Minor effects
Often normal tymps, immittance if HL allows
Women often have decreased compliance

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34
Q

Relation with extended high frequencies and ARHL

A

Lose them early
Most vulnerable part of the cochlea
Over the age of 40, may not have thresholds above 16k

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35
Q

What do extended high frequencies help with?

A

Sound localization, hearing in noise and auditory segregation

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36
Q

Underlying physiological effects with ARHL

A

Down regulation of neural activity that are important for speech processing
Loss of grey matter volume in primary auditory cortex
Resource allocation (sensory abilities affect which and how much brain regions are recruited for functions)

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37
Q

Efferent function changes with ARHL

A

Gain control
Inhibit cochlear amplifier
Role in signal detection in noise
Protective role during acoustic over-stimulation
Likely affected but lack of clinical testing

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38
Q

Cortical responses in older adults

A

Delayed response latency- stimulus audibility, not hearing loss related but rather neurophysiological changes

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39
Q

Presbycusis treatment and rehab

A

Counsel, alleviate symptoms, difficulty separating effects of aging from effects of noise exposure
Rehab options: HA, assistive devices, group rehab
All senses decline with age

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40
Q

Retrograde process

A

Lose ribbon synapses then auditory nerve fibers then spiral ganglion cells

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41
Q

Incidence of Menieres

A

0.2-2%

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42
Q

Common factors of Menieres

A

More common in women, 40s and 50s diagnosis
Associated with history of allergies, smoking, virus or respiratory infection

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43
Q

Pediatric Menieres

A

2.3% of MD are in children
1/3 of the children have a family history
Higher prevalence bilaterally
Overlaps with vestibular symptoms of vestibular migraines, BPV, SSNHL

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44
Q

Sign and symptoms of adult Menieres

A

Classic:
-HL
-tinnitus
-vertigo
-fullness
-fluctuation
Other:
-hydrops can be associated with the classic symptoms without vertigo
Symptoms can vary
Usually unilateral but about 40% of patients will become bilateral
70% of patients vertigo will resolve/burn out in 8-10 years

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45
Q

Differential diagnosis for Menieres

A

-CPA tumor
-BPPV
-Lyme disease
-neurosyphilis
-labyrinthitis
-vestibular neuritis
-perilymph fistula
-vestibular migraine

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46
Q

Meniere Syndrome

A

Very similar to Menieres disease but this is secondary to another disease like thyroid or an endolymphatic tumor

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47
Q

Basic definition of Menieres

A

Disorder of the inner ear characterized by dysfunction in the fluid balance-regulating system

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48
Q

Characteristics of definite Menieres (according to guidelines)

A

-two or more spontaneous attacks of vertigo, each lasting 20 minutes to 12 hours
-audiometrically documented low to midfrequency SNHL in the affected ear on at least 1 occasion before, during or after 1 of the episodes of vertigo
-fluctuating aural symptoms (HL, tinnitus, or ear fullness) in the affected ear
-other causes excluded by other tests

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49
Q

Characteristics of probable Menieres

A

-at least 2 episodes of vertigo or dizziness lasting 20 minutes to 24 hours
-fluctuating aural symptoms (HL, tinnitus, fullness) in the affected ear
-other causes excluded by other tests

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50
Q

Menieres HL characteristics

A

-HL
-low frequency SNHL initially, but declines with time across frequencies
-may not be the most disturbing symptom unless interferes with work
-reduced discrimination, tinny
-recruitment
-diplacusis (ears perceive different pitch)

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51
Q

Menieres fullness characteristics

A

-no objective measures for this so really have to rely on patients
-about 66% report
-associated with gait difficulties, drop attacks and hyperacusis

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52
Q

Menieres vertigo characteristics

A

-spinning when nothing is and neither are you
-earliest symptom
-usually lasts 1-2 hours but can last up to 24
-nausea, vomiting
-afterwrds, feel tired, unsteady, and nauseated
-periods of interim non-symptomatic
-triggers may be diet, menstrual cycle or stress

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53
Q

Drop attacks (Tumarkin crisis)

A

Usually mild (72%), 6% serious
Associated with utricular/saccular dysfunction

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54
Q

Describe the components of perilymph

A

Similar to CSF
High sodium and low potassium

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55
Q

Describe the components of endolymph

A

Similar to intracellular fluid
Low sodium and high potassium
Stria vascularis

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56
Q

What structure separates endolymph and perilymph

A

Membranous labyrinth

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57
Q

How do hydrops affect the membranous labyrinth?

A

Causes distortion of the structure

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58
Q

Pathophysiology of Menieres

A

-build up in pressure may lead to microtears of membranous labyrinth
-temporal bone histology (maybe due to degeneration but could be a secondary cause)
-vascular risk factors/ischemia
-fluid imbalance
-ion imbalance
-endolymphatic hydrops

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59
Q

Natural history of Menieres

A

-eventual resolution of vestibular symptoms
-57-60% of patients in 2 years
-71% in 8 years
-long term PTA in affected ear is about 50
-speech discrimination is about 53%
-caloric response reduction 50%
-vestibular function does not become normal
-symptoms decrease due to loss of function
-hearing issues will progress
-initial audio is tent curve
-5 years is sometimes peak and sometimes flat
-10 years is mostly flat curves

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60
Q

Diagnostic testing for Menieres

A

-unilateral vs. bilateral
-case history
-complete hearing eval including LDLs
-maybe vestibular testing like dix-hallpike
-maybe EcochG, ABR, EEG, DPOAEs, osmotic dehydration
-rule out tests: blood tests, allergy tests, MRI

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61
Q

Menieres and glycerol/urea/mannitol tests

A

-rarely done
-process:
-osmotic diuretics
-measure PTA or low/mid frequency thresholds
-patient ingests
-measure PTA or low/mid frequency thresholds
-compare PTA
-expectation is that it improves in Menieres, no change is not Menieres

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62
Q

EcochG and Menieres

A

-SP/AP ratio is greater than 0.5 or area ratio
-some labs report better sensitivity and specificity with more symptoms but variability
-recent work may improve sensitivity/specificity

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63
Q

What does new research show with Menieres?

