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AUDE 5410 > quiz 3 > Flashcards

quiz 3 Flashcards

1
Q

facial nerve (CN 7)

A

a mixed nerve derived from the second pharyngeal arch
-somatic and visceral motor/sensory innervation occurs

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2
Q

somatic motor innervation

A

muscles of facial expression, post auricular muscle and stapedius muscle
-responsible for post auricular muscle reflex
-responsible for middle ear acoustic reflex

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3
Q

visceral motor innervation

A

lacrimal (tear ducts) and salivary glands
-hard to make tears if CN 7 is affected

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4
Q

visceral sensory innervation

A

taste within the anterior 2/3 of tongue
-chorda tympani nerve

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5
Q

somatic sensory innervation

A

posterior EAC, concha, ear lobe and deep parts of the face

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6
Q

what is the origin of CN 7

A

facial motor nucleus within the anterior pons

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7
Q

what is the insertion of CN 7

A

muscle of facial expression and stapedius muscle

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8
Q

what is the pathway of the facial nerve

A

arises from anterior pons, exits brainstem through pontomedullary junction, goes through cerebellopontine angle to enter the IAC, travels through meatal foramen, passes through the fallopian canal, forms superior aspect of oval window niche, then after passing stapes and SCC turns into the mastoid segment and exits through the stylomastoid foramen

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9
Q

what is the most common site for pathology along the facial nerve

A

when passing through the fallopian canal (labyrinth segment)
-narrowest diameter and causes a site for entrapment and associated disorders

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10
Q

what is the potential problem with the facial nerve pathway

A

it can be very variable from the CPA to IAC in how i runs it course

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11
Q

what ways can facial nerve disorders present in children

A

congenital (occurs during embryogenesis), prenatal acquired (intrauterine trauma or exposure) and postnatal acquired (many of the same conditions present in adults)

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12
Q

osteopetrosis

A

a rare AD genetic conditions that is present at birth with varying severity and presents with bony dysplasia
-cranial neuropathies due to bony obliteration of neural formania with the entrapment or compression of nerves

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13
Q

symptoms of osteopetrosis

A

congenital facial paralysis, vision issue (blindess can occur), HL (deafness can occur)
-due to involvement of CN 2, 5, 7 and 8

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14
Q

treatment of osteopetrosis

A

symptomatic treatment for symptoms and facial nerve decompression if nerve entrapment is associated with the issues presenting

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15
Q

mobius syndrome

A

a rare congenital disorder associated with hypoplasia of the 6th and 7th nerve
-genetic with multiple genes and modes of inheritance or can occur due to exposure in utero to teratogens such as cocaine

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16
Q

symptoms of mobius

A

congenital facial diplegia (paralysis), associated CN 6 paralysis, other cranial nerve deficits, deformities of extremities, musculoskeletal deformities, intellectual disability

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17
Q

treatment for mobius

A

ophthalmologic consolation and nerve reconstruction surgery

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18
Q

bell’s palsy

A

disorder that is the most common cause of acute unilateral facial paralysis
-can be idiopathic, due to being a diagnosis of exclusion meaning that this is what is diagnosed when presenting with facial paralysis
-can occur from herpes simplex virus which leads to compression of the nerve
-begins with sensory fibers and then involves more motor fibers

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19
Q

anything that causes ____________ will cause facial nerve paralysis

A

compression

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20
Q

how is a diagnosis of bell’s palsy given

A

history and clinical examination point to the correct diagnosis
-onset during a 48 hour period
-fever and neck stiffness at onset
-no HL or vertigo
-no other cranial neuropathy
-normal head and neck examination
-drying of eyes
-can be recurrent

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21
Q

audiologic evaluation of bell’s palsy

A

-normal otoscopy
-HL is rare
-normal tymps
-abnormal ARTs if lesion is proximal to stapedial nerve
-present ARTs if lesion is distal to stapedial nerve

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22
Q

if function has not retuned within 6 months post paralysis with bell’s palsy, what is waranted

A

CT scan and MRI as well as electroneurography to assess generation of nerve fibers

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23
Q

treatment for bell’s palsy

A

decompression of nerve, steroids indicated early in the course of the disease, antiviral with steroids and eye care to prevent damage

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24
Q

differential diagnosis for bell’s palsy

A

CPA or skull based tumors, vestibular schwannoma, otitis media, parotid gland tumors

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25
Q

good prognosis for bell’s palsy

A

younger patients, partial paralysis and recovery within 2 months, intact ARTs, less degeneration in ENoG

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26
Q

poor prognosis for bell’s palsy

A

patients older than 65, greater than 90% nerve degeneraion within first two weeks, and diabetic patients

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27
Q

what trauma can cause facial nerve deficits

A

temporal bone fractures, iatrogenic injuries, lacerations and gunshot wounds

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28
Q

malignant otitis externa

A

invasion of bacteria within the soft tissue
-treat with debridement of infected tissue, antibiotics and the decompression of the facial nerve when needed

