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AUDE 5410 Aud-Vestib Disorders > Final Exam Study Guide (New Material) > Flashcards

Final Exam Study Guide (New Material) Flashcards

1
Q

what is a neoplasm

A

abnormal mass tissue

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2
Q

around 45% of intracranial tumors arise from

A

neuroglia cells

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3
Q

what are neuroglial cells

A

non-excitable support cells of CNS & make up about ½ volume of CNS

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4
Q

what are the 4 types of neuroglia cells

A

astrocytes
oligodendrocytes
microglia
ependymal cells

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5
Q

what are astrocytes

A

star shaped cells & provide barrier at synapses that contain NT or hormones (dopamine)

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6
Q

what are oligodendrocytes

A

active in forming myelin sheath in central n fibers

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7
Q

what are migroglia

A

small glial cells that ingest & remove neural residue during inflammation & degeneration in CNS (phagocytic)

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8
Q

what are ependymal cells

A

epithelial cells lining CSF & are ciliated and facilitate CSF circulation & production

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9
Q

what are benign tumors

A

slow growing, well-defined borders for easy removal (surgery is good treatment), no metastasizing or life threatening, will kill if in crucial areas

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10
Q

what are malignant tumors

A

grow fast, invade & destruct structures, life threatening, can metastasize

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11
Q

explain how a benign and malignant tumors are intertwined

A

A large benign tumor, such as a CN VIII schwannoma, pressing against vital brainstem structures can lead to serious medical problems, even death
On the other hand, a small malignant tumor, such as an astrocytoma, although highly invasive, initially, may not interfere with neural function and may temporarily escape detection

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12
Q

what is an intra-axial tumor

A

originate in parenchyma of brain
ex: astrocytoma, glioblastoma

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13
Q

what is an extra-axial tumor

A

tumors that originate not from parenchyma of brain
ex: meningiomas, CN sheaths, pineal & pituitary glands

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14
Q

what are the 4 segments of the temporal bone

A

petrous (IE & hard segment)
Squamous
Mastoid
Tympanic (forms EAC, matures by 3 yrs old)

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15
Q

where do majority of vascular malformations in temporal bone present

A

in IAC or geniculate ganglion of VII N location in fallopian (facial) canal
preference in this region is though to be due to blood supply around ganglion

rarely in ME cavity or EAC

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16
Q

what are the two vascular tumors

A

hemangiomas & vascular malformations

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17
Q

What happens in hemangiomas

A

Extra blood vessels that group together into a dense clump
Most go through phases of growth & then go away on their own

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18
Q

what are findings in hemangiomas/vascular malformations/vascular tumors

A

Symptoms present ~3rd decade of life

-Geniculate Ganglion site→CHL (erodes ME cavity), facial weakness/twirch

-IAC site→ progressive SNHL, vertigo (CN VIII lesion)

-Tinnitus, hemifacial spasm

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19
Q

what are D/D for vascular tumors (H & VM)

A

-from other temporal bone tumors→ by radiographic appearance
-meningiomas→ irregular margins, may contain calcium flecks
-VII N schwannoma→less localized,
-cholesteatomas (also vascular lesion)→ seen in ME cavity

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20
Q

how are vascular tumors diagnosed

A

-Case hx & symptoms
-High res CT→intra tumor calcification shows here
-MRI w/ contrast→fluid is bright on T2 weighted more than acoustic schwannomas