A

-increased attention to vestibular, WAI and EP tests
-imaging
-endolymphatic sac surgery is back in China
-CI’s are a good option

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64
Q

New diagnostic approaches to Menieres

A

-high resolution MRI
-proteomics
-EvestG (electrovestibulography), similar to EcochG but with tilt and measure
-subjective visual vertical (SVV) perception

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65
Q

Gold standard for diagnosing Menieres

A

-imaging
-high pass masking of ABR (CHAMP), maybe this has not been able to replicate
-clinical history
-audiology eval
-exclude other conditions

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66
Q

Conservative management and treatment of Menieres

A

-minimize symptoms, particularly vestibular
-conserve hearing
-complications with this though: consistent diagnosis, fluctuation, assessing effectiveness and time frame
-conservative treatment has good results with about 85% of patients being helped
-lifestyle changes: regular meals, low salt, no MSG, no caffeine, no smoking, avoid triggers

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67
Q

Staging HL in definite/certain Menieres

A

-stage 1 is less than or equal to 25
-stage 2 is 26-40
-stage 3 is 41-70
-stage 4 is greater than 70

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68
Q

Medical management of Menieres

A

-diuretics and salt restriction (salt is believed to alter fluid balance in inner ear leading to depletion of endolymph)
-acute therapy: meclizine, benzodiazepines, corticosteroids, betahistine
-maintenance therapy
-vasodilators (allows the blood to slow more freely, allows for better metabolism of endolymph
-immunologic management (systemic steroids and intratympanic dexamethasone)
-steroids-intratympanic (autoimmune/inflammatory disease), lack of effect on hearing
-PE tubes
-antiviral drugs
-anti-nausea drugs
-homeopathy
-herbal (gingko)
-chiropractic
-acupuncture
-Meniett
-Intratympanic corticosteroids
-endolymphatic shunts
-intratympanic gentamycin
-endolymphatic sac vein decompression

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69
Q

Mechanical management of Menieres

A

-transtympanic micropressure
-Meniett device (portable low intensity alternating pressure generator)

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70
Q

Meniett

A

-has to be prescribed
-low frequency, low amplitude pressure pulses within the middle ear via a close-fitting ear cuff and tympanostomy tube
-use 3x a day, 3 minutes a session

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71
Q

Intratympanic treatment of Menieres

A

-purposefully damage the inner ear to stop vertigo
-injected through the TM using a narrow needle then the drug is left in the ME for a period of time then allowed to drain out
-destroys sensory cells

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72
Q

Intratympanic gentamicin for Menieres

A

-side effects can include temporary imbalance or nygstagmus, hearing loss
-often relieves symptoms but not always

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73
Q

Endolymphatic sac surgery

A

-addresses the site of obstruction causing hydrops
-different types:
-decompression
-shunting
-drainage
-removal of sac
-damage to sac
-blocking the sac

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74
Q

Vestibular nerve selection

A

-possible vestibular suppression without any effect on hearing
-single step procedure
-tricky and can have intraoperative complications of damage to facial nerve, cochlear nerve or CSF leak

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75
Q

Labyrinthectomy

A

-considered for patients with intractable vertigo and no functional hearing
-similar efficacy to vestibular nerve section

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76
Q

Menieres rehab

A

-physical/audiological issues:
-fluctuating HL
-tinnitus
-poor word rec
-rising configuration
-loss of dynamic range
-emotional issues:
-stress of illness
-restriction of activities
-vestibular rehab

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77
Q

Strategies for fluctuating HL

A

-hearing aids
-multiple memories to match the fluctuating hearing

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78
Q

Menieres counseling

A

-recognize emotional and social aspects
-reaosnable expectations
-support for identifying triggers
-reporting back
-use of earplugs
-support use of amplification
-support groups

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79
Q

Secondary endolymphatic hydrops

A

-trauma
-postoperative (CI, stapedectomy)
-otosclerosis
-CPA tumors
-other disease (autoimmune, infection)
-drugs (fluid balance)

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80
Q

Vestibular migraine

A

Vertigo, imbalance, dizziness, unsteadiness, motion sensitivity, muffled hearing, tinnitus, fullness

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81
Q

Genetic component for Menieres and vestibular migraines

A

5-20% familial for Menieres
Some families show a strong association with migraine
Maybe multifactorial

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82
Q

What is the most common vestibular disorder

A

BBPV

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83
Q

Mal de debarquement

A

Intense rocking, swaying sensation
Usually after a cruise
More common in women
Etiology unknown
May not resolve on its own
may resolve with vestibulo-ocular reflex reset

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84
Q

Chiari malformation

A

-1/1000 clinically
-type 1 may not be diagnosed
-symptoms include dizziness, muscle weakness, numbness, vision problems, headahce, progressive SNHL, tinnitus and problems with balance and coordination
-part of the cerebellum is displaced into the spine
-occipital headache with valsalva
-post surgery tinnitus

