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AUDE 5410 > final exam comprehensive > Flashcards

final exam comprehensive Flashcards

1
Q

ABR findings with conductive HL

A

an increase with absolute latencies

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2
Q

ABR findings with SNHL

A

higher wave latencies with early waves disappearing as the intensity decreases

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3
Q

ABR findings with retrocochlear pathologies

A

presence of wave 1 only

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4
Q

ABR findings with ANSD

A

a flattened sum curve, flipped condensation and rarefaction curves

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5
Q

ABR findings with a schwannoma

A

wave 5 increases and therefore interwave latency also increases

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6
Q

OAE findings with PE tubes

A

reduced or obliterated

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7
Q

OAE findings with negative ME pressure

A

variable responses

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8
Q

OAE findings with ANSD

A

present unless blood supply is impacted

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9
Q

neuroglial cells

A

the supporting cells of the brain
-astrocytes : nerve cells and functions as an insulator
-oligodendrocytes : myelin sheath for central nerve fibers
-microglia : activated with inflammation/degeneration in CNA
-ependymal cells : line CSF filled cavities and spinal cord

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10
Q

neoplasms

A

abnormal mass of tissue, can be benign or malignant
-a disorder of the cell cycle in which they prey on the host

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11
Q

classification of neoplasms

A

intracranial, benign, malignant, intra-axial and extra-axial

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12
Q

intracranial neoplasms

A

brain tumor that includes :
-benign and malignant tumors
-masses within brian
-tumors of meninges
-tumors from structures near brain tissue

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13
Q

benign neoplasm

A

slow growing with well defined borders
-generally not life threatening
-does not metastasize

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14
Q

malignant neoplasms

A

tends to grow faster and causes invasion and destruction of structures
-can become life threatening
-able to metastasize to other areas of the body

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15
Q

intra-axial tumors

A

originating within the brain tissue

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16
Q

extra-axial tumors

A

originating from tissue that is not originated from the brain

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17
Q

vascular tumors

A

most found within the temporal bone and are benign
-messy and difficulty to remove due to them becoming involved with blood supply
-typically presenting with symptoms in the 3rd decade of life

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18
Q

two types of vascular tumors

A

hemangiomas and vascular malformations

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19
Q

hemangiomas

A

initial rapid growth with decreasing growth rate

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20
Q

vascular malformations

A

grows in proportion with the body growth without regression
-more common than hemangiomas

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21
Q

site of lesion for vascular tumors

A

IAC or the geniculate ganglion of the 7th nerve
-can also arise from ME cavity

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22
Q

symptoms of vascular tumors

A

CN 7 dysfunction, hemifacial spasm, tinnitus and vertigo (occurs when CN 8 is impacted)

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23
Q

diagnosis of vascular tumors

A

case Hx and presentation of symptoms, high resolution CT scan, MRI with contrast (geniculate lesions may be difficult to view)

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24
Q

what type of MRI is useful with vascular tumors?

A

T2 weighted image as the fluid is brighter

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25
Q

management of vascular tumors

A

surgical removal

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26
Q

differential diagnosis of vascular tumors

A

meningioma, CN 7 schwannoma and cholesteatoma

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27
Q

schwannoma

A

benign tumor of the temporal bone and CPA that is produced by abnormalities of schwann cells and are slow growing
-extra-axial tumors

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28
Q

site of lesions for schwannomas

A

IAC from the 8th nerve, jugular foramen of 10th nerve or the fallopian cavity of the 7th nerve

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29
Q

explain the common growth pattern of a schwannoma

A

grows into the CPA involving the 7th and 8th nerve, it can grow large within the CPA, while in the CPA it can creep into the IAC and with further enlargement it can cause brainstem compression and 5th nerve involvement

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30
Q

symptoms of schwannomas

A

headache, tinnitus, unsteady gait, imbalance/vertigo, facial paralysis, nystagmus and if 4th ventricle compression occurs it can cause hydrocephalus, coma or death

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31
Q

schwannoma symptoms will typically present _________

A

ipsilaterally

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32
Q

audiologic findings of a schwannoma

A

unilateral HF SNHL, normal OAE with not significant HL, OAE suppression is decreased, poor WRS, abnormal ARTs, varied reflex decay (none seen with normal nerve, decay with affected nerve), abnormal ABR in most cases

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33
Q

diagnosis of a schwannoma

A

T1 contrast MRI
-a CT scan is not sensitive

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34
Q

management of a schwannoma

A

observation, radiosurgery or surgery

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35
Q

meningioma

A

the most common benign brain tumor of the CNS that are circumscribes, lobulated and white masses
-extra axial
-appears within middle to late decades of life

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36
Q

meningiomas can be …..

