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AUD spring 19 Medical > Final > Flashcards

Final Flashcards

1
Q

list the five inner ear diseases

A

1) otosclerosis
2) meniere’s disease
3) autoimmune inner ear disease
4) sudden and idiopathic SNHL
5) vascular lesions

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2
Q

another name for otosclerosis

A

otospongiosis

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3
Q

epidemiology of otosclerosis (3 items)

A
  • hereditary in 70% of cases
  • –autosomal dominant/runs in families (50% of cases)
  • –variable penetrance: have the disease but not the clinical symptoms
  • more in females (2:1)
  • –worsen during pregnancy/ estrogen therapy
  • race dependent:
  • –4-8% of caucasian-1% with symptoms
  • –1% of black
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4
Q

when is the onset of otosclerosis?

A

11-30 years of age (70% of cases)

—develops in the third decade of life

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5
Q

how does the hearing loss with otosclerosis develop

A
  • slowly progressive
  • bilaterally, asymmetric conductive/mixed of even SNHL
  • –unilateral in 10% of cases
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6
Q

otosclerosis pathogenesis theories (8)

A
  • hereditary: autosomal dominant
  • congenital=osteospongiosis
  • –more immature bone: on and around the stapes footplate, otic capsule(cochlea/labyrinth)
  • –excessive resorption of bone
  • —-bone breakdown–new bone forms
  • —-new bone is soft and hypervascular–a sclerotic mass
  • developmental problems
  • –embryology cartilage rests in otic capsule–abnormal bone
  • trauma
  • vascular problems
  • –decrease blood supply–otosclerotic foci
  • –acidity or perivascular tissue–decalcification–abnormal
  • immunologic reactivity to collagen molecules: tests show high serum collagen level
  • viral/measles-vaccination=less number of otosclerosis
  • aging
  • –changes in otic capsule=otosclerosis
  • –vascular spaces are replaces by bone
  • —-dense mosaic-patterned
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7
Q

involvement sites for osteospongiosis

A
  • ant to oval window (90%)
  • –anterior crus=root
  • —-site of prevalence)
  • –footplate fixation
  • –annular ligament of stapes

*this leads to persistent CHL

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8
Q

osteospongiosis: how does it occur histologically?

A

focal fixation-diffuse active-quiescent-cochlear otosclerosis

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9
Q

other involvement sites for otospongeosis (6)

A
  • promontory
  • facial canal
  • stapedial tendon
  • incudostapedial joint
  • vestibule and cochlear labyrinth=malignant otosclerosis
  • round window niche=rare, profound loss
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10
Q

symptoms of otosclerosis

A
  • hearin loss
  • –bilateral, asymmetrical CHL depending on the degree of stapes fixation
  • –unilateral in 10% of cases
  • paracusis of willis (when limited to the stapes)
  • –better hearing ability in noisy environment
  • tinnitus (75%)
  • –inner ear degenerative effects of the disease
  • –varies in intensity and character
  • vestibular disturbances-vertigo is rare (25%)
  • –hydrops?
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11
Q

signs of otosclerosis

A
  • in the otoscopic exam: schwartez sign= red descoloration under drum due to active focus on promontory
  • tuning fork test: CHL
  • PTA
  • –unilateral or bilateral CHL
  • –low freq (250-2000HZ)
  • a slight SNHL at 2000Hz= carhart notch
  • –associated SNHL: cochlear involvement
  • WRS: excellent
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12
Q

carhart notch

A
  • a sign of otosclerosis
  • caused by stapedial fixation
  • otosclerosis reduces BC thresholds by:
  • –5dB at 500 HZ
  • –10 at 1000
  • –25 at 2000
  • –15 at 4000
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13
Q

otosclerosis signs in audiometry (3)

A

1) initial stiffening of the stapediovestibular joint
- –low-freq tilt
- –slight ABG
2) footplate becomes fixed
- –friction elements added
- –flat configuration
- –ABG widens
3) cochlear lesion
- –high freq SNHL
- –drop in WRS

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14
Q

signs of otosclerosis in acoustic reflexes

A
  • very sensitive
  • “on-off” phenomenon
  • precedes hearing loss
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15
Q

what types of imaging is used to see otosclerosis?

A
  • CT

* MRI

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16
Q

differential diagnosis for otosclerosis

A
  • congential footplate fixation
  • tympanosclerosis
  • incus/malleus fixation
  • ossicular discontinuity
  • systemic diseases:
  • –osteogensis imperfecta
  • –pagets disease
  • –progressive bone disease of skull and long bone
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17
Q

osteogenesis imperfecta

A
  • aka van der hoeve’s syndrome or brittle bone disease
  • –stapes fixation
  • –blue sclera
  • –fractures-called fragillitas osseus
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18
Q

paget’s disease

A

osteitis deformans (3% of adults over 40 years)

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19
Q

progressive bone disease of skull and lone bone (skeletal bone)

A
  • abnormal bone destruction and regrowth-deformity of the affected area
  • temporal bone involvement= CHL 50%
  • elevated alkaline phosphate
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20
Q

management of otosclerosis

A
  • amplification
  • –in early to moderate stage
  • –refuse surgery
  • –poor surgical candidate
  • medial therapy
  • stapes surgery
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21
Q

flouride as medical treatment for otosclerosis

A
  • flourical:
  • –sodium flouride, Ca carbonate, and vitamin D
  • –food supplement and over the counter
  • benefits
  • –stabilizing bone
  • –slow SNHL
  • –statistical benefit is not equal to the clinical benefit
  • side effects
  • –uncommon
  • –GI upset
  • –musculoskeletal pain
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22
Q

goal of surgery for otosclerosis

A
  • reconstruct sound conducting mechanism
  • excellent results in >90% of cases on 6-8 weeks
  • –10dB or less ABG
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23
Q

what can pts not do after surgery for otosclerosis?

A

valsalva

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24
Q

what would determine a successful otosclerosis surgery

A

10dB or less ABG

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25
Q

post op complications of stapedectomy

A
  • postop vertigo is common (rest to treat)
  • prothesis failure
  • –30-82% of failures=displaced prosthesis
  • –short prosthesis with fractures
  • –floating footplate
  • bleeding
  • –mucosal trauma
  • –active phase
  • –persistent stapedial artery
  • SNHL=0.2-10%
  • –surgical trauma of drilling vs laser
  • –serous labyrinthitis-high freqs
  • –hydrop
  • perilymph fistula
  • –drop or fluctuation in hearing
  • –tinnitus, vertigo
  • —-re-explorationa nd sealing of the problem is a surgical emergency
  • CSF gusher; causes:
  • –congenital footplate fixation
  • rare complications:
  • –facial paralysis
  • –acute otitis media
  • –cholesteatoma
  • rarely, a “dead ear” is the end result
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26
Q

pathogenesis of meniere’s disease

A

Temporal bone studies of membranous labyrinth show:

  • dilation
  • distortion
  • membrane ruptures

sites:

