Final Exam Study Guide (New Material) Flashcards
what is a neoplasm
abnormal mass tissue
around 45% of intracranial tumors arise from
neuroglia cells
what are neuroglial cells
non-excitable support cells of CNS & make up about ½ volume of CNS
what are the 4 types of neuroglia cells
astrocytes
oligodendrocytes
microglia
ependymal cells
what are astrocytes
star shaped cells & provide barrier at synapses that contain NT or hormones (dopamine)
what are oligodendrocytes
active in forming myelin sheath in central n fibers
what are migroglia
small glial cells that ingest & remove neural residue during inflammation & degeneration in CNS (phagocytic)
what are ependymal cells
epithelial cells lining CSF & are ciliated and facilitate CSF circulation & production
what are benign tumors
slow growing, well-defined borders for easy removal (surgery is good treatment), no metastasizing or life threatening, will kill if in crucial areas
what are malignant tumors
grow fast, invade & destruct structures, life threatening, can metastasize
explain how a benign and malignant tumors are intertwined
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
what is an intra-axial tumor
originate in parenchyma of brain
ex: astrocytoma, glioblastoma
what is an extra-axial tumor
tumors that originate not from parenchyma of brain
ex: meningiomas, CN sheaths, pineal & pituitary glands
what are the 4 segments of the temporal bone
petrous (IE & hard segment)
Squamous
Mastoid
Tympanic (forms EAC, matures by 3 yrs old)
where do majority of vascular malformations in temporal bone present
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
what are the two vascular tumors
hemangiomas & vascular malformations
What happens in hemangiomas
Extra blood vessels that group together into a dense clump
Most go through phases of growth & then go away on their own
what are findings in hemangiomas/vascular malformations/vascular tumors
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
what are D/D for vascular tumors (H & VM)
-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
how are vascular tumors diagnosed
-Case hx & symptoms
-High res CT→intra tumor calcification shows here
-MRI w/ contrast→fluid is bright on T2 weighted more than acoustic schwannomas
why use an mri with contrast for vascular tumors
luid is bright on T2 weighted more than acoustic schwannomas
what is the management for vascular tumors
Surgery, thermal ablation, embolization
-Recurrence is low
more common vascular tumor that is present at birth
vascular malformation
rare and comprise 1% of temporal bone tumors
vascular malformation
explain vascular malformation and how they grow
grow w/ body growths w/out regression
-can grow large & s/s present @ any time
ex: AVMs
most common benign tumor of temporal bone & CPA
schwannomas
accounts for ~ 91% of all tumors in and around the temporal bone
schwannomas
most common site of schwannomas
IAC from CN VIII
arises from vestibular division of CN VIII
what are the 3 sites of temporal bone schwannomas
IAC
jugular foramen for CN IX & X
fallopian canal of VII CN
only one where you see multiple schwannomas
NF2
will always be unilateral & singular
schwannoma
where do vestib schwan come from
schwann cells
are vestib schwanns intra or extra axial
extra because they come from schwann cells and not primary brain cells
explain vestib schwans
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
S/S almost always ipsi to lesion & occur when it is ~ 1 to 4 cm in size
vestib schwan
what is the most common symptom of vestib schwan
HL
can also see headache & tinnitus
*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.)
true
what will pure tonesshow for vestib schwannoma
asymmetrical unilateral HF SHNL (may be as low as 10 dB asymmetry)
bs lesion = flat unilateral SNHL
what does tone decay show for vestib schwannoma
+ tone decay in more frequencies & doesn’t diminish w/ high intensity
another name for vestib schwan
acoustic neuroma
OAE findings in acoustic neuroma
normal if HL not significant, decreased contra suppression
speech shows what in acoustic neuroma
WRS worse than expected w/ thresholds, + rollover > 0.45 (> 0.25 for NU-6-word lists)
tymps will be abn in vestib schwan
false, normal
what does reflex decay show in vestib schwan
contra decay + at 500 & 1000
what are Hirsch & Anderson Guidelines for RD
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
what does td show for vestib schwannoma
TD > 30dB + for retro pathology
more frequencies w/ decay = greater probability of retro pathology
test both ears for comparison
how does tone decay work according to rosenburg
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)
why are ABRs not done for every tumor?