A

aggressive and locally invasive
-can invade nerves
-can become involved with vascular structures

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37
Q

site of lesions with meningiomas

A

meninges
-originating within the CPA and may grow into the IAC

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38
Q

risk factors for a meningioma

A

being an NF2 patient, having radiation therapy to the head and certain chromosomal abnormalities

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39
Q

symptoms of a meningioma

A

vertigo, tinnitus, nausea/vomiting

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40
Q

audiologic findings with a meningioma

A

progressive unilateral SNHL, abnormal ARTs on affected side, normal tymp, positive reflex decay, positive roll over and poor WRS in noise

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41
Q

treatment of meningiomas

A

surgical excision followed by radiation
-hearing preservation is more likely for CPA meningiomas rather than CN 8 tumors
-with old or ill patients the approach is more conservative with symptomatic management

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42
Q

differential diagnosis for meningiomas

A

osteoma, paraganlgioma, NF2 and facial nerve schwannoma

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43
Q

cortical tumors

A

tumors that are affecting the auditory cortex which may show normal results for peripheral auditory tests however poor WRS will occur

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44
Q

symptoms of cortical tumors

A

normal ABR if the periphery is normal, headaches, dizziness/unsteadiness

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45
Q

with cortical tumors, the symptoms will be seen _________

A

contralaterally

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46
Q

malignant tumors

A

often diagnoses at late stages with a dismal prognosis
-might show symptoms similar to chronic otitis media

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47
Q

symptoms of a malignant tumor

A

aural discharge, otalgia, HL, tinnitus, facial paralysis, headaches and cochleovestibular deficits (SNHL or vestib issues)

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48
Q

metastatic tumors

A

malignant tumors that are from other site of origins than the brain
-such as breast cancer, lung cancer, renal carcinoma, thyroid cancer, melanoma or osteoblastoma

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49
Q

autoimmunity

A

occurs when the body’s immune system attacks the body itself
-instead of the body protecting itself from disease, it attacks the body’s own cells
-more common within females

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50
Q

immunology of the inner ear

A

cells are connected by the blood labyrinth barrier that controls the movements of circulating inflammatory and other proteins/cells
-this is of importance for the immune response of the inner ear
-this barrier is not immunopriveleged
-this barrier is made of endothelial cells through a tight junction and it affects the EP

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51
Q

inner ear vasculature

A

responsible for the delivery of systemic drugs and steroids for inner ear treatment
-stria vascularis and spiral ligament have homestatic function that requires uncompromised blood flow
-barrier allows for endolymph to maintain high potassium levels required for production and maintenance of the EP and normal cochlear function
-disruption can lead to immediate HL

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52
Q

what can occur to the inner ear in response to a vascular reaction to inflammatory factors

A

breakdown of strial integrity, decreased endolymph production and reduced EP levels
-leading to SNHL

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53
Q

how can steroids negatively impact the immune system

A

suppress the production of inflammatory cells, suppress the production of cytokinesis, suppress the production of antibodies, stimulates production of inhibitory factors and increase production of junctional proteins

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54
Q

autoimmune inner ear disease (AIED)

A

autoimmune disorder that is characterized by progressive bilateral SNHL and its responsiveness to immunosuppressive agents
-reversible SNHL if treated early
-females are affected more with symptoms appears between 20 and 50 years of age

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55
Q

primary AIED vs. secondary AIED

A

condition of the inner ear vs. condition coming from another part of the body

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56
Q

symptoms of AIED

A

bilateral progressive SNHL, aural fullness, tinnitus, imbalance/ataxia and positional/episodic vertigo

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57
Q

diagnosis of AIED

A

lab tests and imaging studies
-physical exams are usually normal

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58
Q

treatment of AIED

A

corticosteroids remain the standard and lasting for around 4 weeks
-can be given longer for repeated or for relapses

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59
Q

differential diagnosis of AIED

A

sudden SNHL, menieres disease, vestibular schwannoma, MS, otosyphillis

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60
Q

sudden sensorineural hearing loss (SSHL)

A

greater than 30 dB SNHL occurring in at least 3 continuous frequencies within 3 days
-typically unilateral
-increased incidence with age and is seen with patients with previous viral infections