  • scala media
  • saccule
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27
Q

causes of meniere’s disease

A
  • poorly understood
  • endolymphatic hydrops
  • –increased pressure into the inner ear
  • —-increased production
  • —-increased resorption
  • autoimmune etiology
  • –response to immunotherapy=32% with anti68kDa antibody
  • anatomic problems
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28
Q

why do the low frequencies become affected by meniere’s disease first

A
  • the degree of endolymphatic space expansion is variable
  • –50% of cases: bulged in the region of helicotrema
  • saccule if bulged
  • –against the footplate (60%)
  • –into a horizontal SSC (1/3)
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29
Q

manifestations of meniere’s disease

A
  • vertigo
  • –episodic with normal intervals
  • –lasts 20 min-12 hours
  • –sudden episodes of fall (pts may think they had a stroke)
  • low freq SNHL
  • –fluctuating=10dB at 2 freq
  • –progressive
  • aural fullness
  • roaring tinnitus
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30
Q

what are the types of meniere’s disease (and tell about them)

A
  • definite MD
  • –2 or more episodes of vertigo (20min-12hours)
  • –low freq SNHL before, during, or after vertigo episodes
  • –fluctuating aural manifestations (hearing, fullness, tinnitus)
  • probable MD
  • –2 or more episodes of vertigo (20min-24hours)
  • –fluctuating aural manifestations
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31
Q

how is meniere’s disease diagnosed?

A
  • otoscopy=norma;
  • Hennebert’s sign in 30%
  • –this is pressure induced vertigo and nystagmus
  • puretone aud= cochlear HL
  • ART, SISI, and ABLB
  • ENG
  • ECochG= enlarged SP-large SP/AP ratio
  • ABR to rule out vestibular schwannoma
  • Vestibular Evoked Myogenic Potential (VEMP)= test the integrity of the saccule portion of the inner ear and may detect meniere’s disease even when a patient is non-symptomatic
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32
Q

two diseases that must be differentiated from Meniere’s disease

A
  • vestibular migraine (2%)
  • –episodic vertigo (sec-days) and migraine headache, intolerance of head motion/motion sickness
  • benign paroxysmal positional vertigo (BPPV)
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33
Q

what is another name for drop attacks

A

otolithic crises of tumarkin

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34
Q

causes of drop attacks and treatment

A
  • cardiac disorders (64%)= medication or pacemakers
  • seizures (7%)= anticonvulsant
  • poor blood flow to brain (TIA) (8%)= lower cholesterol, blood thinners, surgery on arteries to open them up
  • superior canal dehiscence (small%)= plug or patch superior canal
  • meniere’s disease (5%)= surgery or medication to destroy labyrinth
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35
Q

nonsurgical treatment for meniere’s

A
  • diet and vestibular suppression to reduce spells of vertigo
  • –diet and salt restriction
  • –valium during the episodes
  • –diuretics: thiazides, neptazane
  • –meniett device: small pressure pulses (3x daily/ 6 weeks)= displacement of excess endolymph=normal inner ear pressure
  • steroids for the immune component (intratympanic or systemic)
  • gentamicin perfusion (watch)= chemical vestibulectomy
  • –gel foam soaked over the round window
  • vestibular rehabilitation
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36
Q

surgical treatment for meniere’s

A
  • endolymphatic sac decompression- less HL
  • –endolymphatic subarachnoid shunt
  • –endolymphatic-mastoid shunt
  • vestibular nerve sectioning
  • –retrosegmoid procedure (95% effective in controlling vertigo; less risk of HL)
  • –translabyrinthine procedure= dead ear
  • labyrinthectomy= destructive surgery= surgical ablation of end organ= cure vertigo
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37
Q

what % of cases of hearing loss or dizziness does autoimmune disease of the inner ear comprise

A

<1% of all cases of hearing loss or dizziness

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38
Q

what are the two immune principle

A

innate (nonspecific) response

adaptive (specific) response

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39
Q

the innate response of the immune specific

A
  • first line of defense
  • prevent micro-organism from entering body
  • nonspecific
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40
Q

adaptive response of the immune system

A
  • specific
  • destroy invading organism
  • –phagocytic cells= locally
  • –humoral (B cell) and cellular (T) cell
  • —-mediated systems hormones
  • ——stimulate proliferation of
  • —-T lymphocytes= immunoglobin
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41
Q

4 immune functions of the inner ear

A
  • antigen-antibody reaction
  • lymphocytes and immunoglobuling (Ig) production
  • lymphatic drainage
  • barriers
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42
Q

what is the antigen antibody process

A

the antigen stimulates lymphocytes which proliferate and mature into plasma cells which produce antibodies against one antigen

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43
Q

inner ear exposure to antigen

A
  • primary exposure
  • –localized immune response
  • –beneath the basilar membrane of the basal coil of the cochlea
  • 2ry (repeated) exposure
  • –generalized immunologic response
  • –all over the cochlea
  • leads to degeneration of spiral ganglion cells, organ of corti, hemorrhage, etc
  • antibodies are found in serum and perilymph as a result of immune response
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44
Q

how do lymphocytes and immunoglobulin (lg) production work as immune function of inner ear

A
  • cochlea has no lymohocytes
  • –antigens from inner ear migrate to endolymphatic sac which stimulates lymphocytes to produce antibodies
  • systemic lymphocyte entry through spiral modiolar vein
  • immune response decreased when endlymphatic sac (ELS) destroyed
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45
Q

lymphatic drainage as an immune function of the inner ear

A
  • little lymphatic drainage leads to:
  • limited immunosurveillance
  • –perilymph has lgs (m,G,A,) at 1/1000th of serum concentration
  • inner ear is subject to immune surveillance if:
  • –systemic immunization led to inner ear immune response when antigen presented within inner ear
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46
Q

three types of barriers

A
  • blood-labyrinthine barrier
  • CSF-labyrinthine barrier
  • middle ear-labyrinthine barrier
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47
Q

how do the barriers work

A
  • protect the function of the inner ear from changes in the surrounding/extracellular fluids
  • maintain ionic concentration of cochlear fluid
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48
Q

what are autoimmune inner ear diseases (AIED)

A

1) cogan’s disease
2) wegener’s ganulomatosis
3) secondary/other autoimmune disease
* Vogt-Koyanagi-Harada (VKH) syndrome
* Behcet’s disease
* relapsing polychondritis
* systemic lupus erythematosus
* rheumatoid arthritis
* polyarteritis Nodosa

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49
Q

theories of/pathogenesis of autoimmune SNHL

A
  • vasculitis of inner ear
  • autoantibodies (antigenic epitopes=antigenic determinant)
  • –part of the antigen is recognized by the immune system (antibodies, B cells, or T-cells)
  • cross-reacting antibodies
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50
Q

cogan’s disease definition

A
  • rare
  • systemic autoimmune disease of the cornea and inner ear
  • –inflam reaction of temporal bone and membranous labyrinth=bilateral degeneration
  • —-cochlea and vestibular labyrinth
  • —-hydrops
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51
Q

etiology of cogan’s disease

A
  • etiology is unknown
  • –viral or microbial etiology
  • –autoimmune disease
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52
Q

cogan’s disease signs and symptoms

A
  • ocular and otologic (audiovestibular) symptoms
  • otologic: similar to meniere’s
  • –vertigo and HL
  • ocular
  • –nonsyphilitic interstitial keratitis (IK)
  • —-blood vessels grow into the cornea
  • —-loss of the normal clearness of the cornea
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53
Q

history and clinical manifestations of cogan’s disease

A
  • middle aged women with onset 22-29 years
  • –65% female, 35% male
  • progressive SNHL, weeks to months
  • dizziness, aural fullness
  • one ear first then the other
  • –bilateral 79%
  • no acute vestibular symptoms-slow loss of vestibular function
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54
Q

how many with cogan’s disease are originally diagnosed with meniere’s?