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21
Q

why use an mri with contrast for vascular tumors

A

luid is bright on T2 weighted more than acoustic schwannomas

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22
Q

what is the management for vascular tumors

A

Surgery, thermal ablation, embolization
-Recurrence is low

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23
Q

more common vascular tumor that is present at birth

A

vascular malformation

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24
Q

rare and comprise 1% of temporal bone tumors

A

vascular malformation

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25
Q

explain vascular malformation and how they grow

A

grow w/ body growths w/out regression

-can grow large & s/s present @ any time

ex: AVMs

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26
Q

most common benign tumor of temporal bone & CPA

A

schwannomas

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27
Q

accounts for ~ 91% of all tumors in and around the temporal bone

A

schwannomas

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28
Q

most common site of schwannomas

A

IAC from CN VIII
arises from vestibular division of CN VIII

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29
Q

what are the 3 sites of temporal bone schwannomas

A

IAC
jugular foramen for CN IX & X
fallopian canal of VII CN

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30
Q

only one where you see multiple schwannomas

A

NF2

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31
Q

will always be unilateral & singular

A

schwannoma

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32
Q

where do vestib schwan come from

A

schwann cells

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33
Q

are vestib schwanns intra or extra axial

A

extra because they come from schwann cells and not primary brain cells

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34
Q

explain vestib schwans

A

typically unilateral & slow growing, generally present bw 40-60 yrs & diagnosis mostly after 6th decade, slightly more common in females
commonly start in IAC that grows into a larger mass in CPA that compresses BS causing hydrocephalus & death
single tumors are most common but multiple like in NF2 can be seen

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35
Q

S/S almost always ipsi to lesion & occur when it is ~ 1 to 4 cm in size

A

vestib schwan

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36
Q

what is the most common symptom of vestib schwan

A

HL

can also see headache & tinnitus

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37
Q

*ANYTHING PT PRESENTS WITH THAT IS SINGLE SIDED IS ALWAYS A RED FLAG (why is one side more affected than the other? vision loss, hl, vertigo, etc.)

A

true

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38
Q

what will pure tonesshow for vestib schwannoma

A

asymmetrical unilateral HF SHNL (may be as low as 10 dB asymmetry)

bs lesion = flat unilateral SNHL

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39
Q

what does tone decay show for vestib schwannoma

A

+ tone decay in more frequencies & doesn’t diminish w/ high intensity

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40
Q

another name for vestib schwan

A

acoustic neuroma

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41
Q

OAE findings in acoustic neuroma

A

normal if HL not significant, decreased contra suppression

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42
Q

speech shows what in acoustic neuroma

A

WRS worse than expected w/ thresholds, + rollover > 0.45 (> 0.25 for NU-6-word lists)

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43
Q

tymps will be abn in vestib schwan

A

false, normal

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44
Q

what does reflex decay show in vestib schwan

A

contra decay + at 500 & 1000

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45
Q

what are Hirsch & Anderson Guidelines for RD

A

RD+++ → pos retro sign if reflex amp declines > 50% in 5 sec at 500 and 1000 Hz
RD++ → questionable retro sign if reflex amp declines > 50% in 5 sec at 1000 Hz but not 500 Hz
RD+ → not significant retro sign if reflex amp declines < 50% in 5 sec at 500 and 1000 Hz

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46
Q

what does td show for vestib schwannoma

A

TD > 30dB + for retro pathology
more frequencies w/ decay = greater probability of retro pathology
test both ears for comparison

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47
Q

how does tone decay work according to rosenburg

A

begins @ thresh of frequency being tested, lasts for 60s
if PT hears tone all 60s, neg TD
if tone fades before 60s, amount of decay is SL reached at end of 60s (ex: thresh 55 dB HL @ 2kHz & tone raised total of 35 dB @ end of 60s, TD of 35 dB is reported)

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48
Q

why are ABRs not done for every tumor?

A

MRI is more sensitive and definitive than ABR

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49
Q

when is an abr sensitive to vestib schwan

A

sensitive to tumors > 1cm

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50
Q

what will a CN VIII pathology show in ARTs for R

A

right ipsi and contra are affected
l ipsi and contra are unaffected

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51
Q

what would a small extra/intra axial bs path show in ARTs for r pathology

A

abs contras (has to crossover in BS)

r contra & l contra abs

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52
Q

what would a small extra/intra axial bs path show in ARTs for L pathology

A

left & right contras abs

ispis normal

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53
Q

what would a large extra/intra axial bs path show in ARTs for r pathology

A

depending on size and location, all abs

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54
Q

what will a CN VIII pathology show in ARTs for L

A

l ispi and l contra abs
right both normal

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55
Q

what is a common profile for vestib schwan

A

HF asymmetry, R ipsi & contra abn, & word rec drops in R ear w/ noise

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56
Q

what will an ABR show for vestib schwan

A

want to compare abr on one side to the other side

wave v latency increased (>6ms), absence of wave v, inter latency increased (>4ms)(I-V is affected)

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56
Q

what is a postive sign in ABR for vestib schwan

A

compare wave V latency b/w ears with relatively little difference in sensitivity

The inter-ear/interaural latency difference (ILD) of wave V of > 0.3 or 0.4 ms
Also referred to as the interaural time for wave V or “IT5”

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57
Q

what is IT5

A

difference in latency of wave 5 of abnormal ear and of the normal ear

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58
Q

tumor on r side and l is normal
latency of r is 6.5 s
latency of l is 5.5 ms
interaural latency difference?
is this significant bw interaural latencies?