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85
Q

Perilymphatic fistula

A

-abnormal connection between inner and middle ear that allows leakage of perilymph
-like Menieres also a fluid imbalance
-unilateral HL, flucutating SNHL, sudden or progressive and/or fluctuating word discrimination, vestibular symptoms (vertigo, dysequilibrium, tullio, hennebert), tinnitus, aural fullness, flat tymps

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86
Q

Define vertigo

A

sensation of self-motion when no self-motion is occurring or the sensations of distorted self-motion during an otherwise normal head movement

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87
Q

Define dizziness

A

Sensation of disturbed spatial orientation without a false or distorted sense of motion

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88
Q

Most common etiologies of dizziness and vertigo

A

-physical trauma
-acoustic trauma
-barotrauma
-spontaneous
-ear surgery, particularly stapes surgeries
-neoplasms, cholesteatomas
-congenital, especially cochlear abnormalities

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89
Q

Diagnosing and testing perilymphatic fistula

A

-case history
-battery of hearing tests
-fistula test (pressure to ear, look for nystagmus, Henneburt)
-ECOG
-ENG
-VEMP
-exploratory surgery
-MRI with intrathecal gadolinium
-marker to identify perilymph

90
Q

Treatment of perilymphatic fistula

A

-bedrest
-avoidance of straining
-reoccurs in 21-47% of patients
-exploratory tympanotomy and repair

91
Q

Vestibular neuritis

A

Viral or bacterial infection of the vestibular nerve
May have long recovery period or be chronic
Episodic vertigo

92
Q

Labyrinthitis

A

Viral or bacterial infection of the labyrinth
Serous or suppurative
Episodic vertigo with HL

93
Q

Embryology week 3

A

Inner ear:
-formation of the otic placode (thickening of the neuroectoderm), otic pit forms

94
Q

Embryology week 4

A

OE and ME:
-branchial arches
Ossicles and ME:
-first pharyngeal pouch ectoderm extends outward to form the tubotympanic recess and approaches 1st cleft ectoderm
-ossicles form from branchial arches neural crest mesenchyme
Spiral ganglion:
-statoacoustic ganglion
Disorders:
-Michel aplasia
-common cavity malformation
-cochlear hypoplasia

95
Q

Embryology week 5

A

External ear/six hillocks of his:
-1. tragus (first/mandibular arch)
-2. crus of helix
-3. ascending helix
-4. upper helix, scapha and antihelix
-5. middle scapha, antihelix and helix
-6. antitragus
Ossicles and ME:
-neural crest mesenchyme concentrates (ossicles) between cleft and pouch
-cleft widens (future EAM)
-ectoderm plug
TM:
-tubotympanic recess (1st pharyngeal pouch) contacts ectoderm
Stapes:
-ring around stapedial artery
Spiral ganglion:
-cochlear and vestibular ganglia distinct

96
Q

Embryology week 6

A

IE:
-(6-8) saccule and utricle
-(6/7) semicircular canals evaginations of the dorsal sac, crista ampullaris
-neuroepithelial ridge develops at ampullated ends

97
Q

Embryology week 7

A

Pinna:
-moves dorsolaterally
Ear canal:
-tympanic ring forms
Spiral ganglion:
-(7-9) fibers enter cochlear epithelium
Disorders: mondini

98
Q

Embryology week 8

A

Ear canal:
-external canal is thick epithelial plug, migrated inward toward ossicles
-contact with the primordial malleus (beginning of TM)
IE:
-cochlea reaches 2.5 turns
-pars inferior
-semicircular canals reach general form

99
Q

Embryology 9-10

A

Organ of Corti:
-sensory epithelium

100
Q

Embryology week 10

A

TM:
-bony ring of TM in place but incomplete
-ring ossifies 10-19 weeks
Stapes:
-stirrup shape
Organ of Corti:
-(10-20) stria vascularis

101
Q

Embryology week 11

A

Organ of Corti:
-IHC and OHC present
-immature stereocilia
Spiral ganglion:
-synapses on HC
IE:
-gross histological differentiation (presence of hair cells) complete

102
Q

Embryology week 12

A

ME:
-mesenchyme in TM cavity begins to become vacuolated

103
Q

Embryology week 11-16

A

TM:
-increases in size

104
Q

Embryology week 14

A

Organ of Corti:
-HC and stereocilia better developed
-supernumerary HC
-pillar cells and tunnel of corti
Spiral ganglion:
-efferents on IHC

105
Q

Embryology week 15

A

Ossicles and ME:
-malleus and incus are adult size and shape
Spiral ganglion:
-(15-24) myelination

106
Q

Embryology 16-19

A

IE: cochlea reaches adult size

107
Q

Embryology week 18

A

Pinna:
-separates from the head
Ear canal:
-(to week 21) plug starts to recanalize via apoptosis
-forming the external canal
IE:
-semicircular canals reach adult size

108
Q

Embryology week 19

A

Organ of Corti:
-mostly mature appearance

109
Q

Embryology week 20-22

A

Pinna:
-approaches mature shape
Ossicles and ME:
-tympanic cavity grows to enclose ossicles but still full of mesenchyme
Organ of Corti:
-(20-25) modiolus ossification