A

1/4 to 1/2

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55
Q

clinical manifestations of cogan’s disease (typical vs atypical type)

A
  • typical type:
  • –audio-vestibular symptoms occur before or after IK
  • —-sudden IK, photophobia, ocular pain, eye redness
  • —-fluctuating and progressive SNHL, tinnitus, vertigo, and loss of vestibular function
  • atypical type
  • –audio-vestibular symptoms occur with ocular disease other than IK
  • —-eg uveitis, iritis, scleritis, and conjuctivitis
  • systemic autoimmune symptoms (29%)
  • –vasculitis, arthritis rashes, auricular pain
  • –GI hemorrhage, etc
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56
Q

cogan’s diagnosis

A

*clinically
*laboratory
—lymphocyte transformation test
(LTT)
—–93% specific
—–50-80% sensitive
—anti-68kDa protein
—–95% specific
—–insensitive
—–predictor of steroid response
—ESR
—CRP (along with ESR is acute phase)
—C1q binding assay
—anti-cardiolipin
—ANCA=anti-neutrophil cytoplasmic antibody
—syphilis testing
—lyme titers (endemic areas)
—CBC
—chemistries
—thyroid functions
—imaging

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57
Q

treatment of Cogan’s syndrome

A
  • steroid
  • –steroid eye drops
  • –high-dose for hearing loss
  • —-little effect if no measurable hearing before Rx
  • untreated cases=profound bilateral SNHL over several months
  • –cochlear implantation
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58
Q

what is wegener’s granulomatosis?

A
  • necrotizing granulomata and vasculitis
  • –respiratory tract
  • –kidney’s-glomerulonephritis
  • –blood vessels: vasculitis and ischemia
  • —-inner ear= SNHL
  • –serous OM (25%)
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59
Q

diagnosis of wegener’s granulamatosis

A
  • antineutrophil cytoplasmic antibody (cANCA)
  • –90% specific
  • tissue biopsy
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60
Q

general definition of secondary/other autoimmune disease HL

A
  • HL secondary to systemic autoimmune disease

- –lupus rheumatoid arthritis

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61
Q

Diagnosis for secondary/other autoimmune disease

A
  • frequently inferred

* MRI: cochlear inflammation may be seen

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62
Q

treatment of secondary.other autoimmune disease

A

directed at primary disorder

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63
Q

again list the secondary/other autoimmune diseases (76

A
  • vogt-koyanagi-harada (VKH) syndrome
  • behcet’s disease
  • relapsing polychindritis
  • systemic lupus erythematosus
  • rheumatoid arthritis
  • polyarteritis nodosa
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64
Q

vogt-koyanago-harada (VKH) syndrome

A
  • imflammatory disease: biateral panuveitis with involvement of the CNS, ear and skin
  • autoimmunity to melanocytes
  • –depigmentation=poliosis
  • –periorbital hair loss
  • –aseptic meningitis
  • –SNHL, vesitbular signs, uveitis
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65
Q

bechet’s disease

A

*autoimmune disease
*affects: mucocutaneous, ocular, cardiovascular, renal, pulmonary, GSI, vascular, urology, musculoskeletal and CNS systems
*recurrent oral and genital ulcers
(aphthous ulers=cancer sore)

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66
Q

relapsing polychondritis

A
  • recurrent inflam of
  • –ear, nose, trachea, larynx
  • –peripheral joints
  • autoantibodies to cartilage type II and IX
  • —-II: otic capsule and tectorial membrane
  • diagnosis:
  • –elevated ESR and Igs
  • –positive LTT
  • treatment
  • –NSAIDs and steroids
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67
Q

systemic lupus erythematosus

A
  • anti-nuclear, anti-DNA antibodies
  • numerous systemic manifestations
  • –polyarthralgia, arthritis
  • –pleuritis, pericarditis, myocarditis
  • –pneumonitis, nephritis
  • –CN palsies, meningitis, neuritis
  • –scleritis, renal degeneration from vasculitis
  • COM with vasculitis
  • progressive SNHL, dysequilibrium
  • rash=rare
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68
Q

rheumatoid arthritis

A
  • small joints of hands and feet
  • vasculitis, muscle atrophy, subcutaneous, nodules, splenomegaly
  • rheumatoid factors (75%)
  • –lgM 19S and 7S, lgG 7S
  • –reaction to abnormal lgG produced within the synovia
  • CHL–ossicular joint fixation
  • SNHL
  • –cochlear inflammation
  • –side effect of medications
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69
Q

polyarteritis nodosa

A
  • vasculitis of small and medium-sized arteries
  • renal and visceral
  • ischemia=osteoneogenesis fibrosis
  • –temporal bone studies
  • hearing loss=rare
  • –vasculitis
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70
Q

autoimmune disease treatment

A
  • immunosuppressive agents
  • –stabilize the progressive hearing loss
  • –steroids
  • —-systemic
  • —-transtympanic: less commonly used
  • ——-less toxic
  • ——-efficacy unproven
  • –methotrexate: helpful= reduce steroid dose
  • –cyclophosphamide (CTX) + prednisone:
  • —-discontinue CTX after 3 months
  • —-continue with prednisone for another 2 wks, then gradual withdrawal
  • avoid early withdrawal:
  • –2ry immune response is ore robust than the 1ry immune response
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71
Q

long-term steroid treatment: contraindication

A
  • preganacy
  • peptic ulcer
  • hypertension, DM
  • glaucoma
  • TB
  • recent vaccination
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72
Q

long-term steroid treatment: side-effects

A
  • GI reactions
  • edema
  • osteoporosis
  • CNS disorders
  • –euphoria
  • –mood swings
  • –insomnia
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73
Q

steriod treatment alternative

A
  • plasmapheresis
  • circulating antigens, immune complexes, and inflammatory mediators are removed from plasma
  • –improvement in 50-75% of cases
  • indications
  • –when SNHL shows initial response with subsequent failure
  • –when steroids are contraindicated
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74
Q

sudden sensorineural hearing loss (SSNHL)

definition and time course

A
  • 30 dB or greater SNHL
  • over at lease 3 adjacent frequencies
  • occurring within 3 days or less
  • devastating to pts
  • frustrating for physicians
  • definitive diagnosis and treatment unknown
  • –90% of cases are idiopathic
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75
Q

SSNHL statistics

A
  • 4000 cases/year in the US
  • –b/t one and 6 people per 5000 every year
  • 15000 reported cases/year worldwide
  • highest incidence in 50-60 years old
  • lowest incidence in 20-30 year olds
  • men= women
  • 2% bilateral
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76
Q