A

1 ms (the difference between both ears of wave 5 ONLY)

yes, want > .3 or .4 ms

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59
Q

how do you definitively diagnose vestib schwan

A

T1 MRI w/ contras is gold standard

CT scan - not as sensitive to small tumors as above

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60
Q

what is a diagnostic feature of schwannoma on MRI

A

increased lumen size of IAC

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61
Q

what are treatment options for vestib schwan

A

Observation → watch & wait using serial MRIs & audios

Sterotactic radiosurgery

surgery

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62
Q

what is sterotactic radiosurgery and the goal

A

(gamma knife surgery) → Advanced form of radiation therapy that targets small areas with highly focused, intense radiation beams - uses 3D imaging, goal is to reduce size and growth when surgery is contraindicated (NF2 or elderly PTs); preserve hearing/n for <1.5cm tumors

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63
Q

what is the goal of surgery in vestib schwan PTs

A

goal is to alleviate risk of progressive intracranial tumor growth to decrease risk of morbidity and mortality, preserves fn fxn

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64
Q

what is contraindication of vestib schwan surgery

A

NF2 or elderly PTs

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65
Q

What tumors covered so far are considered benign tumors of the temporal bone

A

osteoma→ bony tumor in EAC
paragangloma
NF2
FN schwannoma

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66
Q

3 reasons we see meningiomas

A

nf 2
radiation
genetics

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67
Q

gold standard for diagnosing tumors

A

MRI T1

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68
Q

NF2 PTs on T1 MRI can show multiple meningiomas

A

true

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69
Q

one of most common benign tumors of CNS in adults & ~10% of all tumors involving the CPA

A

meningiomas

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70
Q

where do meningiomas come from

A

arise from meninges of CNS and usually superficial making them extra- tumors

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71
Q

usually found singly
circumscribed, lobulated white-grey masses
appears later in life & more common in females

A

meningiomas

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72
Q

can be associated with DiGeorge syndrome

A

meningiomas

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73
Q

describe the difference in size of meningiomas and how this affects their growth

A

larger size has larger space so they do not push on things and can get very large before they produce symptoms
smaller size has smaller space so it pushes on things making symptoms
i.e. IAC meningiomas mimic acoustic neuromas clinically and on images making diagnosis difficult

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74
Q

can you clinically diagnose the difference bw schwannoma and meningiomas without an mri

A

NO

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75
Q

what are audiometric s/s of meningiomas

A

progressive unilateral SNHL
unlike acoustic neuromas, only ~60% PTs w/ meningiomas in temporal bone have SNHL symptoms
vertigo
tinnitus
pulsatile if it involves jugular foramen
nausea/vomiting
due to irritation of meninges
CN VIII involvement mimics acoustic schwannoma
abn art on affected side & normal tymps’
+RD
+rollover & poorer scores in noise
usually abn ABR
normal OAEs with appropriate loss

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76
Q

what is treatment for meningiomas

A

for benign ones invading CNs→ surgical removal & possible radiation if complete resection not possible
even with removal , high recurrence rate
long term follow up for monitoring of recurrence
small tumors w/ old or ill PTs
conservative symptomatic management

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77
Q

what are d/d for meningiomas

A

OM
paraganglioma
fn neuroma
vestib schwannoma

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78
Q

why is OM d/d for meningiomas

A

if meningioma gets to ME mimics OM
adults don’t get otitis media unless there is an underlying issue
make sure to look out for this and refer when necessary

differences→ red TM , granulation tissue formation & CHL

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79
Q

why is a paraganglioma d/d for meningioma

A

meningiomas more highly vascular on otoscopy, can look like these on MRI, & can present w/ neck mass similar to glomus jugulare

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80
Q

why is FN neuroma d/d for meningiomas

A

if CN VII involved can cause facial numbness/paralysis also seen in FN neuromas

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81
Q

what are cortical tumors and what do they show

A

shows normal peripheral tests→ pure tones, ARTs, ABR & OAEs

WRS will be poor and inconsistent w/ thresholds especially in noise

headaches, dizziness

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82
Q

why are ART and ABR normal in cortical tumors

A

because they only go up to the BS

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83
Q

s/s of cortical tumors are on the same side as the site of lesion

A

FALSE
opposite
if you have a r sides stroke the left side is affected so the same is here with cortical tumors

