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AUDE 5410 Aud-Vestib Disorders > Quiz 3 (FN Disorders) > Flashcards

Quiz 3 (FN Disorders) Flashcards

1
Q

which nerve is involved in eye movements assessed during vestibular testing

A

CN III Occulomotor

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2
Q

which brand of the facial nerve innervates the outer 2/3 of the tongue and can be sacrificed during ME surgery such as removal of a cholesteatoma

A

chorda tympani

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3
Q

osteopetrosis (bony displasia) is a disorder of aging that results in hardening of the cranial bones

A

false

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4
Q

____ syndrome is a rare congenital disorder with possible multifactorial inheritance in hypoplasia of CNs VI & VII

A

mobius

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5
Q

in the case of bell’s palsy, MEAR will be present if the lesion is ____ to the stapedius nerve

A

distal

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6
Q

a left facial nerve schwannoma will show an abnormal left ipsilateral response and an abnormal _____ contralateral response

A

right

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7
Q

largest CN with 3 major branches on each side of the pons, derivative of 1st pharyngeal arch

A

trigeminal CN V

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8
Q

innervates single muscle, superior oblique muscle of eye

A

cn iv
trochlear

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9
Q

lateral rectus of eye, most common overall cause of impairment is diabetic neuropathy

A

CN VI abducens

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10
Q

sensory fibers from posterior ⅓ of tongue, tonsils, pharynx, middle ear, & carotid sinus; supplies parasympathetic fibers to parotid gland through otic ganglion; supplies motor fibers to stylopharyngeus muscle; contributes to pharyngeal plexus

A

CN IX glossopharyngeal

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11
Q

innervates sternocleidomastoid & trapezius

A

CN XI accessory

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12
Q

longest course of all cn - head to abs & supplies diaphragm, derived from 4th pharyngeal arch

A

CN X vagus

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13
Q

supplies motor fibers to all muscles in tongue except palatoglossus muscle (accessory)

A

CN XII hypoglossal

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14
Q

what is the FN intracranial pathway

A

runs complex 3d course
originates in the facial motor nucleus in the anterior part of the pons
exits the BS at the pontomedullary junction
passes through the cerebellopontine angle to enter the IAC
ends by inserting into muscles of facial expression & stapedius muscle

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15
Q

what is the pathway of fn in IAC segment

A

exits bs & lies anterior to vestib nerve & superior to cochlear nerve
AICA runs bw CN 7 & 8 → provides vascular supply to this part of CN 7
chorda tympani runs bw 7 & 8 in IAC
after n enters IAC, it travels 8-10mm to the opening of IAC
in IAC, fn narrows to its lowest diameter & fallopian (facial) canal also narrows

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16
Q

what type of nerve is fn and where is it derived

A

mixed nerve
derived from 2 pharyngeal arch

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17
Q

what else is derived from the second pharyngeal arch

A

stapedius muscle

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18
Q

facial expressions, postauricular muscle, stapedial muscle (MEAR)

A

somatic motor

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19
Q

ear lobe & deep parts of the face

A

somatic sensory

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20
Q

what is somatic motor of fn

A

facial expressions, postauricular muscle, stapedial muscle (MEAR)

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21
Q

what is somatic sensory of fn

A

ear lobe & deep parts of the face

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22
Q

lacrimal & salivary glands

A

visceral motor

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23
Q

what is visceral motor of fn

A

lacrimal & salivary glands

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24
Q

chorda tympani nerve (anterior ⅔ of the tongue)

A

visceral sensory

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25
Q

what is visceral sensory of fn

A

chorda tympani nerve (anterior ⅔ of the tongue)

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26
Q

what supplies CN 7 in IAC

A

AICA

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27
Q

why is IAC segment a site that is at higher risk for entrapment/compression

A

in IAC, fn narrows to its lowest diameter & fallopian (facial) canal also narrows
canal narrowing is a common site for facial nerve entrapment and associated disorders
between the IAC & stylomastoid foramen

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28
Q

what is the fn pathway in the intratemporal portion

A

labyrinthine segment → goes through narrowing of bony canal in temporal bone
tympanic segment → forms superior part of oval window niche
mastoid segment → passes bw stapes & lateral semicircular canal & turns inferiorly to mastoid segment & exits temporal bone via stylomastoid foramen
stylomastoid artery (branch of postauricular arty) supplies this area of FN

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29
Q

common site of pathology: temporal bone fractures & Bell’s palsy

A

labyrinthine segment

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30
Q

what pathology is common in the labrythine segment

A

common site of pathology: temporal bone fractures & Bell’s palsy

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31
Q

fn injured here in pathologic processes & during ME surgery

A

tympanic surgery

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32
Q

what pathology occurs in the tympanic segment

A

fn injured here in pathologic processes & during ME surgery

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33
Q

shows variable branching patterns in the face

A

mastoid segment

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34
Q

what pathology does mastoid segment show

A

shows variable branching patterns in the face

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35
Q

course of FN makes it vulnerable to many neoplastic, traumatic, & infectious conditions