Causes of SSNHL

A
  • symptoms of URT infections (infections)
  • H/O ototoxic drug use (medicatons)
  • H/O head trauma, straining, sneezing, nose blowing, intense noise exposure
  • H/O flying or scuba diving (trauma)
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77
Q

associated symptoms of SSNHL

A
  • vertigo/dizziness
  • aural fullness
  • tinnitus
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78
Q

additional things to look for in history w/ SSNHL

A
  • past medical history:
  • –autoimmune disorders
  • –vascular disease
  • –malignancies
  • –neurologic conditions
  • –hypercoagulable states
  • —-sickle cell disease (African Americans)
  • past surgical history:
  • –stapedectomy or
  • –other otologic surgeries
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79
Q

physcial exam for SSNHL

A
  • complete head and neck exam in everyone
  • neurologic exam of sensory and motor systems
  • –tandem gait (cerebellar vermis)= toes of the back foot touch the heel of the front feet with each step
  • –Rombers=a test of proprioception= stand feet together with eyes open the closed
  • –nose to finger or heel to shin
  • vestibular= Dix-Halpike test
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80
Q

diagnostic testing for SSNHL

A
  • audiologic eval:
  • –pure tone audiometry
  • –speech discrimination
  • –tympanometry
  • –stapedial reflex
  • lab testing
  • –CBC, ESR, VDRL
  • –lymphocyte transformation test (LTT)
  • –western blot for antibodies to 68 KD protein
  • MRI
  • –CPA tumors
  • —-13% of pts with acoustic tumors present with SSNHL
  • —-13% may recover hearing
  • –multiple sclerosis
  • –ischemic changes
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81
Q

treatable causes of SSNHL

A
  • infections
  • autoimmune
  • vascular
  • traumatic
  • neoplastic
  • idiopathic SSNHL (I-SSNHL)
  • –viral infections
  • –autoimmune
  • –vascular compromise
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82
Q

SSNHL from Viral labyrinthitis (what causes it and why does it occur)

A
  • causes: URI viruses, measles, mumps, chicken pox, and herpes zoster
  • pathology can vary
  • –damage to cochlea and vestibular labyrinth
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83
Q

symptoms of SSNHL from viral labyrinthitis

A
  • symptoms may vary
  • –SNHL, tinnitus, and vertigo
  • –if only vertigo without hearing loss
  • —-the diagnosis is likely vestibular neuronitis
  • —labyrinthine concussion
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84
Q

SSNHL from trauma

A

1) acoustic: NIHL
2) barotrauma: visceral rupture
3) perilymphatic fistula
4) rupture of membranous labyrinth

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85
Q

definition of traumatic SSNHL from perilymphatic fistula

A
  • leakage of perilymph from inner ear, round, or oval window to the middle ear
  • rare without: prior surgery or congenital dysplasia
86
Q

causes of perilymph fistula (PLF)

A
  • barotrauma
  • blast
  • acoustic trauma
  • post-traumatic
  • spontaneous
  • increased intracranial pressure due to exertion
87
Q

manifestations of perilymphatic fistula

A
  • H/O exposure to initiating factor:
  • –blow to the head
  • –sneezing; bending over; lifting a heavy object
  • –sudden changes in barometric pressure
  • —-flying, scuba diving
  • sudden fluctuating hearing loss
  • –SNHL, CHL, or mixed HL
  • sudden vertigo: vary–rotatory/unsteadiness
  • –severe, episodic, usually brief
  • –aggravated by valsalva
  • tinnitus
  • fistula sign (vertigo and nystagmus)
  • –using a pneumatic otoscope to vary external canal pressure
  • side of involvement:
  • –eyes closed turning test: pt tends to fall when turning toward the involved ear
  • –positive positional tests: when the involved ear is undermost
  • CT scan
88
Q

how to differentiate perilymphatic fistula from BPPV

A
  • with a fistula there is either no latent period, or it is short
  • with BPPV the nystagmus is less violent
  • with a fistula, the duration is longer so there is fatigue, slowly
  • nystagmus rarely reverses direction when sitting up (with fistula?)
89
Q

treatment for perilymphatic fistula

A
  • absolute bed rest
  • –head elevated
  • –affected ear upwards 30 degrees
  • avoid maneuvers that increase intracranial pressure
  • –lifting > 10lbs; nose blowing; straining
  • serial/daily audiometry to detect fluctuating HL
  • after 5 days:
  • –improvement: can have 6 wks light activity
  • –no improvement:
  • —-surgical exploration and
  • —-patching the fistula to seal the leak
  • —-successful surgery= relief of vertigo and hearing loss
90
Q

SSNHL from rupture of the membranous labyrinth (define)

A
  • breaks in the membranous labyrinth
  • –intracochlear=meniere’s
  • –oval/round window=perilymphatic fistula
  • H/O of inciting event
91
Q

who is at a high risk for rupture of the membranous labyrinth

A
  • post stapedectomy
  • inner ear anomalies
  • –mondini malformation=sac-like cochlea
  • –michel deformity=complete labyrinthine and cochlear aplasia
  • –large vestubular aqueduct
92
Q

diagnosis for traumatic SSNHL

A
  • usually clinical:
  • –H/O inciting event
  • –audio shows sudden or rapid progressive SNHL
  • –Hennebert’s sign= ELH/sup canal dehiscence
  • —-fistula sign=pressure induced vertigo
  • –Tullio’s phenomenon
  • —-sound induced vertigo
  • MRI, ESR, syphilis test
  • –inflammatory process, neoplasia
  • definitive=intraoperative
93
Q

SSNHL from acoustic tumors

A
  • 6% of all 1ry intracranial tumors
  • 0.8-1.2 cases/100,000 population
  • SNHL:
  • –10-19% may present with SSNHL
  • –1% of pts with asymmetric SNHL have acoustic tumors
  • –gradually progressive SNHL
94
Q

labyrinthine diseases to cause SNHL (7)

A
  • presbycusis
  • infections
  • ototoxic
  • trauma
  • vascular disease
  • meniere’s
  • autoimmune
95
Q

acoustic nerve probs to cause SNHL (4)

A
  • trauma
  • meningitis
  • tumors
  • disseminated sclerosis
96
Q

AIED clinical manifestations

A
  • middle aged females
  • bilat, asymmetric SNHL
  • –sudden, rapidly progressive, or protracted
  • absence of systemic immune disease
  • 50% with dizziness
  • light-headedness and ataxia more common than vertigo
  • episodes=multiple, daily
97
Q

Summary of SSNHL

A
  • many medical causes for HL
  • few are amenable to direct intervention:
  • –medical or surgical
  • treatment is usually aimed at limiting progression
98
Q

vascular diseases to cause SSNHL

A
  • vascular loop
  • vertebrobasilar ischemia
  • hemolabyrinth: hemorrhage into the inner ear
  • atherosclerosis
  • diabetes mellitus
99
Q

treatment for SSNHL caused by vascular disease

A
  • prevent occlusion
  • keep cholesterol and blood sugar level under tight control
  • surgical decompression in cases with vascular loop
100
Q

vascular loop definition

A

a loop of anterior inferior cerebellar artery compresses VIII and VII nerves
—occlusion is due to hypertension or arteriosclerosis