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84
Q

diagnosed often late and present a poor prognosis
ex: adenocarcinoma & osteosarcoma

A

malignant tumors

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85
Q

what symptoms of malignant tumors are they similar to

A

chronic suppurative OM
usually treated as such and why true diagnosis is delayed

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86
Q

what are audiometric s/s of malignant tumors

A

aural discharge→ w/ or w/out blood
otalgia
HL
tinnitus

87
Q

what are s/s of cranial neuropathies in malignant tumors

A

facial paralysis
headache
SNHL & vestib symptoms

88
Q

what tumors mestasize from other sites to the temporal bone

A

Breast cancer (most common)
Lung cancer
Renal carcinoma, GI, and liver adenocarcinoma
Lymphoma and leukemia
Thyroid cancer
Osteoblastoma (childhood cancer of the bone)
Melanoma (skin cancer)

89
Q

what does the immune system do

A

protects from disease & can distinguish bw body’s own cells and foreign cells

90
Q

what is autoimmunity

A

happens when immune system goes awry and attacks body itself
instead of protecting from external pathogens the immune system produces autoantibodies or T lymphocytes reacting with host own antigens

91
Q

3rd most common category of disease in US

A

autoimmune disease

92
Q

important determinant for immune response of the IE

A

blood-labyrinth barrier

93
Q

what carry immune cells, inflammatory cells & hormones that can affect IE fxn & is responsible for delivery of systemic drugs & steroids for IE treatment

A

blood vessels

94
Q

what are first treatment in autoimmune, inflammatory & infectious conditions of IE because they suppress immune system

A

steroids

95
Q

what is AIED characterized by

A

progressive bilateral SNHL (quick) happening weeks to months and is responsive to immunosuppressive agents (corticosteroids)
some can have unilateral fluctuating SNHL that complicates diagnosis

96
Q

what are the 2 types of AIED

A

primary→ restricted disease to the ear only
secondary→something that can come from other parts of the body that cause the problem (Cogan & Wegener granulomatosis)

97
Q

What are s/s associated with AIED

A

rare, females more, symptoms bw 20-50 yrs
progressive bilateral SNHL (quick) happening weeks to months
aural fullness and/or tinnitus, vestibular symptoms

98
Q

which autoimmune disorder is SNHL reversible

A

AIED

99
Q

what is the primary treatment for AIED

A

corticosteroids→ standard of care for primary AIED for 4 wks
must happen ASAP; irreversible within 3 mos of onset
Steroids given longer than 4 wks or for repeated relapse

100
Q

what are D/D for AIED

A

SSHL
most common confusion
SSHL is usually unilateral and not progressive and is sudden and here it is bilateral and progressive
Meniere’s
mimics because of fluctuating SNHL, tinnitus, aural fullness & vertigo
Others to rule out→ vestib schwan, MS, & otosyphilis

101
Q

occurs within less than 3 days

A

sudden

102
Q

occurs slower, over more than 3 days (seen in AIED)

A

rapidly progressiv3

103
Q

what is SSHL

A

> 30 dB HL SNHL occurring in at least three contiguous frequencies within < 3 days

HL always sudden & SN & can occur w/ a pre-existing SNHL & unilateral

104
Q

If one ear has been affected, the risk of the other ear being affected by SSHL during a patient’s lifetime rises by 4 to 17% (same or the other ear)

A

SSHL

105
Q

when should treatment begin for SSHL

A

should begin < one week of onset
-Corticosteroid therapy for ~ 4 wks
-Intratympanic steroids→higher concentration w/ less side effects/risks of sytemic administration

106
Q

what is a good prognosis for SSHL

A

mild LF SNHL, symptoms persist for shorter time, WRS may not fully recover

107
Q

poor prognosis for SSHL

A

age, HF/flat SNHL, greater SNHL severity, diabetes, vertigo

108
Q

what is MS

A

Results in demyelination of myelin sheath surrounding n fibers in brain & SC

Progressive neurological autoimmune disorder

Affects white matter pathways in CNS

109
Q

what is hallmark of MS

A

Plaques are the hallmark in white matter

110
Q

what are s/s of MS

A

~ 85% have bilateral HF SNHL but can be any audio pattern
-Some LF rising SNHL
young adults, females, caucasian and they have fluctuating SNHL
poor WRS especially in noise

111
Q

LF SNHL rising that is not an autoimmune disorder?