MRI is more sensitive and definitive than ABR
when is an abr sensitive to vestib schwan
sensitive to tumors > 1cm
what will a CN VIII pathology show in ARTs for R
right ipsi and contra are affected
l ipsi and contra are unaffected
what would a small extra/intra axial bs path show in ARTs for r pathology
abs contras (has to crossover in BS)
r contra & l contra abs
what would a small extra/intra axial bs path show in ARTs for L pathology
left & right contras abs
ispis normal
what would a large extra/intra axial bs path show in ARTs for r pathology
depending on size and location, all abs
what will a CN VIII pathology show in ARTs for L
l ispi and l contra abs
right both normal
what is a common profile for vestib schwan
HF asymmetry, R ipsi & contra abn, & word rec drops in R ear w/ noise
what will an ABR show for vestib schwan
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)
what is a postive sign in ABR for vestib schwan
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”
what is IT5
difference in latency of wave 5 of abnormal ear and of the normal ear
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?
1 ms (the difference between both ears of wave 5 ONLY)
yes, want > .3 or .4 ms
how do you definitively diagnose vestib schwan
T1 MRI w/ contras is gold standard
CT scan - not as sensitive to small tumors as above
what is a diagnostic feature of schwannoma on MRI
increased lumen size of IAC
what are treatment options for vestib schwan
Observation → watch & wait using serial MRIs & audios
Sterotactic radiosurgery
surgery
what is sterotactic radiosurgery and the goal
(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
what is the goal of surgery in vestib schwan PTs
goal is to alleviate risk of progressive intracranial tumor growth to decrease risk of morbidity and mortality, preserves fn fxn
what is contraindication of vestib schwan surgery
NF2 or elderly PTs
What tumors covered so far are considered benign tumors of the temporal bone
osteoma→ bony tumor in EAC
paragangloma
NF2
FN schwannoma
3 reasons we see meningiomas
nf 2
radiation
genetics
gold standard for diagnosing tumors
MRI T1
NF2 PTs on T1 MRI can show multiple meningiomas
true
one of most common benign tumors of CNS in adults & ~10% of all tumors involving the CPA
meningiomas
where do meningiomas come from
arise from meninges of CNS and usually superficial making them extra- tumors
usually found singly
circumscribed, lobulated white-grey masses
appears later in life & more common in females
meningiomas
can be associated with DiGeorge syndrome
meningiomas
describe the difference in size of meningiomas and how this affects their growth
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
can you clinically diagnose the difference bw schwannoma and meningiomas without an mri
NO
what are audiometric s/s of meningiomas
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
what is treatment for meningiomas
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
what are d/d for meningiomas
OM
paraganglioma
fn neuroma
vestib schwannoma
why is OM d/d for meningiomas
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
why is a paraganglioma d/d for meningioma
meningiomas more highly vascular on otoscopy, can look like these on MRI, & can present w/ neck mass similar to glomus jugulare
why is FN neuroma d/d for meningiomas
if CN VII involved can cause facial numbness/paralysis also seen in FN neuromas
what are cortical tumors and what do they show
shows normal peripheral tests→ pure tones, ARTs, ABR & OAEs
WRS will be poor and inconsistent w/ thresholds especially in noise
headaches, dizziness
why are ART and ABR normal in cortical tumors
because they only go up to the BS
s/s of cortical tumors are on the same side as the site of lesion
FALSE
opposite
if you have a r sides stroke the left side is affected so the same is here with cortical tumors
diagnosed often late and present a poor prognosis
ex: adenocarcinoma & osteosarcoma
malignant tumors
what symptoms of malignant tumors are they similar to
chronic suppurative OM
usually treated as such and why true diagnosis is delayed
what are audiometric s/s of malignant tumors
aural discharge→ w/ or w/out blood
otalgia
HL
tinnitus
what are s/s of cranial neuropathies in malignant tumors
facial paralysis
headache
SNHL & vestib symptoms
what tumors mestasize from other sites to the temporal bone
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)
what does the immune system do
protects from disease & can distinguish bw body’s own cells and foreign cells
what is autoimmunity
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
3rd most common category of disease in US
autoimmune disease
important determinant for immune response of the IE
blood-labyrinth barrier
what carry immune cells, inflammatory cells & hormones that can affect IE fxn & is responsible for delivery of systemic drugs & steroids for IE treatment
blood vessels
what are first treatment in autoimmune, inflammatory & infectious conditions of IE because they suppress immune system
steroids
what is AIED characterized by
progressive bilateral SNHL (quick) happening weeks to months and is responsive to immunosuppressive agents (corticosteroids)
some can have unilateral fluctuating SNHL that complicates diagnosis
what are the 2 types of AIED
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)
What are s/s associated with AIED
rare, females more, symptoms bw 20-50 yrs
progressive bilateral SNHL (quick) happening weeks to months
aural fullness and/or tinnitus, vestibular symptoms
which autoimmune disorder is SNHL reversible
AIED
what is the primary treatment for AIED
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
what are D/D for AIED
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
occurs within less than 3 days
sudden
occurs slower, over more than 3 days (seen in AIED)
rapidly progressiv3
what is SSHL
> 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
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)
SSHL
when should treatment begin for SSHL
should begin < one week of onset
-Corticosteroid therapy for ~ 4 wks
-Intratympanic steroids→higher concentration w/ less side effects/risks of sytemic administration
what is a good prognosis for SSHL
mild LF SNHL, symptoms persist for shorter time, WRS may not fully recover
poor prognosis for SSHL
age, HF/flat SNHL, greater SNHL severity, diabetes, vertigo
what is MS
Results in demyelination of myelin sheath surrounding n fibers in brain & SC
Progressive neurological autoimmune disorder
Affects white matter pathways in CNS
what is hallmark of MS
Plaques are the hallmark in white matter
what are s/s of MS
~ 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
LF SNHL rising that is not an autoimmune disorder?