101
Q

symptoms of vascular loop (vague?) and diagnosis

A
  • atypical vertigo that is episodic, followed by:
  • SNHL: sudden
  • VII nerve symptoms are less common
  • cerebellar asynergy

*diagnosis: MRI

102
Q

vascular loop treatment

A

is controversial

  • antiarrhythmics:
  • –carbamazepine: phenytoin
  • antidepressant:
  • –denzodiazepines: klonopin
  • antihypertensives
  • surgical decompression
103
Q 
vertebrobasilar ischemia (VBI)
definition
A

decreased blood flow of the vertebral and basilar arteries

104
Q

vertebrobasilar ischemia (VBI) causes

A
  • artherosclerosis
  • mechanical compression: cervical spondylosis= drop attack
  • –posterior inferior/ anterior inferior cerebellar artery
105
Q

vertebrobasilar ischemia (VBI) symptoms

A
  • vertigo is the most common
  • followed within few days by visual and brainstem signs
  • –may be cochlear or vestibular depending on the vessels involved
106
Q

vertebrobasilar ischemia (VBI) management

A
  • full audiological/vestibular eval
  • reassure pts
  • vertigo: labyrinthine sedatives (prochlorperazine)
  • hearing loss: HA
  • tinnitus: distraction technique
107
Q

ISSNHL treatment

A
  • steroids
  • antiviral agents: in no improvement with steroids
  • diuretics
  • blood viscosity reducers to facilitate blood flow
  • antithrombotic
  • vasodilators
  • outcomesL
  • –full recovery in 1/3 of pts
  • –partial recovery: 1/3
  • –no recovery: 1/3
  • –the more HL, the less likely of having improvement
108
Q

the three different types of temporal bone radiology

A
  • conventional: X-ray
  • CT: 3D CT
  • MRI: 3D MRI
109
Q

X-Ray basics

A
  • “plain films”= rarely used
  • to confirm the position of CI
  • oblique or transorbital A-P
110
Q

advantages of X-Ray

A
  • much less expensive than CT or MRI in terms of equipment and interpretation
  • less subject to artifact or smoothing by reconstruction algorithms
111
Q

disadvantages of X-ray

A
  • limited post-processing/reprocessing of image
  • unable to perform computer reconstructions in different planes
  • ionizing radiation
  • less clarity of info
  • ionizing radiation can cause biologic damage
112
Q

CT basics

A
  • computed tomography
  • basic technique for the temporal bone
  • the word “tomography” is from the Greek word tomos which means slice
  • soft tissue windows
  • bone windows
113
Q

orientation of vestibular receptors from the lateral view

A

the horizontal semicircular canal and utricle lie in a plane that is tilted anterodorsally relative to the naso-occipital plane

114
Q

orientation of vestibular receptors from the axial view

A

anterior and posterior semicircular canals and saccule are arranged vertically in the head at 90 degree angles to the horizontal canal
*the anterior and posterior canals also lie at 90 degree angles to each other

*the anterior canal on one side is co=planar with the posterior canal on the other

115
Q

what is the scutum?

A

a spur-shaped bony projection on top of the TM

*often eroded by cholesteatoma

116
Q

what makes up the snake eyes?

A

the distal labyrinthine and proximal tympanic segments of the facial nerve
*located anterior to the snail (cochlea)

117
Q

what is the anterior genu?

A

the first turn of the facial nerve

*labyrinthine segment in fallopian canal turns into tympanic segment

118
Q

what makes up the signet ring in the axial view?

A

the vestibule and the lateral semicircular canal

119
Q

what makes up the ice cream cone in the axial view?

A

the mallear head and the incus body

120
Q

what makes up the duck shape in the axial view?

A
  • the lateral semicircular canal
  • vestibule
  • basal turn of the cochlea
121
Q

what is the incidence of facial palsy with a longitudinal fracture of the temporal bone?

A

20%

122
Q

what is the incidence of facial palsy with a tranverse fracture of the temporal bone>

A

50%

123
Q

where is a transverse fracture of the temporal bone located

A

lateral to the cochlea and runs into the vestibule and out to the back of the skull

124
Q

advantages of CT

A
  • faster than MRI
  • good for bony structures
  • 3D CT scan
125
Q

disadvantages of CT

A
  • uses ionizing radiation
  • much more expensive than x-rays
  • –exam
  • –interpretation
126
Q

MRI why?

A
  • CT can’t display the membranous labyrinth and the nerve pathways leaving it
  • based on the principle of NMR (nuclear magnetic resonance)
  • uses strong magnetic field pulsed radio waves and antennae
  • info reconstructed into digital image
127
Q

effects of radiation exposure

A
  • stochastic (probabilistic) effects
  • –increase in probability (risk) of effect
  • –non threshold dose
  • non-stochastic (deterministic) effects
  • –dose determines magnitude of effect
  • —–skin erythema
  • —–cataracts
  • –threshold dose
  • somatic effects= person who is irradiated
  • genetic effects= offspring and future generations affected
128
Q

four parts of the temporal bone

A
  • squamous (largest)
  • tympanic (smallest)
  • mastoid
  • petrous (hardest)
129
Q

the mastoid portion of the temporal bone

A
  • superiorly is the tegmen tympani which is the bone underlying the middle cranial fossa
  • posteriorly is the indentation of the sigmoid sinus
  • anteriorly is the posterior wall of the EAC and the VII nerve
  • medially is the labyrinth, SCCs, sigmoid sulcus and the bone overlying the posterior fossa dura
  • inferiorly is the digastric ridge which is a landmark for the VII canal
130
Q

the petrous portion of the temporal bone

A
  • the medial petrous portion relates to:
  • –internal carotid artery
  • –the sigmoid sinus
  • –the VII nerve
  • –the labyrinth and IAC
131
Q

what are the three layers of the development of the temporal bone

A
  • there are three layers
  • –squamous: from the membranous bone
  • –tympanic: from membranous bone
  • —–the primitive mastoid air space
  • ———-mucosal epithelium from the 1st branchial pouch
  • –petrous: originates from cartilage
  • appear by the 4th month (all but the petrous part)
132
Q

what is the importance of histopathology

A
  • to distinguish normal anatomic variants from structural and functional alterations caused by disease processes
  • to understand the effect of different diseases on the structures of the ear
  • to enhance our understanding of etiopathologies of some disorders
133
Q

the process of harvesting and preparation of histopathology

A

1) consent
2) coordination with the family, PCP, ENT,and funeral people
3) harvesting the bone within 24 hours of death
4) sectioning of temporal bone
5) immersing into fixative neutral buffered formalin
6) decalcification in a specific solution (6-9)
7) neutralization for the acid process
8) dehydration in increasingly concentrated alcohol (2 weeks)
9) hardening: embedded in celloiden and undergoes hardening (1 month)
10) slicing of temporal bone (horizontal or vertical sections)
- –a slice is 20 um thick
- –average human temporal bone specimen makes 500 slices
* labeling of the slides
* photomicrograph
* **the preparation of temporal bone for standard microscope takes 1 yr after harvesting

134
Q

how are axial sections of the temporal bone made?