A

SSCD but this is conductive not SNHL
*Meniere’s

112
Q

normal audio but I have a hard time hearing. what are things to consider?

A

could be retro
hidden hearing loss
synaptopathy
depends where the damage is on the 8th n are or there could be an issues in the CNS

113
Q

What is used for diagnosis of MS

A

CT & MRI→>/=2 plaques in white pathways w/ hx, clinical presentation provides diagnosis

114
Q

runs a slow and protracted course of > 5 to 20 years

A

MS

115
Q

is there treatment for MS

A

Manageable but no cure
-No therapy is universally successful for all PTs

116
Q

what are d/d for MS

A

Susac’s & Schilder’s (other ai)
-Diabetes→HL, visual problems, disequilibrium, poor WRS
-Stroke→poor wrs, visual problems, cognitive/memory issues, poor motor skills
-SSHL

117
Q

what are the triad for susac syndrome

A

cognitive issues
vision problems
asymmetric LF HL

118
Q

what is the difference bw susac and ms

A

no psychological issues in MS early like in susac
susac is self limiting but ms gets worse
MS may or may not have HL but Susac does have HL
MS has two or more lesions and Susac has less

119
Q

why is susac mistaken for ms

A

mistaken for MS due to white matter defects present on MRI
dead tissue due to lack of blood supply

120
Q

how does susac resemble ms

A

affects women 20-40 yrs
fluctuating disease progression like MS
asymmetric SNHL in LF & fluctuates
sometimes vertigo/dizziness and tinnitus

121
Q

what is schilder’s disease

A

rare, progressive degenerative demyelinating disorder of CNS
begins in childhood
some consider is childhood variant of MS
Adrenal glands & myelinated nerves and their axons are affected
bilateral
motor sensory & cognitive problems develop in 1st decade and progress

122
Q

what are s/s of schilders

A

personality changes, poor attention, progressive loss of intellectual fxn, vision, hearing and balance problems, muscle weakness, headaches, seizure

123
Q

how is schilders diagnosed

A

MRI, presence of > 2 large (> 2 cm), often bilateral plaques
peripheral nervous system is normal
Additional lesions in brain/spinal cord may suggest MS

124
Q

rare chronic autoimmune inflammatory disorder
young adults, peak around third decade, no gender or racial dominance

A

cogan syndrome

125
Q

what is seen in cogan’s syndrome

A

vestibular auditory symptoms and interstitial keratitis is the hallmark characteristics
these happen quickly after each other
red painful light sensitive eyes, blurred & decreased vision
they have cardiovascular issues or they have inflammation of the blood vessels

126
Q

what is difference bw cogan and menieres

A

meniere’s
hearing goes down and goes back up and back down etc but never end with a profound hL
diff diagnosis for Meniere’s because it is an endolymphatic hydrops
cogan
HL is here, fluctuating but it will progress to profound SNHL and it will not in meniere’s

127
Q

Three signs/symptoms are important for differential diagnosis of cogan and meniere

A

Eye symptoms of CS that are absent in Meniere’s
CS patients report imbalance and ataxia vs. objective vertigo as reported by Meniere’s disease patients
Systemic manifestations observed in CS are not seen in Meniere’s

128
Q

d/d for cogans

A

meniere’s
labyrinthitis/neuritis - hearing loss, vertigo, tinnitus, nausea/vomiting, but NO eye symptoms
wegener’s - SNHL & vertigo but generally NO eye symptoms

129
Q

Chronic incurable manageable metabolism disorder
Inadequate production of insulin
results in hyperglycemia & glycosuria

A

diabetes

130
Q

s/s of diabetes

A

HL could be caused by vascular impairment or metabolic pathways
HL & poor wrs if there is neuropathy especially in noise
LF HL is most common; HF SNHL fluctuating is also reported

131
Q

how does hypertenstion affect hearing

A

BP exceeds 140/90
heart pumps harder & increased pressure damages blood vessels which cause auditory deficits due to reduced blood and oxygen to cochlea
HF SNHL