SSCD but this is conductive not SNHL
*Meniere’s
normal audio but I have a hard time hearing. what are things to consider?
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
What is used for diagnosis of MS
CT & MRI→>/=2 plaques in white pathways w/ hx, clinical presentation provides diagnosis
runs a slow and protracted course of > 5 to 20 years
MS
is there treatment for MS
Manageable but no cure
-No therapy is universally successful for all PTs
what are d/d for MS
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
what are the triad for susac syndrome
cognitive issues
vision problems
asymmetric LF HL
what is the difference bw susac and ms
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
why is susac mistaken for ms
mistaken for MS due to white matter defects present on MRI
dead tissue due to lack of blood supply
how does susac resemble ms
affects women 20-40 yrs
fluctuating disease progression like MS
asymmetric SNHL in LF & fluctuates
sometimes vertigo/dizziness and tinnitus
what is schilder’s disease
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
what are s/s of schilders
personality changes, poor attention, progressive loss of intellectual fxn, vision, hearing and balance problems, muscle weakness, headaches, seizure
how is schilders diagnosed
MRI, presence of > 2 large (> 2 cm), often bilateral plaques
peripheral nervous system is normal
Additional lesions in brain/spinal cord may suggest MS
rare chronic autoimmune inflammatory disorder
young adults, peak around third decade, no gender or racial dominance
cogan syndrome
what is seen in cogan’s syndrome
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
what is difference bw cogan and menieres
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
Three signs/symptoms are important for differential diagnosis of cogan and meniere
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
d/d for cogans
meniere’s
labyrinthitis/neuritis - hearing loss, vertigo, tinnitus, nausea/vomiting, but NO eye symptoms
wegener’s - SNHL & vertigo but generally NO eye symptoms
Chronic incurable manageable metabolism disorder
Inadequate production of insulin
results in hyperglycemia & glycosuria
diabetes
s/s of diabetes
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
how does hypertenstion affect hearing
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
how does cigarette smoking affect hearing
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
how does chronic alcoholism affect hearing
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
what is korsakoff’s
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
what was beaver dam and what did it reveal
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
awareness of body in space
proprioception
tells us where the head is in relation to the environment
somatosensory portion of nervous system
what does the vestibular system do
provides awareness of our position of head and body (somatosensory) and awareness of active/passive limb movements and body position
what are the 3 vestib components
peripheral sensory - in inner ear
central - bs and cerebellum structures in here
motor - connections w/ different motor nuclei & muscles
housed in the inner ear and consists of two types of motion sensors
3 semicircular canals
2 otolith organs - utricle & saccule
peripheral sensory apparatus - vestibular labyrinth
two types of motion sensors
3 semicircular canals
2 otolith organs - utricle & saccule
sensors for angular or rotational acceleration of the head
They can detect movements in three-dimensional space
3 semicircular canals
linear acceleration with respect to gravity because of their orientation in the head
utricle & saccule
what does the utricle sense
sensitive to a change in linear movement (e.g., sideways or up/down head tilt)
what does the saccule sense
gives information about vertical acceleration (e.g., when in an elevator)
where are otoconia
utricle and saccule
clock of the body
cerebellum
rate of speech is impacted, impacts how we walk (timed motion),
cerebellum damage
why do older adults fall so much?
ankles w/ arthritis and other issues cause bad ankle sway to sop them from falling
what is the central vestib system
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
2 hallmarks of cerebellar issues:
gait & nystagmus
Whenever the vestibular mechanism is damaged/diseased, common clinical manifestations that result are
sense of imbalance
dizziness/vertigo
nystagmus
type of dizziness specific to vestibular system disorders
associated with an illusory sense of motion or rotation over which the individual has no control
vertigo
can be of peripheral or central origin
vertigo
what are major conditions that can produce episodic vertigo
menieres (lasts the longest)
BPPV
migraine associated vertigo
SSCD
what condition will give you congenital cataracts
norrie
rubella
cmv in some cases
can someone who is blind have nystagmus? why or why not
yes because nystagmus is not initiated by visual impulses
cna nystagmus be congenital
yes
if someone has vertigo, nystagmus will be present
yes
Bilateral peripheral deficits generally do show vestibular compensation
FALSE
do not
Central vestibular pathology does show vestibular compensation
FALSE
doesn’t
if you have issue with inner ear and have SNHL is there compensation that will get this back?