A
  • superior to inferior

* starting at the top and going down to understand relationships between various structures

135
Q

diseases that can be seen in histopathology

A
  • exostoses
  • TM perf
  • chronic OM
  • otosclerosis
  • vestibular schwannoma
  • temporal bone metastases
  • petrous apex lesions
  • fallopian canal lesions
  • internal carotid artery disorders
  • labyrinthitis ossificans
136
Q

exotoses

A

bony protuberances of the EAC

137
Q

temporal bone metastases

A
  • histopathology: 1ry or 2ry (R metastatic breast carcinoma occupies the IAC and the petrous apex)
  • clinically-similar to AN:
  • –sudden-onset
  • –VII paralysis
  • –SNHL
  • –vertigo
138
Q

labyrinthistis ossificans

A
  • osteoneogensis that obliterated the fluid spaces of the labyrinth manily S. tympani
  • 2ry to trauma, meningitis, vascular insult
  • –advanced otosclerosis
  • –AIED
  • complications-CI surgery
139
Q

effects of aging on the outer ear

A
  • loss of tissue elasticity of the pinna
  • loss of tissue elasticity of the ear canal
  • stiffening of the eardrum
140
Q

effects of aging on the middle ear

A
  • degeneration of the middle ear musculature
  • calcification of middle ear ligaments
  • ossification of middle ear bones
141
Q

effects of aging on the inner ear

A

*research has classified six different types of presbycusis involving the inner ear and its related structures

142
Q

presbycusis

A
  • hearing loss related to aging
  • the most common type of SNHL industrialized countries
  • begin as early as age 30
  • 25-40% of americans age 65 or older experience hearing loss
  • more than 90% of individuals age 90 or older experience hearing loss
143
Q

gender and presbycusis

A
  • men are more likely to be affected
  • –more severe loss at earlier onset
  • women=better high frequency hearing
  • men=better low freq hearing
144
Q

signs of presbycusis

A
  • silent onset
  • symmetric SNHL
  • progressive loss
  • no other ear diseases
  • normal ear examination
145
Q

effects of HL

A
  • can affect people in many different ways
  • psychological effects:
  • –depression
  • –inattentiveness
  • –increased tension/negativity
  • health effects:
  • –poor general health
  • –reduced mobility
  • –reduced interpersonal communication
146
Q

causes of presbycusis

A
  • no definitive etiology but many potential contributing factors
  • hereditary may also contribute to the development of SNHL in up to 50% of individuals
147
Q

contributory factors of presbycusis

A
  • noise exposure
  • vascular disease
  • systemic disease
  • ototoxic meds
  • head injuries
  • tumors
  • inflammatory processes
  • environmental toxins
148
Q

sensory presbycusis

A
  • description: degeneration of HCs and supporting cells at the base of the cochlea
  • audiometruc findings
  • –slow, progressive, steeply sloping high freq hearing loss
  • –good WRS
149
Q

neural presbycusis

A
  • description: loss of cochlear neurons
  • –loss of effective transmission of the neural signal (information coding)
  • most common form of degeneration seen in the aging cochlea
  • audiometric findings:
  • –high freq HL
  • –disproportionate WRS
150
Q

other degenerative central nervous systems changes those with neural presbycusis exhibit

A
  • lack of coordination
  • weakness in arms and legs
  • tremors
  • irritability
  • intellectual deterioration
  • memory loss
151
Q

strial (metabolic) presbycusis

A
  • degeneration of the stria vascularis
  • loss of nutrient supply for cellular function
  • changes in cochlear potentials (less effective neural impulses)
  • audiometric findings:
  • –flat HL
  • –typically good WRS
152
Q

cochlear conductive (mechanical) presbycusis

A
  • changes in the basilar membrane mass/stiffness
  • degeneration of spiral ligament
  • changes to cochlear mechanics
  • audiometric findings:
  • –sloping loss of both low and high freqs
153
Q

mixed presbycusis

A
  • an individual may demonstrate one or more types of presbycusis simultaneously
  • the resulting HL is then a combo of the degenerative effects described within the inner ear
154
Q

indeterminate presbycusis

A
  • about 25% of individuals with presbycusis may exhibit audio findings similar to sensory or strial presbycusis
  • but not evident site(s) of injury related to these forms of presbycusis
  • audio findings:
  • –flat or sloping high freq HL
  • –reasonable good WRS
155
Q

other degenerative changes with age

A
  • vascular and/or osseous changes:
  • –thickening of internal auditory artery=reduced blood supply to cochlea and sensory cells
  • –abnormal growth of bony tissue within internal auditory canal= compression of 8th cranial nerve and internal auditory artery
  • —-may cause dysfunction/degeneration of nerve fibers and inner ear tissue
156
Q

central auditory pathways and presbycusis

A
  • HL in the presence of a normal inner ear may be related to a central auditory system dysfunction
  • degenerative changes within the auditory pathway include:
  • –loss of functional neurons in the brainstem and auditory cortex
  • –leads to ineffective transmission of neural impulses from the inner ear to the brain
157
Q

tympanometry findings with presbycusis

A
  • aging shows no significant differences with middle ear transmission
  • –findings may suggest: compliance may decrease with age, and negative pressure increases with age
  • limited research done with tymps in the elderly population
158
Q

acoustic reflex thresholds findings with presbycusis

A
  • age does not necessarily cause significant changes in ARTs
  • –it is the peripheral hearing that causes elevated or absent ARTs
  • amplitude of reflex: suggested decrease of amplitude with aging
159
Q

pure tone audiometry findings with aging

A
  • SNHL worsen with age
  • –higher freq (>1000Hz) affected earlier
  • —-by the age of 40
  • –low freq affected later
  • —-around the age of 60
  • bilateral, symmetrical SNHL
160
Q

speech audiometry and aging

A
  • SRT worsens with age
  • –in accordance with pure-tone hearing loss
  • speech discrimination assessed in quiet:
  • –dependent upon type and significance of presbycusic loss
  • speech understanding in noise or with degraded signal:
  • –difficulty increases with function of age
161
Q

central deficits and their effect on speech discrimination with age

A
  • central (brain processing) deficits must contribute to speech understanding difficulty in the aging
  • peripheral hearing loss+ cognitive decline+ central processing decline= poor speech understanding in noise or with a degraded/rapid speech signal
162
Q

auditory processing measures in elderly

A
  • increased (20-70%) prevalence in elderly
  • –confounded with peripheral hearing loss
  • behavioral measures to assess:
  • –monotic speech and tone tests
  • —-how well does the pt process signals in only one ear at a time
  • –dichotic tests
  • —-how well does the pt take in information from both ears at the same time and process it correctly in the brain
  • –binaural tests
  • —-how well does the pt use both ears together to listen and localize sounds
163
Q