132
Q

how does cigarette smoking affect hearing

A

affects hearing through effects on cochlear vasculature & anti-oxidative mechanisms of cochlea
blood vessels go into spasm (vasospams) and cause higher risk of blood clotting in cochlea

133
Q

how does chronic alcoholism affect hearing

A

can affect central auditory processing
can have normal audio but issues understanding and processing what is said
delays transmission time in the brain - lag time with what is heard and what is processed

134
Q

what is korsakoff’s

A

related to chronic alcoholism

causes chronic memory disorder due to lack of nutrients from not eating
issues learning new info, cannot remember newer events & long term memory gaps

135
Q

what was beaver dam and what did it reveal

A

examined correlation bw different risk factors and HL like smoking, diabetes, alcohol etc.

only risk factor w/ HL was cardiovascular disease with inflammation, atherosclerosis, and hypertension

136
Q

awareness of body in space

A

proprioception

137
Q

tells us where the head is in relation to the environment

A

somatosensory portion of nervous system

138
Q

what does the vestibular system do

A

provides awareness of our position of head and body (somatosensory) and awareness of active/passive limb movements and body position

139
Q

what are the 3 vestib components

A

peripheral sensory - in inner ear
central - bs and cerebellum structures in here
motor - connections w/ different motor nuclei & muscles

140
Q

housed in the inner ear and consists of two types of motion sensors
3 semicircular canals
2 otolith organs - utricle & saccule

A

peripheral sensory apparatus - vestibular labyrinth

141
Q

two types of motion sensors

A

3 semicircular canals
2 otolith organs - utricle & saccule

142
Q

sensors for angular or rotational acceleration of the head
They can detect movements in three-dimensional space

A

3 semicircular canals

143
Q

linear acceleration with respect to gravity because of their orientation in the head

A

utricle & saccule

144
Q

what does the utricle sense

A

sensitive to a change in linear movement (e.g., sideways or up/down head tilt)

145
Q

what does the saccule sense

A

gives information about vertical acceleration (e.g., when in an elevator)

146
Q

where are otoconia

A

utricle and saccule

147
Q

clock of the body

A

cerebellum

148
Q

rate of speech is impacted, impacts how we walk (timed motion),

A

cerebellum damage

149
Q

why do older adults fall so much?

A

ankles w/ arthritis and other issues cause bad ankle sway to sop them from falling

150
Q

what is the central vestib system

A

takes info from peripheral apparatus through CN VIII vestib portion and goes to cerebellum and nuclei in pons to be processed along with visual and somatosensory input
this influences eye movements staying up and walking, and spatial orientation

151
Q

2 hallmarks of cerebellar issues:

A

gait & nystagmus

152
Q

Whenever the vestibular mechanism is damaged/diseased, common clinical manifestations that result are

A

sense of imbalance
dizziness/vertigo
nystagmus

153
Q

type of dizziness specific to vestibular system disorders
associated with an illusory sense of motion or rotation over which the individual has no control

A

vertigo

154
Q

can be of peripheral or central origin

A

vertigo

155
Q

what are major conditions that can produce episodic vertigo

A

menieres (lasts the longest)
BPPV
migraine associated vertigo
SSCD

156
Q

what condition will give you congenital cataracts

A

norrie
rubella
cmv in some cases

157
Q

can someone who is blind have nystagmus? why or why not

A

yes because nystagmus is not initiated by visual impulses

158
Q

cna nystagmus be congenital

A

yes

159
Q

if someone has vertigo, nystagmus will be present

A

yes

160
Q

Bilateral peripheral deficits generally do show vestibular compensation

A

FALSE
do not

161
Q

Central vestibular pathology does show vestibular compensation

A

FALSE
doesn’t

162
Q

if you have issue with inner ear and have SNHL is there compensation that will get this back?

A

no it is gone and will be HI in that side

163
Q

if you have unilateral problem (periphery), the other side and central system compensates

A

true

164
Q

when will you undergo vestibular compensation?