A

true

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36
Q

stylomastoid artery (branch of postauricular arty) supplies this area of FN

A

mastoid segment in the intratemporal segment pathway of FN

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37
Q

what supplies vascular supply to the mastoid segment in the intratemporal portion pathway of FN

A

stylomastoid artery (branch of postauricular arty) supplies this area of FN

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38
Q

incidence of NFP

A

~ 0.2%

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39
Q

NFP can be

A

congenital
prenatal acquired
postnatal acquired

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40
Q

what causes congenital NFP

A

developmental errors in embryogenesis

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41
Q

what causes prenatal acquired NFP

A

intrauterine trauma: forcep compression in delivery or facial compression against sacrum during labor
exposure to teratogens in utero (maternal rubella)

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42
Q

what causes postnatal acquired

A

most commonly trauma & infections that can also be seen in adults

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43
Q

AD genetic, a bony displasia that progresses/fluctuates and can cause blindness, HL, and facial paralysis (treatment: nerve decompression)
\

A

osteopetrosis

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44
Q

what is inheritance of osteopetrosis

A

AD
present at birth (congenital)
severity varies
milder than AR

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45
Q

AR of this disorder is more severe than AD

A

osteopetrosis

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46
Q

treatment of osteopetrosis

A

symptomatic
FN decompression if n entrapment results in facial dysfunction

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47
Q

aka Albers-SchÖnberg Disease

A

osteopetrosis

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48
Q

symptoms of osteopetrosis

A

involvement of CN II, V, VII, VIII that is progressive/fluctuating
multiple cranial neuropathies due to bone growth that compresses or entraps CNs
congenital facial paralysis
vision (even blindness) & HL (even deafness)

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49
Q

what is bony dysplasia

A

hardens & becomes denser
bone growth, “stone”

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50
Q

rare congenital disorder with hypoplasia/underdevelopment of CN 6 and 7 (multifactorial etiology with teratogens like drugs causing it)

A

mobius

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51
Q

Signs: bilateral facial paralysis, LR eye muscle not working, ID, musculoskeletal deformities (cross eyes, cant look to the side)

A

mobius

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52
Q

what is a teratogen

A

a substance that can cause or increase the risk of a birth defect in a baby. Teratogens can be drugs, alcohol, chemicals, or toxic substances. They can also be found in the environment, such as in street drugs, disease, or BPA

53
Q

what is mobius

A

rare congenital hypoplasia of CN 6 & 7 nuclei

54
Q

what is hypoplasia

A

condition where tissue or organ fails to grow to normal size

55
Q

etiology of mobius

A

genetic → has multiple genes & modes of inheritance (multifactorial)

teratogens (exposure in utero) → cocain ergotamine
misoprostol

56
Q

what is ergotamine (teratogen that can cause mobius)

A

alkaloid that is vasoconstrictor to treat migraines, induce birth, & prevent post-partum hemorrhage

57
Q

what is misoprostol (teratogen that can cause mobius)

A

vasodilator that prevents stomach ulcers or treats tinnitus

58
Q

what are signs & symptoms of mobius

A

bilateral facial paralysis
CN VI uni or bilateral paralysis (eye is turned in - cross eyed)
other cn deficits
deformities of extremities
musculoskeletal deformities
ID

59
Q

what is the treatment for mobius

A

ophthalmologic consult
nerve reconstructive surgery

60
Q

epidemiology of bell’s palsy

A

idiopathic
most common cause of acute unilateral facial paralysis
can be recurrent in small % of people
right side more often
affects both sexes equally (more frequency in women 10-19 yrs)
pregnancy increase risk 3 fold

61
Q

pregnancy increases risk of bell’s palsy by 3 fold

A

most commonly during 3rd trimester
preeclampsia can increase occurrence

62
Q

what is preeclampsia

A

disorder of pregnancy with high blood pressure and proteins in the urine

63
Q

idiopathic, herpes virus also involved, begins with sensory then moves to motor

A

bells palsy etiology

64
Q

what is etiology of bells pasly

A

idiopathic
usually diagnosed by exclusion (most common)
main infectious agent → herpes simplex virus
begins with sensory then moves to motor

65
Q

what else can cause bell’s palsy that is rare

A

OM, CPA, parotid gland, or skull based tumors or metastatic lesions

66
Q

explain how herpes simplex virus causes Bell’s palsy

A

entrapped → inflammatory response (swelling) leading to compression/ischemia of nerve at the meatal foramen and labyrthine segment
can cause n degeneration