OAEs with aging

A
  • all classes of OAEs reported to be changed with aging
  • –incidence decreases
  • –amplitude decreases
  • attributed to inner hair cell loss associated with age
164
Q

auditory evoked potentials and aging

A
  • latency:
  • –all evoked potentials show increased latency with age (it takes longer for the brain to give a response)
  • amplitude:
  • –ABR
  • —-amplitude decreases with age
  • —-peripheral hearing loss to be considered when analyzing waveforms
  • –AMLR:
  • —-amplitudes significant increase with age
  • –ALR and P300:
  • —-amplitude decrease with age (peripheral HA doesn’t affect these potentials
165
Q

two things to consider when working with the elderly populations

A
  • typical audiological characteristics may not truly represent handicap or impairment
  • –benefit might not be represented appropriately through behavioral and objective measures
  • using functional tools, being aware of medical contraindications and understanding social behavior of the elderly population are key to rehabilitative success
166
Q

the physical and mental health of the aging

A

not all individuals of the same age experience aging the same way

  • the senior adult is required to adjust to a certain amount of physical disability and reduced activity level
  • this can affect the individual’s attitude toward self-fulfillment
167
Q

why do older people with HL seem senile?

A
  • inattentive
  • inappropriate responses
  • could actually be attributed to HL
  • HL has shown to have adverse effects on quality of life and on emotional, behavioral, and social well-being
168
Q

pre-fit counseling for elderly

A
  • many may have difficulty with accepting diagnosis of HL
  • it’s important to address the psychosocial aspect of HL
  • allow pt to tell their story
  • –many elderly just want to talk
  • –you want pt to trust you
  • clarify their problems
  • allow them to accept the problem
169
Q

pre-fit hearing rehab assessment

A
  • these cases require longer appointments and it is important to give these patients the time they need
  • obtain info about the pt’s lifestyle, goals, and expectations
  • –expectations need to be realistic
  • visual aids are used to aid in having the pt understand their HL
  • cost is discussed
170
Q

counseling aids

A

tools before and after a hearing aid fitting to confirm benefit

  • HHIE: hearing handicap inventory for the elderly
  • COSI: client orientated scale of improvement
  • ABHAP: abbreviated profile of hearing aid benefit
171
Q

post-fit aural rehab

A
  • provides care and instruction by assisting pts in “learning how to hear”
  • hearing aid orientation (HAO): it is vital to the success of the hearing aid wearer that the individual be completely oriented with their hearing instrument
  • questionnaires readdressed to quantify benefit
172
Q

aural rehab

A
  • give a support system during a period of adjustment
  • classes and support groups: HA activities and practicing good communication strategies
  • knowledge about HL
  • educate family members
  • accept responsibility
  • negative effects of HL on communication
  • realistic expectations and limitations of amplification
  • pt satisfaction
173
Q

the course the VII nerve runs

A
  • intracranial part (12mm)
  • meatal part (IAC) (10mm)
  • intratemporal
  • –labyrinthine (3-4mm)
  • –tympanic part (11mm)
  • –mastoid part (13mm)
  • extratemporal/extracranial (15-20mm)
  • –frontal/temporal
  • –zygomatic
  • –buccal
  • –mandibular
  • –cervical
174
Q

components/fibers of the VII nerve

A
  • motor
  • parasympathetic
  • sensory, taste fibers
175
Q

the facial nerve structural anatomy

A
  • the basic unit of the VII nerve is the Axon

* the axonal processes are surrounded by a myelin sheath

176
Q

epineurium

A

(nerve sheath)

  • outermost collagenous layer
  • is continuous with the dura matter
  • houses vas nervosa for nutrition
177
Q

perineurium

A

dense connective tissue, surrounds the endoneurium and groups the nerve fibers
—barrier to infection

178
Q

endoneurium

A

surrounds each axon

  • adherent to Schwann cell layer
  • vital for regeneration
179
Q

nodes of ranvier

A

small constrictions at the myelin sheath

*rapid propagation of AP along the VII nerve

180
Q

histological classifications of facial nerve lesions

what is is and the basic names of the classifications

A
  • based on the histologic changes and physiologic implications of the injurt
  • –determining the severity of a peripheral injury
  • –predicting the potential for spontaneous recovery of function

classifications:
1st degree: neuropraxia
2nd: axonotmesis
3rd: neurotmesis (wallerien degeneration)
4th: partial disruptic
5: complete disruption (no spontaneous recovery)

181
Q

specifics on the 3rd degree lesion of the facial nerve

A

neurotmesis

*injury to nerve trunk= wallerien degeneration, incomplete recovery, no organized regrowth= synkinesis

182
Q

how is the severity of facial paresis stated clinically?

A

the House-Brackmann classification

  • –to follow the course of a facial disorder
  • –6 categories
183
Q

what are the 6 categories of the house-brackman system

A 
1=none
---normal function in all areas
2=mild
---slight weakness of close inspection , synkinesis
3=moderate
---obvious but not disfiguring asymmetry
4=moderately severe
---obvious, disfiguring asymmetry; normal appearance rest
5=severe
---barely perceivable motion; asymmetry at rest
6=total
--- no perceptible motion
184
Q

what would a lesion at or proximal to the chorda tympani affect?

A
  • taste of the anterior 2/3 of the tongue–metallic taste
  • secretory= submaxillary and sublingual glands
  • sensation on posterior wall of EAC
185
Q

Schirmer test

A
  • site of lesion= greater superficial petrosal nerve
  • test lacrimal gland function
  • schirmer or filter paper strips are inserted between the lower lid and the conjunctiva of each eye
  • a difference of 25% or less is abnormal
186
Q

what are the electrodiagnostic/monitoring tests for facial nerve lesions

A
  • electroneuronography (ENoG)
  • –with trauma you need to wait 72 hours after injury
  • electromyography (EMG)
  • –determine nerve regeneration
  • Trigeminal-Facial reflex testing (eye-blink)
  • antidromic testing
  • intracranial stimulation
  • Radiography: CT/MRI
187
Q

what is the anterior genu of the facial nerve

A

the 1st turn of the facial nerve

*labyrinthine segment in fallopian canal turns to tympanic segment

188
Q

four groups of facial nerve lesions

A
  • inflammatory disorders
  • congenital syndromes
  • traumatic and Iatrogenic lesions
  • tumors
189
Q

four inflammatory disorders causing facial nerve lesions

A
  • Bell’s Palsy
  • Ramsey Hunt syndrome
  • otitis media
  • lyme disease
190
Q

Bell’s Palsy (number of cases and cause)

A
  • idiopathic facial paralysis
  • 20 cases per 100,000 annually
  • Herpes Simplex Virus
191
Q

Ramsay Hunt Syndrome

A
  • herpes zoster oticus
  • 5 cases per 100,000 annually
  • herpes zoster virus
192
Q

how do viruses cause damage to nerves?

A
  • the virus passes down the axons=radiculitis (pain due to irritation of nerve root)
  • then passes upward to brainstem=meningoencephalitis
  • –seen on gadolinium-enhanced MRI
  • if the virus infects schwann cells they become inflamed and this causes demyelinization of VII nerve cells
193
Q

what two things are used to diagnose facial paralysis?