A

unilateral peripheral pathology

165
Q

single most common complication of acute or chronic OME

A

serous labyrinthitis

166
Q

what is the difference between labyrnthitis and neuritis

A

lab - affects as and vestibular system (inflammation of IE labyrinth)
neuritis = only vestibular nerve (inflammation of vestibular n)

167
Q

inflammation of inner ear labyrinth

A

vestibular labyrinthitis

168
Q

inflammation of the vestibular nerve

A

vestibular neuritis

169
Q

vestibular neuritis & labyrinthitis are preceded by what kind of infections

A

Cold/Influenza/Otitis media
Measles/Mumps
Meningitis
Infectious mononucleosis

170
Q

very common to have infection 2-3 wks prior to having symptoms

A

neuritis & labyrinthitis

171
Q

involves both cochlea and vestib symptoms

A

labyrinthitis

172
Q

will not see HL but will see vestibuolar symptoms

A

neuritis

173
Q

when will you have cochlear issue and when will you not?

A

cochlear - labyrinthitis

174
Q

what symptoms can be seen in vestibular labyrinthitis

A

Cochlear symptoms - HL
Aural fullness
Tinnitus
High frequency SNHL
in approx 50% cases, HL resolves completely or partially

Vestibular symptoms
Acute vertigo
Nausea/vomiting
Nystagmus

175
Q

what symptoms can be seen in vestibular neuritis

A

Vestibular symptoms
Acute vertigo
Nausea/vomiting
Nystagmus

176
Q

what is seen in vestibular occlusion of labyrinthine artery

A

labyrinthine artery is primary arterial supply to cochlea w/ no anastomosis so occlusion here by an emboli causes sudden & profound SNHL & vestibular dysfunction - vestibular compensation occurs in ~ 4 to 6 months but SNHL is permanent
more common in older adults but happens at all ages

177
Q

CNS disorder that causes vertigo/dizziness along with migraine headache symptoms

A

migraine associated vertigo

178
Q

symptoms of MAV

A

dizziness/vertigo is aura of the headache
can last > 24 hours
MAV can also have
Headache, nausea, vomiting, and pallor
Photophobia (insensitivity to light) and loss of peripheral vision
Motion intolerance and noise sensitivity
Ataxia and numbness/weakness of the extremities

HL is uncommon

179
Q

what is a diagnosis of MAV based on

A

based on case Hx & subjective
symptoms

family hx of migraines ids key

180
Q

most cause common cause of vertigo of peripheral origin

A

BPPV

181
Q

what does bppv stand for (medical list)

A

Benign – it is not life-threatening
Paroxysmal – it comes in sudden, brief spells
Positional – it gets triggered by certain head positions or movements
Vertigo – a false sense of rotational movement

182
Q

ccounts for ~ 20% of all vestibular complaints

A

bppv

183
Q

what structure is sensitive to gravity

A

otolith/otoconia
in the utricle and saccules

184
Q

diagnostic test and teratment for BPPV

A

dix hallpike
epley

185
Q

where is BPPV common location

A

posterior scc if in horiz more complicated to treat

186
Q

3 forms of BPPV

A

acute (resolves spontaneously over 3 mos), intermittent (active & inactive periods over several years), chronic (continuous symptoms over long durations

187
Q

describe BPPV

A

Brief episodes of mild-intense vertigo that last for 1 min & may have nausea/vomiting
-Triggered by head position
-Worse in mornings or evenings
Avg. Age of onset is ~ 55 years but can occur at any age

188
Q

how to otoconia cause BPPV

A

otoconia dislodge & migrate into SCCs & move fluid when it shouldn’t causing false signals to the brain resulting in vertigo
otolith organs (u and s) contain otoliths sensitive to gravity and these can become dislodged and make there way into one or more scc where they shouldnt be
the fluid in the SCC doesn’t move to gravity but otoliths do so when they are dislodged into SCC it moves the fluid when there are enough accumulations the SCC canals that are used to sense head motions so this causing IE to send false signals to the brain that the head is moving based on gravity even though it isn’t resulting in vertigo

189
Q

are audio & mri normal for bppv?