110
Q

Embryology week 22

A

Spiral ganglion:
-afferent synapses morpholol mature

111
Q

Embryology week 26-30

A

Ossicles and ME:
-ossicles ossified

112
Q

Embryology week 32

A

Ossicles and ME:
-stapes adult size and ossified

113
Q

Embryology week 33

A

Ossicles and ME:
-early pneumatization of mastoid air cells

114
Q

Embryology age 3

A

TM:
-changes in verticality
-changes in face

115
Q

Embryology age 9

A

Pinna:
-adult size and consistency

116
Q

Vestibular schwannoma incidence and prevalence

A

-makes up 80-85% of CPA tumors
-makes up 5-10% of intracranial tumors
-sporadic
-slightly more common in females
-mean age at diagnosis is about 50
-about 1 in 100,000
-symptomatic incidence is 1.4-9%
-more common in caucasian population; for black, hispanic and asian populations the tumors are likely larger
-usually rare and genetic

117
Q

Vestibular schwannoma pathophysiology

A

-inflammation
-immune response
-aging of system-more vulnerable
-inactivation or loss of tumor suppressor gene
-possible role of epigenetic changes
-idiopathic

118
Q

Vestibular schwannoma effects

A

-nerve compression (but size of tumor no relation to degree of HL usually until the tumor is large)
-effect on blood flow
-change in gene expression-secretion, cytokines
-possible contralateral, delayed effects
-endolymphatic hydrops

119
Q

Vestibular schwannoma CN symptoms

A

-CN V: loss of corneal reflex (blink on cotton wisp to edge of cornea), facial numbness (3 divisions, test with cotton ball and end of paperclip/blunt needle)
-CN VII: Hitselberger sign (paresthesia of posterior canal, motor effects, taste disturbances anterior 2/3 of tongue) rare, eye twitch
-CN IX, X, XI: swallowing, coughing, etc.

120
Q

Meningiomas

A

-15% of intracranial tumors and 3% of CPA tumors
-benign and does not metastasize
-can be locally aggressive because it can invade bone
-put pressure on nerves, brain and vascular
-close to brain tissue, may have a tail

121
Q

Other types/locations of tumors (10)

A

-facial nerve schwannoma
-hemangioma
-cholesteatoma
-lipoma
-arachnoid cyst
-glomus
-malignancies
-petrous apex
-external ear canal
-vascular loop

122
Q

Vascular loop (location, symptoms)

A

-anterior inferior cerebellar artery puts pressure on CN VIII
-similar symptoms to vestib schwannoma
-tinnitus, HL, vertigo, imbalance

123
Q

CPA locations

A

-inverted triangular cistern
-anterior inferior cerebellar artery and superior petrosal vein
-lateral wall, back wall of petrous bone
-medial wall by the pons
-top wall of the tentorium
-contains CSF

124
Q

CPA and CN issues

A

-may affect V, VII, VIII
-VII and VIII packaged together (the vestibular nerves posterior- inferior and superior-, facial nerve anterior superior portion, cochlear division of VIII anterior inferior portion)

125
Q

IAC

A

-8.5mm in length
-lined with dura
-filled with spinal fluid
-VII and VIII
-where peripheral and central systems meet

126
Q

Likely location for vestibular schwannoma

A

-where the schwann cells and oligodendrocytes meet (Obersteiner-Redlick zone)
-level of the porus (opening of IAC) in 56% of cases and inside the IAC in 44%

127
Q

Neurofibromatosis 2 (NF II)

A

-benign CNS tumors
-symptoms: HL, vision loss, gain abnormalities, paralysis, pain, seizures, risk of early mortality from brainstem compression
-hereditary, AD
-cellular transformation and proliferation of schwann cells
-non-expression of normal protein schwannomin/merlin by these cells
-usually unilateral but if initially diagnosed before 18, high chance of developing bilateral
-Cafe au lait spots, HL, tinnitus, dizziness
-may be mosaic (if suspected, need to test tumor)
-management involves surgery, CI is not helpful, ABI (auditory brainstem implant)

128
Q

Neurofibromatosis I (NF I)

A

-neurofibromas, many peripheral nerve tumors
-1/3000
-AD
-chromosome 17, encodes the tumor suppressor neurofibromin
-cafe au lait spots

129
Q

Malignant tumors of the temporal bone may look like what?

A

Chronic suppurative ME disease

130
Q

Unusual nystagmus

A

-will usually only occur for large tumors
-Brun’s nystagmus (bilateral; low frequency, low amplitude horizontal nystagmus when looking toward the side of the lesion; high frequency, small amplitude nystagmus when looking away from the lesion)

131
Q

BPPV

A

-about 20% of all vertigo, 2% lifetime prevalence
-brief mild to intense vertigo
-triggered by changes in head position
-episodes usually less than 30 seconds
-otoconia/otoliths out of the utricle
-peak incidence in the 50s
-rare in people less than 35 unless there is a history of head injury
-associated with vestibular neuronitis
-may be present with vestibular schwannoma
-nystagmus with Diz-Hallpike diagnostic
-treated with epley and semont
-fullness- may be unilateral of bilateral
-may affect CN V and CN VII (reflexes)

132
Q

Common symptom for retrocochlear pathology

A

Unilateral tinnitus
-need to look at context however because may be from shooting or asymmetric noise/trauma

133
Q

Most common symptom of retrocochlear pathology

A

Unilateral/asymmetric SNHL
-usually high frequency
-can be mid but rarely low
-sudden or fluctuating HL

134
Q

Diagnostic tests for retrocochlear pathology

A

-pure tones
-speech discrimination
-PI/PB function for rollover (run at appropriate then at 80/85)
-immittance audiometry
-ABR, stacked ABR
-vestibular testing
-VEMPs
-OAEs

135
Q

Speech discrimination for retrocochlear pathology

A

Poor scores for thresholds

136
Q

Immittance audiometry for retrocochlear pathology

A

Reflexes (about 60% sensitivity is present)
Tone decay

137
Q

Evoked potential testing

A

-ABR peaks can be absent
-may be a big difference between ABR and behavioral
-EcochG
-stacked ABR
-may give more information about tumor location (VEMPs- saccule may indicate inferior vestibular nerve-, ENG, ABR- cochlear nerve-, ENOG)

138
Q

Tymps for retrocochlear pathology

A

Normal

139
Q

Reflexes for retrocochlear pathology

A

Elevated or absent

140
Q

Do tumors here grow fast or slow?