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29
Q

acute suppurative otitis media

A

caused by bacteria and can lead to invasion into the facial canal through a dehiscence that may evoke an inflammatory response with edema or compression resulting in facial weakness
-treat with myringotomy, antibiotics and a trans mastoid decompression

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30
Q

chronic otitis media

A

facial nerve paralysis secondary to this is common
-needs surgical intervention such as a tympano-mastoidectomy followed by decompression of the facial nerve

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31
Q

herpes zoster oticus

A

caused by shingles
-presents with otalgia and pain, vesicular eruption on the concha and/or external canal and along sensory distribution of the 7th nerve
-treat with antiviral medication
-less change of complete spontaneous recovery than bell’s palsy

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32
Q

facial neruoma

A

primary facial neruomas or schwannomas are rare bengin neopalsms of schwann cells
-these are less common than schwannomas

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33
Q

symptoms of a facial neruoma

A

facial weakness, HL (any type), tinnitus, otorrhea, ear canal mass, otalgia, vestibular symptoms and you can see redness in the canal due to the masses needing a blood supply

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34
Q

what are the various facial neuroma locations

A

tympanic segment (most common), vertical segment, labyrinth segment, IAC, CPA, stylomastoid foramen
-many involve multiple segment

35
Q

audiologic evaluation of facial neuoma

A

-generally SNHL due to cochlear nerve compression
-normal tymps
-abnormal ARTs with proximal lesion and present ARTs with distal lesion
-ENoG can be normal

36
Q

what is a useful tool for differentiating a facial neuroma from other tumors

A

CT scan or MRI

37
Q

how can ABR’s be helpful with facial neuromas

A

determines if it is acoustic or a facial neuroma
-with a normal ABR you should think about CN 7

38
Q

management of facial neuromas

A

management is generally conservative
-radiotherapy often sued to decrease size prior to surgery if it is causing pressure on structures
-decompression of nerve of paralysis occurs
-tumor resection if warranted

39
Q

differential diagnoses of facial neuromas

A

otits media with CHL, cholesteatoma, glomus tumor, meningiomas and acoustic neuroma

40
Q

auditory neuropathy spectrum disorder

A

hearing disorder characterized by the disruption of temporal coding of acoustic signals in the auditory nerve fibers resulting in impairment of auditory perceptions relying on temporal cues
-disruption of neural synchrony occurs

41
Q

how is ANSD characterized

A

intact otoacoustic emissions but an absent or abnormal ABR response

42
Q

neural integrity of the __________ and the __________________ pathways are affected in ANSD

A

8th nerve ; lower brainstem

43
Q

what are some common site of lesions for ANSD

A

selective loss/damage of synaptic junctions, disordered release of NTs by IHC synapses, injury to the spiral ganglion, demyelinations to myelin sheath and the auditory nerve absence or undergrowth

44
Q

how can ANSD occur

A

genetic based (syndromic or nonsyndromic or mitochondrial), immune disorders, metabolic disorders or due to environmental factors

45
Q

risk factors for ANSD

A

-prematurity and low birth weight
-prolonged stay within the NICU
-anoxia/hypoxia
-seizures
-hyperbilirubinemia

46
Q

why is low birth weight a risk factor for ANSD

A

shows limited growth and mature rate when in utero
-underdevelopment of structures

47
Q

explain hyperbilirubineamia and how it can result in transient ANSD

A

the primary site is not the 8th but but rather the CANS then shifts outward to the 8th nerve
-bilirubin deposits in the auditory brainstem and 8th nerve ganglion
-nerve death or dysfunction will occur but the IHCs are unaffected
-in some cases improves within 2 years but unsure if neural synchrony restores with normal auditory processing

48
Q

diagnostic criteria for ANSD

A

case Hx, OAEs, ABR, reflexes, behavioral assessment, speech audiometry, ECochG, vestibular assessment followed by functional assessment for young children

49
Q

OAEs in ANSD

A

typically will be preset in early years but may be abnormal if OHC blood supply is compromised
-will not see OAE suppression, which is typically observed

50
Q

ABR in ANSD

A

no true ABR result seen but will observe a cochlear microphonic
-will not increase the latency as the stimulus decreases
-the CM rings for longer

51
Q

how to present a ABR to a patient with suspected ANSD

A

useing reverse polarity and performed at high level click stimulus
-present rarefaction and condensation in separate trails
-if not reverals this confirms true auditory nerve response
-once ANSD has been identified stop

52
Q

middle ear reflexes in ANSD

A

abnormal reflexes even with normal/mild SNHL due to the nerve being involved

53
Q

why are pure tones not useful with diagnosing ANSD

A

due to the high variability of thresholds there can be

54
Q

speech audiometry in ANSD

A

significant impact on speech even with normal or near normal thresholds due to the nerve involvement
-WRS will have a bigger impact
-speech in noise is recommended