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61
Q

what is SSHL associated with

A

viral infections, ototoxic drugs, trauma, tumors, autoimmune diseases, menieres disease, drug abuse, nonorganic HL and vascular pathology

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62
Q

what do histiopathic findings show with SSHL

A

atrophy of organ of corti, stria vascularis or tectorial membrane
-most damage seen on the basal turn of the cochlea
-results in a more narrow spiral ganglion than the normal cochlea

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63
Q

audiologic findings with SSHL

A

unilateral sudden SNHL, rapid deteriorating speech understanding, may present with dizziness or vertigo, normal tymp and ARTs are consistent with HL

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64
Q

diagnosis of SSHL

A

case Hx, test battery, MRI to help rule out other disorders and lab tests (hormone levels, autoimmune conditions or diabetes)

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65
Q

treatment of SSHL

A

oral corticosteroids for around 4 weeks is typical but can be intratympanic steroids in higher concentration
-should begin within one week of onset

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66
Q

what are some consequences of long term steroid usage

A

increased appetite and weight gain, increased susceptibility to infection, organ damage, bone loss, increased hyperglycemia, fluid retention or increased blood pressure

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67
Q

prognosis of AIED

A

-good prognosis with mild low frequency SNHL or short term symptoms
-poor prognosis with old and young patients, high frequency or flat SNHL, vertigo or patients with diabetes

68
Q

what are demyelinating diseases

A

resulting in damage of the myelin sheath that surrounds nerve fibers within the brain and spinal cord
-results in impaired conduction of signals and neurological problems in affected nerves

69
Q

multiple sclerosis (MS)

A

progressive neurological autoimmune disease that is multifactorial
-affects the white matter pathways within the CNS
-causing focal areas of inflammation (plaques)
-unknown cause but is believed to have both intrinsic (genetic) and extrinsic (environmental) factors

70
Q

what is the hallmark of MS

A

plaques (sclerosis or scars)
-more typical within white matter showing preference for the optic nerve and optic chiasm

71
Q

symptoms of MS

A

visual problems (diplopia meaning double vision is seen first), fatigue/malaise, spinal cord issues leading to abnormal reflexes and poor coordination, numbness, dysarthric speech and ataxia

72
Q

audiologic findings with MS

A

SNHL, variable ARTs, poor WRS and may show central auditory processing deficits

73
Q

diagnosis of MS

A

history, periods of intensified symptoms and periods of diminished symptoms, high levels of immunoglobin found in CSF and imaging (CT or MRI)

74
Q

how many plaques are present within an MS patient

A

over two must be seen

75
Q

treatment of MS

A

no cure but is manageable
-immunosuppressive agents are recommended but not goo long term
-symptomatic treatment

76
Q

differential diagnosis of MS

A

susacs, schilders, diabetes, stroke, SSHL

77
Q

susac syndrome

A

self limiting syndrome characterized by encephalopathy (cerebral problems), retinal artery occlusion (vision problems) and asymmetric fluctuating SNHL
-more common in women between 20 and 40 years

78
Q

why is susac often diagnoses as MS

A

due to the presence of white matter defects in the corpus callosum
-high rates within women 20-40 years of age
-fluctuating disease
-asymmetric SNHL that is often low frequency and fluctuating
-associated with dizziness/vertigo

79
Q

schilder’s disease

A

progressive, degenerative demyelinating disorder of the CNS
-begins within childhood/young adulthood however is present in any age
-course in unpredictable
-often bilateral

80
Q

symptoms of schilder’s disease

A

personality changes, poor attention, irreversible and progressive loss of intellectual function, vision and hearing impairments, headaches, seizure, muscle weakness, paralysis and atrophy of adrenal glands

81
Q

diagnosis of schilder’s disease

A

MRI with plaques, no other lesions present and PNS is normal

82
Q

treatment of schilder’s

A

corticosteroids are used and symptomatic treatment

83
Q

cogan syndrome

A

rare chronic autoimmune inflammatory disorder
-impacts young adults with peak incidences in the third decade of life

84
Q

pathology findings of cogan syndrome

A

cell infiltration of spiral ligament, endolymphatic hydrops, degenerative changes in the organ of corti, extensive new bone formation in the inner ear and demyelination of the vestibular and cochlear branches of the 8th nerves