no it is gone and will be HI in that side
if you have unilateral problem (periphery), the other side and central system compensates
true
when will you undergo vestibular compensation?
unilateral peripheral pathology
single most common complication of acute or chronic OME
serous labyrinthitis
what is the difference between labyrnthitis and neuritis
lab - affects as and vestibular system (inflammation of IE labyrinth)
neuritis = only vestibular nerve (inflammation of vestibular n)
inflammation of inner ear labyrinth
vestibular labyrinthitis
inflammation of the vestibular nerve
vestibular neuritis
vestibular neuritis & labyrinthitis are preceded by what kind of infections
Cold/Influenza/Otitis media
Measles/Mumps
Meningitis
Infectious mononucleosis
very common to have infection 2-3 wks prior to having symptoms
neuritis & labyrinthitis
involves both cochlea and vestib symptoms
labyrinthitis
will not see HL but will see vestibuolar symptoms
neuritis
when will you have cochlear issue and when will you not?
cochlear - labyrinthitis
what symptoms can be seen in vestibular labyrinthitis
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
what symptoms can be seen in vestibular neuritis
Vestibular symptoms
Acute vertigo
Nausea/vomiting
Nystagmus
what is seen in vestibular occlusion of labyrinthine artery
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
CNS disorder that causes vertigo/dizziness along with migraine headache symptoms
migraine associated vertigo
symptoms of MAV
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
what is a diagnosis of MAV based on
based on case Hx & subjective
symptoms
family hx of migraines ids key
most cause common cause of vertigo of peripheral origin
BPPV
what does bppv stand for (medical list)
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
ccounts for ~ 20% of all vestibular complaints
bppv
what structure is sensitive to gravity
otolith/otoconia
in the utricle and saccules
diagnostic test and teratment for BPPV
dix hallpike
epley
where is BPPV common location
posterior scc if in horiz more complicated to treat
3 forms of BPPV
acute (resolves spontaneously over 3 mos), intermittent (active & inactive periods over several years), chronic (continuous symptoms over long durations
describe BPPV
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
how to otoconia cause BPPV
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
are audio & mri normal for bppv?
yes
common etiology of BPPV
idiopathic
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
menieres
waht symptoms do you need for menieres
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
what does a definitive diagnosis of menieres need
2 or more episodes lasting more than 20 mins
2/4 characteristic symptoms present
what is considered a significant change in hearing in menieres
shift of > 15 dB HL for average threshold of 0.5, 1, 2, & 3 KHz
shift in WRS of >/= 15-20%
describe the 3 stages of menieres
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
can menieres progress to profound hL
RARELY usually just severe
what does immittance show for menieres
normal tymps
reflexes - present usually at lower SL
king of recruitment
what does ecohg show for menieres
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
what s treatment for menieres
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
rare, usually unilateral, can affect all ages
SSCD
what are vestibular symptoms of SSCD
evoked by loud noises/maneuvars that change ME pressure (coughing, sneezing, etc.)
vertigo/dizziness
nystagmus
sound induced vertigo (Tullios phenomenon)
oscillopsia
What are audio symptoms of SSCD
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
what are d/d for menieres and why
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
how is SSCD diagnosed
vestib assessment
CT
ECohG
increase in endolymphatic pressure
unlike menieres almost all PTs show abn SP/AP
what is the difference in ecohg of Meniers vs SSCD
menieres can only show sign if in active episode or some symptom present
SSCD almost always shows abn SP/AP (>42%)
what is mal de debarquement
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
what are s/s of de debarqument
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
vestib dysfunction is often accompanied by HL in kids
true
why are vestib disorders not caught in kids
underdiagnosed due to compensation, few vocab to express symptoms & these kids walk ony slightly later than typically developing peers
wsome cannot ride bikes, skate, swim, do gymnastics
vestib disorders in kids
If a child has a hearing loss >60 dB HL and has not walked by 14.5 months, suspect
vestibular dysfunction
what are the most common causes of vestib dysfunction in kids
CMV & OMEw
how does OME cause vestib issues in kids
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
what are s/s of vestib disorders in kids
dizziness/vertigo
visual problems
balance problems
how to diagnose vestib issues in kids
good case hx - length of symptoms hx of falls, etc.
identify provoking movements like motion sensitibty