A

yes

190
Q

common etiology of BPPV

A

idiopathic

191
Q

multifactorial
no gender difference
usually unilateral but can be bilateral later
family hx
peak bw 30-60 years, rare in kids, can occur any time

A

menieres

192
Q

waht symptoms do you need for menieres

A

SNHL that comes and goes (LF SNHL like also seen in MS)
LF/roaring tinnitus
intermittent vertigo that can last a long time - nystagmus is always present
aural fullness/pressure

193
Q

what does a definitive diagnosis of menieres need

A

2 or more episodes lasting more than 20 mins
2/4 characteristic symptoms present

194
Q

what is considered a significant change in hearing in menieres

A

shift of > 15 dB HL for average threshold of 0.5, 1, 2, & 3 KHz
shift in WRS of >/= 15-20%

195
Q

describe the 3 stages of menieres

A

Early stage
LF rising SNHL (worse from 250-1000 w/ NH from 2000-8000
moderate to moderately severe flat SNHL
w/ bilateral cases, asymmetry of >25 dB HL
Middle stage
reduced at all frequencies but worse in high and lows
reverse cookie bite
late stage (burn out)
hearing stabalizes
flat severe SNHL w/ peaks at 1 & 2 kHz

196
Q

can menieres progress to profound hL

A

RARELY usually just severe

197
Q

what does immittance show for menieres

A

normal tymps
reflexes - present usually at lower SL
king of recruitment

198
Q

what does ecohg show for menieres

A

SP/AP ratio of > 0.42 or > 42% is considered significant/positive for Ménière’s disease
not 100% accurate test

only see during active episode or symptoms of some sort are present

199
Q

what s treatment for menieres

A

for some, low sodium diet & diuretics
shunt to unblock endolymphatic duct
altering immune activity that could be causing it
Amplification is not always successful because of the distortion and recruitment that makes speech perception difficult
CIs can be beneficial, if candidacy criteria are met

200
Q

rare, usually unilateral, can affect all ages

A

SSCD

201
Q

what are vestibular symptoms of SSCD

A

evoked by loud noises/maneuvars that change ME pressure (coughing, sneezing, etc.)
vertigo/dizziness
nystagmus
sound induced vertigo (Tullios phenomenon)
oscillopsia

202
Q

What are audio symptoms of SSCD

A

chl/fluctuating HL (mimics OTSC or Meniere’s
most have LF ABG (worse from 250-1000)
due to increases sensitivity of BC by increased perilymph movements improving BC thresholds, energy from AC is pushed away from cochlea making them lower

203
Q

what are d/d for menieres and why

A

patulous ET - aural fullness/pressure & autophony that is common with both
ARTs differentiate OTSC from SSCD
NORMAL in SSCD - because not a ME pathology or true ABG
ABN in OTSC

204
Q

how is SSCD diagnosed

A

vestib assessment
CT
ECohG
increase in endolymphatic pressure
unlike menieres almost all PTs show abn SP/AP

205
Q

what is the difference in ecohg of Meniers vs SSCD

A

menieres can only show sign if in active episode or some symptom present

SSCD almost always shows abn SP/AP (>42%)

206
Q

what is mal de debarquement

A

illusion of movement long after travel on water/boat
most seen in sailors or other long travel like airplane, car, train, waterbed
most resolves in 24 hours others persist
spontaneous resolution decrease after it has persisted for >12 mos
etiology
unknown
middle aged women

207
Q

what are s/s of de debarqument

A

rocking/swaing/disequilibrium but rarely accompanied by true vertigo
anxiety & depression
symptoms worsen when lying down or stress/fatigue
improve or disappear during continuous movement ike driving

208
Q

vestib dysfunction is often accompanied by HL in kids

A

true

209
Q

why are vestib disorders not caught in kids

A

underdiagnosed due to compensation, few vocab to express symptoms & these kids walk ony slightly later than typically developing peers

210
Q

wsome cannot ride bikes, skate, swim, do gymnastics

A

vestib disorders in kids

211
Q

If a child has a hearing loss >60 dB HL and has not walked by 14.5 months, suspect

A

vestibular dysfunction

212
Q

what are the most common causes of vestib dysfunction in kids

A

CMV & OMEw

213
Q

how does OME cause vestib issues in kids

A

chronic OME can cause delayed walking & balance problems
this is by invasion of bacterial toxins in IE or cholesteatoma that causes labyrinthitis or perilymphatic fistula resulting in vestib issues

214
Q

what are s/s of vestib disorders in kids

A

dizziness/vertigo
visual problems
balance problems

215
Q

how to diagnose vestib issues in kids

A

good case hx - length of symptoms hx of falls, etc.
identify provoking movements like motion sensitibty

AUDE 5410 Aud-Vestib Disorders (18 decks)

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