67
Q

diagnosis of Bell’s palsy

A

exclusionary diagnosis

68
Q

what to look for in hx & clinical exam for bell’s palsy

A

partial/total unilateral facial paralysis → onset with 48 hr period
fever & stiff neck @ onset
no hl/vertigo
no other cranial neuropathy
eye drying (due to lack of eye closure & lacrimation)
recurrence is rare
spontaneous recovery w/in 3-6 mos in some

69
Q

what is an exclusionary diagnosis

A

diagnosis of a medical condition reached by a process of elimination, which may be necessary if presence cannot be established with complete confidence from history, examination or testing

70
Q

what is done for diagnosis w/ in 3-6 mos of onset of paralysis

A

audiometric eval & hiv/lyme test if applicable

71
Q

what do audio evals show for bell’s palsy

A

normal otoscopy, HL rare for pure tones, normal tymps, abnormal ARTs (proximal lesion to stapedius nerve), present ARTs (distal lesion to stapedius nerve)

72
Q

Abnormal ARTS due to a lesion ________ to the stapedius nerve

A

proximal

73
Q

Presence of ARTs indicates lesion ______ to the stapedius nerve

A

distal

74
Q

what is done if no return of function after 3-6 mos post paralysis

A

ENog to assess n fiber degeneration
CT & MRI to differential diagnose from VIIN tumors

75
Q

what are common FN tests used

A

ENoG, electromyography (EMG), nerve excitability test (NET), & max stim test (MST)

76
Q

how does an enog work

A

A stimulating electrode is placed proximally over the nerve trunk and a second electrode is placed distally over muscle. Current is applied in the first electrode and response is detected in the second electrode. The response is measured bilaterally and the healthy side is compared to the weak side. The magnitude of the response on the weak side is calculated as a percentage of the response on the healthy side.

Degeneration greater than 90% is correlated with a poor prognosis

77
Q

what is the adv of an enog

A

it is an objective measure of the amount of intact axons relative to the healthy side.

78
Q

what is the treatment for bell’s palsy

A

nerve decompression → some surrounding bone may need removed
steroids in early course of disease
antiviral w/ steroids
eye care → prevents permanent damage w/ eye dryness

79
Q

90% of degeneration happens w/in

A

2 wks of onset

80
Q

what is the differential diagnosis for bell’s palsy

A

CPA/skull based tumors
vestib schwannoma
OM
Parotid gland tumors

81
Q

most recover fxn w/ no medical or surgical intervention within

A

3-6 mos

82
Q

young PT’s, partial paralysis & fxn recovery w/in 2 mos, distal lesion to stapedius nerve (lesion in mastoid or extratemporal segment of fn), EMG evidence of voluntary activity, ENoG shows <90% degeneration of electrically evoked muscle action potential after ~ two weeks of onset

A

good prognosis

83
Q

what is a good prognosis for bell’s palsy

A

young PT’s, partial paralysis & fxn recovery w/in 2 mos, distal lesion to stapedius nerve (lesion in mastoid or extratemporal segment of fn), EMG evidence of voluntary activity, ENoG shows <90% degeneration of electrically evoked muscle action potential after ~ two weeks of onset

84
Q

what is a poor prognosis for bell’s palsy

A

PT >65 yrs, >90% nerve degeneration within the first two weeks as diagnosed with ENoG & diabetic PT’s

85
Q

PT >65 yrs, >90% nerve degeneration within the first two weeks as diagnosed with ENoG & diabetic PT’s

A

poor prognosis

86
Q

why do diabetic PT’s show increased incidence/greater risk for Bell’s palsy?

A

because of a peripheral circulatory disorder that develops in the feeding vessels to the facial nerves

87
Q

traumas that lead to fn dysfunction

A

temporal bone fractures
iatrogenic injuries (surgery)
lacerations
gunshot wounds

88
Q

most common site is next to geniculate ganglion
HL → CHL, mixed SNHL

A

temporal bone fractures

89
Q

common site is tympanic segment over oval window
injury from otosclerosis or cholesteatoma surgery

A

iatrogenic injuries from surgery

90
Q

most common infection to affect the facial nerve

A

shingles
herpes zoster oticus

91
Q

what is the most likely lesion where FN gets entrapped that causes symptom problems if there is tumor growth in children

A

facial nerve paralysis

92
Q

what are infectious conditions that can affect the FN

A

malignant OE
facial paralysis caused by ME disease inflammation
chronic OM
herpes zoster oticus

93
Q

etiology of malignant OE

A

invasion of pseudomonas pneumoniae & other bacteria into the soft tissue, cartilage & bone