85
Q

symptoms of cogan

A

interstital keratitis (red, painful, light sensitive eyes), SNHL, nausea, ataxia, oscillopsia, tinnitus, progressive, musculoskeletal symptoms, fever, weight gain and fatigue

86
Q

testing of cogan

A

positive ECochG, caloric testing shows absent peripheral vestibular function, and generally high frequency slopping SNHL

87
Q

diagnosis of cogan

A

based on presence of inflammatory eye disease and vestibulocochlear dysfunction

88
Q

treatment of cogan

A

collaborative medical approach, corticosteroids for hearing and ocular symptoms, amplification (CIs are more successful) and vestibular rehabilitation

89
Q

wegener’s syndrome

A

autoimmune vasculitis that affects the upper and lower respiratory tracts, ear and kidneys with variable expressivity
-swelling of pinna may occur
-conductive HL associated with OM due to infection of nasopharynx

90
Q

treatment of wegener’s

A

immunosuppressive drugs, cytotoxic drugs
-without treatment it can be fatal

91
Q

diabetes and HL

A

due to vascular changes that affect the stria vascularis and spiral ganglion
-low frequency HL is common
-high frequency SNHL and fluctuating HL can also be seen
-WRS not affected unless neuropathy is present

92
Q

hypertension and HL

A

blood supply is affected and therefor reduced blood and oxygen supply to the cochlea
-increased incidence of high frequency SNHL

93
Q

vestibular system

A

the somatosensory portion of the nervous system that provides awareness of the spatial position of the head and body
-provides proprioception and kinesthesia
-peripheral sensory apparatus, vestibular system and motor ouput

94
Q

peripheral sensory apparatus (vestibular labyrinth)

A

located within the inner ear and is comprised of the following :
-semicircular canals that are sensory for angular or rotational acceleration
-otolith organs (utricle and saccule) that sense gravitational changes in which the utricle is linear and saccular is vertical

95
Q

central vestibular system (structures within the brainstem and cerebellum)

A

receives input from the peripheral vestibular mechanisms by the vestibular divisions of CN 8
-input from labyrinth is processed alongside visual sensory and somatosensory input
-influences eye movement, truncal stability and spatial orientation

96
Q

motor output (connection to motor nuclei and muscles)

A

comprised of vestibulo-ocular reflex (VOR), vestibulospinal reflex (VSR) and vestibulocollic reflex (VCR)

97
Q

VOR

A

gaze stabilizing reflex that helps keep the environment steady and stable
-when the head rotates one way, the eyes are rotated the opposite direction within the same axis to keep the visual field steady
-oscillopsia occurs when this is not working properly

98
Q

VSR

A

stabilizes posture
-maintaining posture, the back is involved

99
Q

VCR

A

stabilizes the head
-head is involved

100
Q

common symptoms of vestibular disorders

A

sense of imbalance, dizziness, nystagmus and vertigo

101
Q

nystagmus

A

disturbances of ocular movement characterized by nonvoluntary rhythmic oscillations or rapid jerky movements of one or both eyes
-either idiopathic or associated with disorders
-can occur spontaneously in response to vestibular upsets
-detection through ENG or VNG

102
Q

vertigo

A

a type of dizziness that is specific to vestibular system disorders
-subjective (self) or objective (environment)
-episodic vertigo occurs with sudden onset in distinct episodes

103
Q

vestibular compensation

A

typically vestibular symptoms are unilateral however over time symptoms may improve due to compensatory mechanisms
-this process involves changes in the central vestibular nucleus that lead to partial restoration of lost neural activity within affected nuclei

104
Q

what will not show vestibular compensation

A

bilateral peripheral deficits and central vestibular pathologies

105
Q

vestibular labyrinthitis

A

inflammation of the inner ear labyrinth
-shows both cochlear and vestibular symptoms

106
Q

vestibular neuritis

A

inflammation of the vestibular nerve
-shows only vestibular symptoms

107
Q

what causes vestibular labyrinthitis/neuritis

A

can occur after infections such as a cold, OM, measles/mumps, meningitis or infection mononucleosis

108
Q

symptoms of vestibular labyrinthitis/neuritis

A

cochlear : aural fullness, tinnitus and high frequency SNHL
vestibular : acute vertigo, nausea/vomiting, nystagmus

109
Q

treatment of vestibular labyrinthitis/neuritis

A

antibiotics or antiviral drugs, symptomatic treatment with vestibular suppressant drugs and steroids have been used for anti-inflammatory effects or to revere HL