A

Slow or not at all

141
Q

Will word discrimination decline if the tumor is not growing?

A

Yes, even if little to no growth

142
Q

Translabyrinthine approach

A

-advantages: no retraction of cerebellum, allows for good identification of CN VII, allows for good exposure of IAC, less risk of CSF leak
-disadvantages: hearing is sacrificed

143
Q

Retrosigmoid approach

A

-advantages: hearing preservation is possible, access to CPA
-disadvantages: limited access to lateral IAC/fundus, difficult to repair or graft CN VII, increased risk of air embolism/CSF leak/post-op headache, cerebellar retraction is necessary

144
Q

Middle fossa approach

A

-advantages: excellent for intracanalicular tumorsm especially at the lateral end of the IAC, hearing preservation is possible, extradural with low risk of CSF leak
-disadvantages: lack of access to CPA and posterior fossa

145
Q

Management considerations for retrocochlear pathologies

A

-best course for patient
-preservation of hearing
-preservation of facial nerve function
-avoid morbidity and mortality

146
Q

Complications from surgery

A

-HL
-facial nerve injury
-CSF leak
-cerebellar damage
-arterial occlusion
-migraine

147
Q

Gamma knife radiation

A

-advantages: decreased length of stay, decreased cost, rapid return to full employment, lower immediate posttreatment morbidity and mortality
-disadvantages: necessity for regular monitoring and frequent re-scanning, does not eliminate the tumor and has higher recurrence rates and sometimes requiring salvage surgery, higher incidence of trigeminal nerve injury, unknown long-term incidence of secondary malignancies, higher incidence of postoperative dosabling vestibular dysfunction

148
Q

Rehab options

A

-HA
-CROS
-BAHA
-CI
-ABI
-vestibular rehab

149
Q

What is the basic clinical presentation of ANSD?

A

OAE are often robust in early life (may become absent or reduced with time)
AR are absent or significantly elevated
CM is present but is not drowned out by the waves, typically the only thing visible
ABR is grossly abnormal or absent
Audios are variable
Speech perception is typically poorer than audiogram

150
Q

Acquired AN

A

-prematurity
-hyperbilirubinemia
-exchange transfusion
-anoxia
-artificial ventilation
-ototoxic drugs
-low birth weight
-anemia
-sepsis
-meningitis

151
Q

AN and temporal processing

A

AN is characterized by poor representation of timing information in the auditory system

152
Q

AN and CAP

A

Latency will be larger and will keep going

153
Q

Synaptopathy

A

Location- IHC ribbon synapse, IHC-SGN synaptic soace
Mechanisms- impaired packaging/release of glutamate, disordered replenishment of vesicles to ribbon synapse
Results- receptor potentials are measurable, but excitatory postsynaptic potentials do not generate action potentials well-times to the stimulus

154
Q

Post-synaptic neuropathy

A

Location- SGN cell body, auditory nerve fibers
Mechanism- often, demyelinating disorders result in poor ability to encode time information; reduced number of auditory fibers results in poorly timed encoding to the brainstem
Result- early potentials may reveal a CAP, but later brainstem responses are absent or abnormal

155
Q

AN and corticals

A

-precise neural synchrony is required for ABR recordings (even a 0.5ms variations in firing rate can degrade the ABR response)
-cortical potentials are more tolerant of timing variations
-several studies suggest cortical potentials can be used to establish hearing thresholds in some individuals with AN

156
Q

When treating AN what would be helpful to know?

A

Detailed medical history, detailed audiologic exam/hearing threshold estimation, genetic evaluation, developmental history, imaging, family engagement

157
Q

Treatment options for AN

A

-audiologic: environmental modifications, HA, CI
-SLP
-manual communication
-alternative augmentative communication

158
Q

Other considerations for AN

A

What other developmental concerns are involved for the child?
- do they have head and trunk stability?
- do they have access to a wheelchair/stander?
- what other skills are they working on?
- what are the parents goals for child?
- what is the childs medical history?
Should we involve other specialties in treatment?
- OT, PT, SLP

159
Q

Atresia

A

-no ear canal due to a birth defect
-usually accompanied by abnormalities of ME bones and OE
-three forms
-may be genetic if there is a family history
-microtia may be associated
-can have maximum CHL (60 dB)
-CNT tymps
-BAHA is a good intervention
-can have surgery to restore hearing but may put facial nerve at risk

160
Q

Otitis externa

A

-infection of the skin of the EAC, often called swimmers ear
-can be caused by fungi and bacteria, worse in hot/humid environments and can develop following lacerations of the canal, may be a chronic issue, can be infectious so use gloves
-symptoms: ear pain, otorrhea, itching, aural fullness, tenderness/pain, fever, cellulitis, mild CHL if there is swelling, localized furuncle, redness