94
Q

treatment for malignant OE

A

infected tissue removal
FN decompression → if needed
antibiotics

95
Q

what ME disease inflammations cause FN paralysis

A

acute suppurative OM
chronic OM
herpes zoster oticus

96
Q

what is ramsay hunt syndome

A

aka herpes zoster oticus
caused by varicella virus (shingles)
remains dormant in the sensory ganglia of the fn & reactivates causing characteristic vesicles along the nerve pathway

97
Q

symptoms of herpes/shingles

A

otalgia, HL, vertigo, more severe facial paralysis, & vesicles on concha, external canal or along sensory parts of 7th n

98
Q

characteristic sites of pathology of shingles

A

labyrinthine segment of FN
can involve V, IX, X, XI
herpes zoster cephalicus

99
Q

what is herpes zoster cephalicus

A

disease affecting CN’s including auditory, vestibular, trigeminal, glossopharyngeal & vagus; rare & involves cervical dermatomes

100
Q

what is a dermatome

A

skin area supplied by a single spinal nerve

101
Q

what is acute suppurative OM

A

gram-positive bacteria & haemophilus influenza (gram negative bacteria)

102
Q

how does acute suppurative OM causae FN paralysis

A

caused by invasion into the facial canal through dehiscence causing inflammation w/ edema, compression & ischemic resulting to facial weakness

103
Q

what is dehiscence

A

erosion or discontinuity in bony structure of facial canal causing a communication bw facial nerve & ME cavity

104
Q

treatment for acute suppurative OM

A

myringotomy, antibiotics & trans-mastoid decompression if progression of nerve degeneration

105
Q

FN paralysis secondary to this is common
can have paralysis w/ or w/out cholesteatoma

A

chronic OM

106
Q

treatment of OM

A

urgent indication of surgery; tympano-mastoidectomy needed for chronic OM w/ FN decompression if FN is involved; removal of cholesteatoma if present on the nerve

107
Q

treatment for herpes z o

A

antiviral med acyclovir

108
Q

prognosis of herpes z o

A

less chance of spontaneous recovery than Bell’s palsy & recover is low even w/ steroids

109
Q

what can be used to diagnose facial neuroma

A

audio eval
ENoG
CT & MRI
ABR

110
Q

what will ARTs show w/ facial neuroma

A

abnormal ARTs w/ lesion PROXIMAL to stapedius n & present ARTs w/ lesion DISTAL to stapedius n (most likely in mastoid or extratemporal segment of FN)

111
Q

what does pure tones & tymps show for facial neuroma

A

SNHL → due to cochlear n compression by tumor
normal tymps

112
Q

what can ENoG show

A

if tumor is in CPA can be normal
can cause HL but no facial fxn effect

113
Q

why do we use CT & MRI for facial neuromas

A

to differentiate the diagnosis bw VIII N tumors & other conditions

114
Q

why use an abr for facial neuroma

A

determines whether tumor is acoustic or facial neuroma

115
Q

Abnormal ARTS if a lesion is ______ to the stapedius nerve

A

proximal

116
Q

ARTs present if a lesion is ______ to the stapedius nerve

A

distal

117
Q

ARTs are ABNORMAL when measured on _______ side

A

AFFECTED

118
Q

what would a R ART show for facial neuroma on R side

A

ART on R (right ispi & left contra) = absent
ART on L (left ipsi & right contra = normal?

119
Q

if the tone is presented and measured on the probe side, then it is an _______ ART

A

ipsilateral

120
Q

if the tone is presented on the earphone side and measured on the probe side, it is a ______ ART.

A

contralateral

121
Q

should small facial neuromas be removed?

A

controversial

122
Q

if facial tumor is slow growing what is management

A

conservative
observe only unless VII N paralysis or other symptoms occur (BS compression)

123
Q

what are some managements of facial neuroma

A

observe
radiotherapy
decompression of fn if paralysis/other symptoms present
tumor resection w/ fn grafting

124
Q

why do radiotherapy for facial neuromas

A

decreases the size before therapy
or used if it is causing pressure on critical structures (BS)

125
Q

where does graft come from after facial tumor resection

A

sensory nerve
usually greater auricular or sural n

126
Q

grafting results in excellent facial muscle tone post-surgery after 6-8 mos (some weakness remains)

A

true

127
Q

sensory n in calf of leg & made of collateral branches of tibial n and common fibular n

A

sural n

128
Q

what are differential diagnosis for facial neuromas

A

OM W/ CHL (w/ or w/out cholesteatoma
cholesteatoma (needs decompression of n & removal)
glomus tumor (paragangliomas → ME & jugular vein bulb)
meningiomas
acoustic neuroma

129
Q

both VII & VIII n schwannomas reported in some cases of ____

A

NF2

AUDE 5410 Aud-Vestib Disorders (18 decks)

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