110
Q

vascular occlusion of the labyrinth artery

A

occlusion of this artery causes sudden and profound SNHL as well as vestibular dysfunction
-most common within older adults
-patients may complain of episodic vertigo causing a transient ischemic attack prior to occlusion

111
Q

migraine headaches

A

severe, episodic and disabling neurological condition
-activation and sensitization of the pain pathway of trigeminal and cervical nerves
-more common in females with a genetic component
-throbbing unilateral head pain with sensitivity to movement
-triggers for episodes
-associated with aura (sensory disturbance)

112
Q

migraine associated vertigo (MAV)

A

dizziness/vertigo is the aura of the headache and in most they present with true vertigo and no headache
-diagnosis is based on case history and subjective symptoms

113
Q

treatment for MAV

A

medication prescribed for migraines, migraine diet and avoid trigger, low dose of vestibular suppressant medicines for acute attacks, vestibular rehabilitation and prophylactic migraines for severe cases

114
Q

benign proximal positional vertigo (BPPV)

A

most common cause of vertigo of peripheral origin and can become triggered by certain head positions or movements
-false sensation of rotational movement
-average age is 55 but can occur at any age and is generally idiopathic

115
Q

risk factors for BPPV

A

head trauma, vestibular neuritis, stapes surgery, menieres disease, migraines, diabetes and osteoporisis

116
Q

symptoms of BPPV

A

brief episodes of mild to intense dizziness/vertigo that is triggered by head positioning
-involves posterior semicircular canal

117
Q

types of BPPV

A

acute (resolves over 3 months), intermittent (active and inactive periods) and chronic (continuous symptoms)

118
Q

what causes BPPV to occur

A

otolith organs (sensitive to gravity) become dislodges and migrate to the SCC which do not move with gravity
-when the otoliths are triggered to move, they move the fluid within the SCCs which causes the inner ear to send false signals to the brain that the head is moving on gravity

119
Q

diagnosis of BPPV

A

audiogram and MRI is typically normal so testing through dix-hallpike test (head maneuver that moves the head into a position which makes the otoliths move within the SCC)
-this signal will cause nystagmus that can be observed and assessed

120
Q

nystagmus occurs due to ……

A

a mismatch of information going to the brain

121
Q

management of BPPV

A

most are corrected mechanically by maneuvers such as the epley maneuver
-vestibular suppressants are not typically helpful
-surgery can help with vertigo in rare cases

122
Q

meniere’s disease

A

idiopathic syndrome characterized by the histopathological finding of endolymphatic hydrops
-a multifactorial condition
-equal incidence between gender with a peak occurring between 30 and 60 years

123
Q

symptoms of menieres

A

intermittent episodes of vertigo lasting from minutes to house, fluctuating SNHL, tinnitus and aural fullness/pressure

124
Q

diagnosis of meniere’s

A

two or more definitive episodes lasting 20 minutes or longer and at least 2 of the characteristics present

125
Q

hearing loss with meniere’s

A

SNHL that progresses as time goes on
-acoustic distortion initially with speech understanding affected
-loudness recruitment with low UCL as a result
-low frequency or flat to reverse cookie bite to flat severe SNHL

126
Q

acute cases of meniere’s

A

often will present the same across all patient’s
-unilateral aural fullness, vertigo, tinnitus and SNHL
-hearing can return to normal after the episode
-lasts for a couple of hours to a day

127
Q

as meniere’s progresses ….

A

attack becomes more frequent and severe
-HL does not return to normal
-vertigo stops but patients may still feel dizzy
-diplacusis (perceiving the sound as the same despite it being different)

128
Q

audiologic findings with meniere’s

A

normal tymp, reflexes present but low, abnormal ECochG (large)

129
Q

management of meniere’s

A

symptomatic treatment to control vertigo and nausea, low sodium diet and diuretics to decrease endolymph, corticosteroids are recommended for patients unresponsive to vestivular suppressants and CIs have been found helpful

130
Q

differential diagnosis for meniere’s

A

acoustic neurome, labyrinth viral infections, idiopathic vertigo, perilymphatic fistula and cogan

131
Q

superior semicircular canal dehiscence (SSSCD)

A

typically a unilateral condition that is the absence of the bone overlying the SCC facing towards the dura and middle cranial fossa
-not every patient will show symptoms, more uncommon to show them
-relating to pressure!