161
Q

Ramsay-Hunt

A

-reactivation of the varicella-zoster virus at geniculate ganglion
-viral infection of the OE, ME and IE
-trigeminal in origin
-symptoms: vesicular rash, ear pain, HL (SNHL), tinnitus, eyelid palsy, facial palsy, vertigo, change/loss of taste, will see if on pinna/canal/TM, reflexes will look weird due to affects of the facial and auditory nerve
-treatment is vaccination, steroids and anti-virals

162
Q

Collapsing canals

A

-most common in elderly and very young children
-use inserts instead of headphones
-ABG in mid-high frequencies (10-50) especially at 6kHz

163
Q

Mondini

A

-often associated with LVAS, Waardenburg, DiGeorge, CHARGE and Pendred
-cochlea will be about 1.5 turns
-at risk for perilymphatic fistula, meningitis
-severe to profound SNHL with some preservation of the high frequencies due to the basal turn still being present
-may also be severe rising to mild SNHL, bilateral, congenital
-degree of SNHL depends on degree of malformation
-SRT and WRS could be better than PTA
-OAEe will be absent where there is HL
-absent reflexes where there is HL

164
Q

ELVAS/EVA/LVA

A

-associated with incomplete partition, Pendred, BOR, perilymphatic gusher, Mondini
-3rd window theory
-similar symptoms to perilymphatic fistula
-needs to be diagnosed with CT or MRI
-more common in kids
-progressive (related to 250) and fluctuating HL, cochlear in cause, fake ABG but normal tymps and reflexes, usually mixed
-unilateral more common
-possibly severe to profound CHL but may have extremely good bone at low frequencies
-characterized by sudden drops and fluctuations

165
Q

SSCD

A

-seen in young children but incidence increases with age
-symptoms- tullio, hennebert, gaze evoked tinnitus, hypersensitive to sound, autophony, conductive hyperacusis
-may complain of feeling fullness, unsteadiness when sneeze/cough, onset of symptoms
-usually unilateral with gradual onset
-no evidence of TM or ossicular abnormality
-CHL will be similar to otosclerosis but will have reflexes and tymps, DPOAEs if HL allows, VEMP and WAI findings
-fake ABG

166
Q

AOM (acute otitis media)

A

-adult complaints- mild intermittent pain, fullness, popping, balance problems, clumsiness
-infants complaint- ear rubbing, irritability, fever, headache, cough, rhinitis, listlessness, anorexia, vomiting, diarrhea, sleep interruption
-otoscopy- moderate to severe bulging, new onset of otorrhea, ear pain
-may have CHL

167
Q

OME

A

-presence of fluid in ME, no signs or symptoms of acute ear infection, HL may be present
-otoscopy- amber, grey, white, blue
-HL may be mild
-will see best air frequency at 2000

168
Q

Mastoiditis

A

-may be due to untreated bacterial AOM
-high fever, pain/tender behind ear, may not have acute pain
-risks of meningitis, absess, CN palsy
-tymps may be flat B or not
may see CHL
-possible poor WRS

169
Q

Otosclerosis

A

-AD, variable expressivity
-progressive CHL, tymps are variable
-more common in women in middle age
-bluish cast of whites of eyes
-Schwartze sign/rising sun
-paracusis willisii (speech is easier to understand in noise than in quiet)
-bone will decrease at 2000
-AR is absent

170
Q

Osteogenesis imperfecta

A

-AD and variable expressivity
-blue sclera
-progressive SNHL in kids to mostly mixed in older ages
-chance of having having significant ABG

171
Q

Cholesteatoma

A

-painless smelly drainage, maybe dizziness, pain progressive unilateral CHL, retraction of TM, perf, granulation tissue, unresponsive to antibiotics, maybe see white mass medial in otoscopy, retraction pocket, dizziness
-tymps may be consistent with perf, may have reduced mobility due to mass
-absent AR

172
Q

Ossicular discontinuity

A

-tymps is Ad
-acquired CHL may have SNHL
-may have max CHL
-maybe reflexes

173
Q

Perf

A

-will see it in otoscopy, tymps will have large volume
-CHL increases in size as perf increases with largest at lowest frequencies

174
Q

Barotrauma

A

-pain, HL, tinnitus, vertigo

175
Q

Temporal bone fracture

A

-may present with facial nerve with facial paresis or paralysis
-case history may include black eye, bruising and blood behind the ear; can be from car accident or blunt trauma
-SNHL if there is a transverse fracture and CHL if longitudinal
-balance disturbances, tinnitus, vertigo

176
Q

OAV (oculo-auriculo-vertebral spectrum)

A

-heart and kidney issues
-ocular findings
-auricular abnormalities- microtia most common, ossicular malformation common, absence of the IAC or inner ear abnormalities
-50% have CHL and/or SNHL

177
Q

Treacher Collins

A

-OE abnormalities, CHL, rarely SNHL
-cleft palate 30% of the time
-60% sporadic
-AD, 100% penetrance, variable expressivity
-maximum CHL (60)

178
Q

JLN

A

-syncope most often elicited by emotion or exercise
-AR
-due to cardiac issues, risk of sudden death without treatment is high
-congenital profound bilateral SNHL