55
Q

ECochG in ANSD

A

action potentials generated by the 8th nerve are affected so abnormal

56
Q

what is speech results with patients that have ANSD

A

poor speech intelligibility and it worsens in noise

57
Q

overview of what you find with ANSD

A

present OAE, absent ABR (with CM present), abnormal ARTs, poor WRS in noise, audiogram variable, patient vary in characteristics and management needs

58
Q

management of ANSD

A

-HAs and FM systems provide limited benefits
-continuing education for them, so potentially manual communication
-CIs are most successful, but need trial with amplification prior to surgery
-gene therapy

59
Q

vestibular assessment in ANSD

A

not always associated in every case
-there can be compensation due to the vestibular system being more than just the 8th nerve so this could be why not every child shows the symptoms

60
Q

functional assessment for young children

A

development evaluation/history, otologic evaluation with imaging of cochlear and nerve, vestibular assessment if otologic evaluation and history warrants it, genetic evaluation, ophthalmologic assessment is associated with peripheral neuropathies, neurologic evaluation to asses peripheral and cranial nerve function and communication assessments

61
Q

CIs are successful if underlying pathophysiology is …..

A

biochemical abnormality of NT substances or synaptic defects between IHCs and auditory nerve

62
Q

presbycusis

A

age related hearing loss
-a gradual decline in hearing, highly variable in age of onset and rate of progression
-slow progression

63
Q

presbycusis results from progressive loss/degeneration of

A

encocochlear potential, sensory hair cells, synapses and other degenerative changes within the peripheral and central auditory system

64
Q

what are the three systems implicated in presbycusis

A

cochlear amplifier (OHCs), power supply and transduction mechanism (IHCs)

65
Q

cochlear amplifier (OHCs)

A

the active processes located in the OHCs that amplify sound vibrations inside the cochlea
-amplification is dependent on the potential difference between scala media and scala tympani

66
Q

power supply

A

cochlear lateral wall tissue, including stria vascularis that provides the power the cochlear amplifier needs to function effectively

67
Q

transduction mechanism (IHCs)

A

final step are the IHCs and afferent nerve fibers of the auditory nerve that receives the amplified vibrations of the OHCs
-convert or transduce
-send to the brain

68
Q

presbycusis is highly varible due to various aspects, what is laid out in the formula for showing this variability

A

ototoxic drugs, noise exposure and age all in relation to genetics will result in hearing abilities

69
Q

presbycusis is typically what type of HL

A

progressive, sloping, high frequency SNHL
-due to the basal end of the cochlear being damaged most often

70
Q

what are common manifestations of presbycusis

A

loss of sensitivity for high frequency sounds resulting in a sloping high frequency SNHL, difficulties with speech perception especially in noisy environments and distorted loudness perception (recruitment)

71
Q

characteristics of presbycusis

A

speech discrimination abilities become worse as high frequency HL increases, audibility of low energy with attenuatution of HF, upward spread of masking, flat configurations are reported, word recognition is affected by age and hearing sensitivity

72
Q

schunknechts classification

A

sensory, neural, metabolic/strial and mechanical presbycusis

73
Q

sensory presbycusis

A

loss of primary cochlear OHCs and supporting cells

74
Q

neural presbycusis

A

loss of afferent cochlear neurons

75
Q

metabolic/strial presbycusis

A

atrophy of stria vascularis and lateral wall and loss of EP

76
Q

mechanical presbycusis

A

stiffening of BM and organ of corti

77
Q

killion and fikret-pasas classification

A

type 1 HL, type 2 HL and type 3 HL

78
Q

type 1 HL

A

mild to moderate SNHL
-normal loudness sensation
-findings are consistent with loss of outer hair cell function with normal inner hair cell function

79
Q

type 2 HL

A

moderately severe HL with no region of completely normal loudness sensation
-presence of partial recruitment
-loss of 60 dB HL is too large to be explained by loss of OHCs alone so it is assumed to have IHC loss as well
-less information being transmitted to the brain
-will have deficits for intelligibility for speech

80
Q

type 3 HL

A

severe hearing loss
-loudness and intelligibility are both affected
-when HL has progressed to 70-80 range, loudness ceases to be the primary concern
-IHC loss is so great that intelligibility dominates the concerns
-range over which speech can be understood in noise is greatly narrowed
-individuals do best when speech is presented close to UCL

81
Q

what is the relationship between NIHL and ARHL

A

early NIHL can exacerbate ARHL
-NIHL will meet up with presbycusis

82
Q

what can be seen in relation to a noise notch with NIHL in comparison to ARHL

A

in early stages of NIHL, there is a noise notch but as time progresses this will flatten out
-so hard to tell if the flattened out version is ARHL or a later stage of NIHL

83
Q

what is age related hearing loss anatomically characterized by

A

degeneration of stria vascularis/lateral cochlear wall, compromised blood supply, presence of normal sensory cells except on basal turn, and degeneration of spiral ganglion in sensory cells

84
Q

what is age related hearing loss physiologically characterized by

A

reduction of endocochlear potential (EP)

AUDE 5410 (4 decks)

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