132
Q

SSCD is the lack of ________ of the bone covering the superior semicircular canal

A

thickening

133
Q

how does SSCD alter fluid mechanics

A

it creates a third window into the inner ear in which energy then can de transmitted out to the cranial vault of from the cranial vault into the endolymph
-this alters the circulation of pressure
-signs are due to this third window

134
Q

etiology of SSCD

A

congneital (poor development of temporal bone), head trauma and idiopathic

135
Q

how do symptoms present in SSCD

A

presents with either vestibular or auditory symptoms, presents with both symptoms or no symptoms

136
Q

vestibular symptoms of SSCD

A

vertigo/dizzinrss, nystagmus, tulio’s (sound induced vertigo)or oscillopsia

137
Q

auditory symptoms of SSCD

A

conductive or fluctuating HL with low frequency ABGs and normal ARTs

138
Q

why do bone threshold get better in the low frequencies with SSCD

A

vibration of the skull from the transducer and with the pressure being altered in a different way it improves these thresholds

139
Q

diagnosis of SSCD

A

vestibular assessment, high resolution CT scan, ECochG (abnormal SP/AP ratio)

140
Q

management of SSCD

A

mild to moderate symptoms have a conservative approach and with debilitating symptoms surgical repair with bony cement or a soft tissue plug occurs

141
Q

differential diagnosis of SSCD

A

patulous ET and otosclerosis

142
Q

mal de debarquement

A

sickness of disembarquement
-illusion of movement experienced after traveling
-unknown case, more common in women
-diagnosis through subjective history

143
Q

symptoms of mal de debarquement

A

rocking or disqeuallibrium after return to land, anxiety and depression, worse when in enclosed spaces or when motionless and it often improves during continuous movement

144
Q

management of mal de debarquement

A

drugs for motion sickness, vestibular rehabilitation may help along with avoidance of trigger

145
Q

why are vestibular disorders often underdiagnosed in children

A

it is often compensated and they do not have the vocabulary to express the symptoms and

146
Q

more often than not, vestibular dysfunction in children often accompanies by ___________

A

hearing loss

147
Q

what are some disorders that can affect the pediatric vestibular system

A

genetic conditions, neurological conditions, trauma/infection and other conditions including ANSD and SSCD

148
Q

OM is a common cause of vestibular symptoms in children, what are two explanations for this

A

invasion of bacterial toxins in the inner ear and formation of cholesteatoma that causes labyrinthitits or perilymphatic fistula

149
Q

a good case history is a critical diagnosis for children, what should be focused on

A

identifying provoking movements or activities such as motion sensitivity

150
Q

you should suspect a vestibular dysfunction in children if what occurs

A

if a child has a HL greater than 60 dB HL and has not walked by 14.5 months

151
Q

hearing level cutoffs for hearing loss

A

shift of greater than or equal to 15 dB HL for the average thresholds 500, 1000, 2000 and 3000 Hz

152
Q

WRS change to be significant

A

shift of 15-20% or greater

153
Q

what is an ECochG

A

electrophysiological test that reflects elevation of the inner ear pressure
-sensitive to pressure changes within the cochlea
-records a summating potential (from organ or corti) and a action potential (from the nerve)

154
Q

what is the action potential in an ECochG in terms of the ABR

A

wave 1

155
Q

ECochG levels to be significant

A

greater than 0.42 or 42% SP/Ap ratio is positive

156
Q

examples of disorders where a ECochG would be helpful to diagnosis

A

meniere’s, SSCD and cogans

157
Q

type Ad tympanogram associates with

A

ossicular disarticulation

158
Q

type B tympanogram associated with

A

ME fluid (OM) or choelsteatoma

159
Q

type B high volume tympanogram associated with

A

perforation or PE tube

160
Q

type B low volume tympanogram associated with

A

occlusion within the canal

161
Q

type C tympanogram associated with

A

auditory tube dysfuntion or middle ear fluid

162
Q

unilateral ME pathology will show what reflex pattern

A

when anything is coming or going from the affected ear

163
Q

cochlear pathology will show what reflex pattern

A

affects anything when it is presented to the bad ear
-STIM affects

164
Q

CN 8 pathology will show what reflex pattern

A

reflexes affected when the tone is presented to the bad ear
-STIM effect

165
Q

brainstem lesions will show what reflex pattern

A

contralateral reflexes are absent

166
Q

CN 7 pathology will show what reflex pattern

A

affected when it is measured on the affected side
-PROBE effect

AUDE 5410 (4 decks)

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