179
Q

GJB2

A

-most common genetic cause of congenital HL
-usually severe to profound SNHL

180
Q

Glomus tumors

A

-may ha e hoarseness, tongue paralysis, vocal weakness, shoulder drop, aspiration, pulsatile tinnitus is the characteristic symptom, sawtooth tymps, reddish/blue mass behind TM in otoscopy, contralateral decay for AR
-CHL if tumor is large enough
-glomus tympanicum- reddish/blue mass behind intact TM, pulsatile tinnitus, late non-auditory symptoms, sawtooth tymps
-glomus jugulare- pulsing tinnitus, CHL, swallowing difficulties, possible dizziness, slow growth, may eventually invade the brain/brainstem

181
Q

Pendred syndrome

A

-AR
-can be congenital or late onset often progressive hearing loss (may be sudden or fluctuate) but often bilateral
-associated Mondini and EVA
-possible thyroid enlargement
-testing- imaging, genetic testing, vestibular, counseling, issue of progression with treatment

182
Q

Waardenburg

A

-heterochromia irides, white forelock
-AD or AR
-HL is not typically progressive usually profound but can be mild in high frequencies, unilateral or bilateral SNHL (usually profound bilateral SNHL)
-expressivity extremely variable

183
Q

Connexin 26

A

-AR and non-syndromic
-most common form of congenital deafness
-family history important here
-normal tymps and otoscopy
-down sloping audiogram with HL in the high frequencies are the worst
-severe to profound deafness
-early onset with minimal progression
-not as frequent symptoms- progressive HL< mild to moderate deafness, asymmetry, AD, associated with skin conditions

184
Q

Crouzon

A

-75% of these patients have HL in addition to stenosis, atresia, microtia
-CHL most common but ME structural anomalies are rare
-OME

185
Q

Stickler

A

-HL most common specifically high frequency SNHL but CHL may also be common
-midfacial underdevelopment, cleft palate, eye problems, joint problems
-hypermobile TM 46% of the time

186
Q

Rubella

A

-usually flat severe bilateral SNHL but may be any mild to profound and can be unilateral and/or asymmetric
-typically congenital, can be late onset
-tymps should be normal, no AR
-usually flat severe bilateral SNHL but can be mild or profound

187
Q

Measles

A

-bilateral moderate to profound SNHL

188
Q

Mumps

A

-may cause profound HL that is often unilateral

189
Q

Meningitis

A

-intracranial complication of OM

190
Q

CMV

A

-symptomatic is at a greater risk of HL and more severe
-HL is mostly late onset, can be progressive and fluctuating
-asymptomatic may have moderate to profound bilateral HL

191
Q

Syphilis

A

-can involve ME, mastoid and IE
-fluctuating low frequency SNHL

192
Q

Hyperbilirubinemia

A

-neonatal jaundice due to build up of bilirubin
-yellow whites of eyes and skin
-temporary and permanent HL, specifically mild to severe HL

193
Q

Prematurity

A

-low birth weight
-many co-existing factors that may cause HL

194
Q

Age related HL

A

-clinical characteristics- bilateral, symmetric SNHL, progressive HL with age, initially word recognitions scores consistent with PTA but progressively poorer, gradual onset, negative history for noise exposure, normal otologic exam, no other otologic disease
-delayed cortical response latency
-SRT increases with age, greater difficulty understanding comfortably loud speech

195
Q

Noise induced HL

A

-common, preventable, can affect any age, cumulative
-2nd most commonly acquired HL
-other effects- fatigue, annoyance, reduced processing capacity, physical effects, tinnitus, hyperacusis, vestibular
-other factors- ear canal, genentics, cerumen, frequency, temperature, response to the sound
-often occupational

196
Q

Acoustic trauma

A

-permanent cochlear damage after one exposure to very high SPLs
-symptoms- otalgia, drainage, perf, hemotympanum, vertigo, muffled hearing, tinnitus

197
Q

Vestibular Schwannoma

A

-more common in caucasian population; usually rare and can be genetic or sporadic
-CN V- loss of corneal reflex, facial numbness
-CN VII- Hitselberger sign (paresthesia of posterior canal)
-CN IX, X, XI- swallowing, coughing
-benign and usually slow growth
-effects- nerve compression, effect on blood flow, change in gene expression

198
Q

PLF

A

-abnormal connection between inner and middle ear that allows leakage of perilymph
-fluid imbalance
-fluctuating CHL, sudden progressive word discrimination, vertigo, disequilibrium, nausea, vomiting, tullio, hennebert, tinnitus, aural fullness

199
Q

BPPV

A

-brief mild to intense vertigo that is triggered by changes in head position, episodes usually last less than 30 seconds
-peak incidence in the 50s
-may experience fullness and affect CN V and CN VII (reflexes)

200
Q

Chiari

A

-dizziness, muscle weakness, numbness, vision problems, headache, progressive, SNHL, tinnitus and problems with balance and coordination

201
Q

NF2

A

-symptoms- HL, vision loss, gait abnormalities, paralysis, pain, seizures, risk of early mortality from brainstem compression, cafe au lait spots
-usually unilateral but if diagnosed prior to 18, high chance of it developing bilateral

202
Q

Mal de Debarquement

A

-feeling of movement when not
-usually after a cruise

203
Q

Sudden sensorineural hearing loss (SSNHL)