A
  • medical history

* physical exam

194
Q

bells’ palsy vs Ramsay Hunt on severity, onset, prognosis, and age

A

bells palsy

  • severity: less severe
  • –paresis and complete recovery
  • onset: acute (10 days)
  • prognosis: recovery within 10-14 days
  • age
  • –females aged 10-19 years
  • –males after age 40

Ramsay hunt

  • severity: herpes zoster is more severe
  • –complete paralysis and denervation
  • –incomplete recovery and synkinesis
  • onset: may take 2-3 weeks
  • prognosis: spontaneous recovery within 3 wks after onset
  • age: incidence increases after age 50; herpes zoster remains dormant on nerve ganglia for decades
195
Q

differential diagnosis of bells palsy vs ramsay hunt

A

bells palsy

  • acute onset
  • peripheral in origin
  • no systemic disease
  • additionally:
  • –family history in 10% of cases
  • –pregnant women and diabetic are at higher risk
  • –recurrence: 10% rate
  • —-if you have 3 recurrences, you have a 50% chance of having a 4th

Ramsay hunt

  • gradually increased severity of symptoms
  • auricular vesicles
  • rising titer of antibody to varicella-zoster virus
196
Q

treatment for both bells palsy and Ramsay hunt

A
  • corticosteroid agents
  • –best Rx for inflammatory, virally induced, immune-mediated disease
  • acyclovir
  • –treats causative agent (herpes simplex virus)
  • —-new versions of acyclovir= valacyclovir and famciclovir and are absorbed more rapidly

not that with bells palsy, treatment takes time and patience

  • corticosteroids and antivirals can help
  • most pts recover completely within three months
  • it rarely recurs
197
Q

lyme disease

A
  • a multisystem inflammation caused by infection with the spirochete
  • –borrelia burgdorferi (bacteria, worm-like/spiral-shaped)
  • prevalent in the northeastern states and west coast
  • the principal vectors for lyme disease in the US are deer ticks
198
Q

lyme disease… early manifestations

A
  • erythema migrans/rash
  • –caused by hematogenous spread of the spirochete within the first few months after the bite
  • characteristic painless rash at the site of the tick bite 3-32 days after the bite
  • –in few days spreads into concentric circles with a central white zone
  • they have no symptoms or flulike symptoms
  • neurologic symptoms die to cranial neuropathy
  • –unilateral or bilateral facial paralysis
  • –soon after 1ry infection or late progressing
199
Q

late manifestations of lyme disease

A
  • occurs months to years after the pt is bitten:
  • –polyarthralgia (main symptom is pain)
  • –arthritis
  • –tendinitis
  • –fibromyalgia (pain in muscles, ligaments, and tendons)
  • –progressive neurologic symptoms
  • pathology of VII paralysis
  • –unknown
  • –spirochete, neural invasion
200
Q

diagnosis and treatment of lyme disease

A
  • mainly by clinical diagnosis and
  • confirmed by serologic testing that uses
  • –enzyme-linked immunosorbent assay and
  • –western blot techniques
  • treatment
  • –controversy about treatment protocols because little data is available
201
Q

what are the three traumatic and neoplastic disorders of the facial nerve

A

*traumatic VII lesions: penetrating, blunt, and Iatrogenic trauma, temporal bone fracture

202
Q

penetrating trauma

A
  • intratemporal VII injury due to gunshot
  • –bullet, 2ry fracture in 20% temporal bone involvement
  • –CNS or vasular injury in 30% of cases
  • –immediate or delayed paralysis
  • compression injury at pre-auricular or styomastoid foramed
  • –good prognosis without surgical intervention
  • transveres vs longitudinal–CT scan
203
Q

temporal bone fractures

A

longitudinal

  • –parallels long axis of petrous pyramid
  • –70-90%
  • –caused by lateral force to mastoid or squamous bone
  • –FN injury in 10-25%

Transverse

  • –perpendicular to long axis of petrous pyramid
  • –10-30%
  • –caused by frontal, parietal, or occipital blow
  • –FN injury in 30-50%
204
Q

three common findings in temporal bone fractures

A
  • hemotympanum
  • “raccoon” sign for anterior skull base
  • battle sign= postauricular ecchymosis
205
Q

facial paralysis in the neonate

A
  • Rare: incidence 0.05-0.23%
  • birth trauma: forceps delivery, C-sections
  • –delayed symptoms (3-7); good prognosis: >90%
206
Q

mobius syndrome for congenital facial paralysis

A
  • VI and VII lesions
  • partial VII paralysis and
  • inability to move eyes from side to side
  • dysmorphic features of the skull, face, and ear
  • abnormalities of the chest, limbs, or cardiovascular system
207
Q

Melkersson-Rosenthal syndrome for congenital facial nerve paralysis

A
  • neurological disorder
  • onset: childhood/ or early adolscence
  • manifestations:
  • -recurring facial paralysis
  • –swelling of the face and lips (usually upper)
  • –folds and furrows in the tongue
  • –recurrence–reddish brown, swollen lips
  • unknown cause
  • -genetic predisposition
  • –symptomatic of crohn’s disease or sarcoidosis
208
Q

iatrogenic facial nerve injury

A
  • accidental/unexpected
  • –incidence 0.6-3.6%
  • –2nd most common reason for malpractice lawsuits
  • —-plastic, head, neck, and otologic surgery
  • ——-IOM of facial nerve decreases risk
  • intentional/expected
  • –during the removal of parotid tumor, acoustic neuroma and skull base tumors
209
Q

neoplasms of the facial nerve

A

cause of approximately 5% of peripheral facial nerve palsies

  • often misdiagnosed
  • –facial neuroma: blanket term
  • –schwannoma: schwann cell
  • –neurofibromas: neurofibromatosis
  • –traumatic neuromas: 2ry to traumatized nerves
  • –vascular tumors-pulsatile tinnitus
  • –other
  • diagnosed by CT and/r MRI
210
Q

differentiating between VII tumor and bell’s palsy

A
  • tumors do not recover after 6 months from origional diagnosis of “bell’s palsy”
  • –could fluctuate-recurrent Bell’s palsy
  • hearing loss: CHL, sensory or neural loss
  • CT or MRI
211
Q

treatment for neoplasms

A
  • goals:
  • –remove tumor
  • –preserve or restore facial function
  • —-good with vascular tumors
  • —-bad with neurofibroma
  • –preserve hearing
  • timing of the procedure is controversial
  • -some advocate aggressive, early removal
  • –others: “watchful waiting” or partial removal
212
Q

three main types of facial nerve repair plus two other

A
  • primary anastomosis: best option
  • –epineural repair except at Pes Anserina
  • –then fasicular repair
  • cable graft (from the sural nerve): for gaps >1.5cm
  • XII to VII jump
  • –only when proximal VII not available
  • –within 18 mos of injury
  • others:
  • –mid-face lift
  • –botox
  • –muscle transfer
  • —-when can’t use nerve you use the temporalis and masseter and attach to the upper lip

AUD spring 19 Medical (3 decks)

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