A

-not CHL; characterized by a greater than 30 dB loss at 3 contiguous frequencies occurring within 24-72 hours
-typically unilateral and very sudden
-idiopathic but there is a higher incidence with various other syndromes
- need to exclude: pre-existing fluctuating HL, bilateral HL, low frequency HL (only), oscillopsia, signs of neurological or optical dysfunction (double vision, ataxia), signs of stroke, head trauma, acoustic trauma
-typically occurs between 40-54 years old
-50% of cases will experience tinnitus, fullness is less common and vertigo is less common
-pathophysiology- idiopathic, vasospasm, autoimmune, intracochlear membrane rupture, trauma, toxins, viral infections
-differential diagnosis: viral (syphilis, meningitis, encephalitis), other infections, Meniere, neoplasm, verterbrobasilar insufficiency, vascular abnormalities, endocrine abnormalities, MS, congenital abnormalities, trauma, PLF, ototoxicity, Lyme
-risk factors: genetic polymorphisms, endothelial function, migraine, statin use, cardiovascular risk factors, periodontal disease, chronic otitis media, smoking, alcohol use, diabetes
-work up: good history, pure tone, speech, immittance including reflexes, OAEs, EHF, ABR, vestibular tests only if vestibular symptoms
-refer!!!!
-high spontaneous recovery rate
-treatment: anti-inflammatories, hyperbaric oxygen, steroids
-negative prognostic factors: younger than 15 or older than 65, vertigo, HL in the opposite ear, profound HL, HF HL, previous HL, late presentation, family history
-bilateral- more likely to be profound, 50% no recovery, life threatening conditions more commonly associated
-pharmacological- speedballing, imatinib, heroin, cocaine, methadone overdose

204
Q

Autoimmune inner ear disease (AIED)

A

-bilateral SNHL of at least 30 dB at any frequency with progression in at least one year
-usually between 20-50
-pathophysiology- immune reaction to inner ear antigens, circulating immune complexes
-signs and symptoms: progressive, often fluctuating bilateral asymmetric SNHL over a period of weeks to months (excludes SSNNHL occurring in less than 24 hours), poor speech discrimination, vertigo, generalized imbalance, ataxia, tinnitus, aural fullness
-testing: audiometry, maybe vestibular, antigen specific and antigen non-specific tests
-differentials: PLF, Meniere and SSNHL
-some autoimmune disorders may be associated: Cogan, rheumatoid arthritis, Wegeners granulomatosis, eosinophilic granulomatosis, vitiligo, vasculitis, IBD, lupus, scleroderma

205
Q

Lyme disease

A

-CN VII palsy especially in kids it is a significant symptom, SSNHL, possible HF HL, tinnitus is common

206
Q

Vestibular migraine

A

-vertigo, imbalance, dizziness, unsteadiness, motion sensitive, muffled hearing, tinnitus, fullness

207
Q

MS

A

-inflammatory, demyelinating disease of the CNS
-two types: chronic progressive, relapsing remitting
-most debilitating illness among young adults; more common in females
-HL is sudden and usually fluctuates
-testing includes: pure tones, speech (may be poorer), reflex pattern, ABR, vestibular and MRI
-vertigo is relatively common but imbalance/disequilibrium is more common

208
Q

Labyrinthitis

A

-inflammation of the membranous labyrinth
-SSNHL/gradual HL, vestibular dysfunction, vertigo, fullness, tinnitus but also headache, vomiting, history of recent URI; may look like vestibular neuritis

209
Q

Vascular lesions

A

-ischemic: blood flow is interrupted, TIA (temporary blockage), thrombus (blood clot)
-hemorrhagic- bleed, aneurysm
-more common for people over 65, may be secondary to other conditions

210
Q

Superficial siderosis

A

-iron accumulation in the brain due to slow bleed into subarachnoid space, rare, may be related to amyloid angiopathy
-early symptoms for otovestibular system: progressive HL but may also have vestibular loss, loss of smell, after repair usually no recovery

211
Q

Stroke

A

-anterior inferior cerebellar artery: vertigo, tinnitus, HL, alone or with facial weakness, hemiataxia, hypalgesia
-retrocochlear: middle cerebellar peduncle, cerebellar flocculus, inferolateral tegmentum of the pons or cochlear
-vascular loops
-associated of stroke with both increased HL and increased risk of SSNHL

212
Q

Neurotoxins

A

-mercury, styrene, lead, hyperbilirubinemia

213
Q

TBI

A

-may affect thinking, concentrating, attention, word finding, tinnitus, balance disorders, HL, continuing headaches

214
Q

Non-otological surgery and anesthesia

A

-nitrous oxide, general, spinal/epidural (temporary low frequency loss)

215
Q

Cerebellopontine angle

A

-triangular space near the temporal bone, tumors may be here

216
Q

Incidence and prevalence of ARHL

A

-65-75 years old is 30-35%
-75+ years old is 40-50%
-90+ years mold is greater than 90%

217
Q

Pathophysiology of ARHL

A

-loss of tissue elasticity of pinna and ear canal
-stiffening of TM
-degeneration of ME musculature
-calcification of ligaments
-ossification of ossicles
-IE structures will degenerate independently

218
Q

Presbycusis treatment/counsel

A

-alleviate symptoms
-rehab options: HA, assistive devices, group rehab

219
Q

Vestibular Schwannoma surgery approaches

A

-translabyrinthine: hearing is sacrificed, good identification of CN VII, less risk of CSF leak
-middle fossa approach: hearing preservation possible, excellent for intracranial tumors, need to retract temporal bone though (no access to CPA)
-retrosigmoid: hearing preservation possible, access to CPA, limited access to IAC, difficulty repairing CN VII
-gamma knife: decreased length of stay and cost, does not eliminate tumor and high recurrence state

220
Q

4 stages of hearing loss in Menieres

A

1: less than 25
2: 26-40
3: 41-70
4: greater than 70

Disorders (3 decks)

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