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w10 &11 Flashcards

1
Q

Presbycusis prevalence

A

30-35% adults 65-75 40-50% those over 75

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2
Q

what is presbycusis

A

Hearing loss associated with the degenerative effects of aging

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3
Q

components of presbycusis

A

Peripheral components (cochlear and neural)
o Central components affecting CANS function
o Word recognition (worse relative to PT audiogram and worse compared to younger patients

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4
Q

presbycusis Etiology & pathology

A
  • Presbycusis specific genes yet to be identified in humans
  • Multifactorial condition involving age, ototoxic/noise and disease related factors over lifespan
    Environmental: health status (e.g., cholesterol, BP, heart disease), history of noise & ototoxic chemical exposure, lifestyle (stress, diet, exercise, smoking)
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5
Q

presbycusis Medical assessment

A
  • Physical exam & case history
  • Exclusion of other etiology’s if indicated by history or patient (retrocochlear pathologies, other medically managed disorders)
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6
Q

presbycusis audiology assessment

A

Should include speech in noise testing
- Standard (Otoscopy, tymps, OAEs, audiometry, reflexes)
- APD assessment (particularly if sig. complaints relative to PT audiogram)
- Impact on QOL *standardized assessment tools

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7
Q

Presbycusis categories by Schuknecht et al

A

Based on underlying pathophysiology and histopathological study of human temporal bone
6 different categories
4 main: sensory, neural, strial (metabolic), cochlear conductive
2 additional: mixed, indeterminate

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8
Q

Sensory presbycusis

A

Audiological: bilateral sloping high freq SNHL, speech discrimination generally good
Histopathology: degeneration of basal cochlea, IHC and OHC, OHC loss predominant, loss of supporting cells, leads to degeneration of organ of corti

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9
Q

Neural presbycusis

A

Audiological: bilateral SNHL, flat-gradual sloping audiogram, steeply sloping also possible, poor speech discrimination
Histopathology: loss of spiral ganglion cells in all 3 cochlear turns, relative preservation of organ of corti, neuronal loss greater than expected based on status of organ of corti

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10
Q

Metabolic (strial) presbycusis

A

Audiological: slow progressive bilateral SNHL, flat to gradually sloping, good speech rec.
Histopathology: atrophy of stria vascularis, pattern of degeneration can vary (patchy & more severe in middle and apical turns, diffuse throughout cochlea), sometimes associated with cyst formation, familial component identified (likely genetic)

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11
Q

Cochlear conductive presbycusis

A

Audiological findings: bilateral SNHL, gradually sloping high freq HL, good speech descrim.
Histopathology: hair cell and neural loss minimal, proposed (not observed): altered thickness and stiffness of BM, presumed effect: altered mechanical properties of BM

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12
Q

mixed presbycusis

A
  • 2 or more of the classical types of presbycusis
  • Varied audiometric findings
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13
Q

Revised conclusions about presbycusic pathology from Schuknecht et al

A
  1. Atrophy of stria vascularis common
  2. Neuronal loss common
  3. Sensory cell loss common
    Cochlear conductive removed bc no anatomical evidence to support this pathology
    Indeterminate added.
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14
Q

Prevailing dogma 1993-2020

A

Stria/metabolic and neural presbycusis predominant lesion in aging cochlea
Pure age-related HL due to degeneration of lateral wall
- Lateral wall cells degenerate (stria vascularis, spiral ligament)
- Critical structure for supporting basic physiology of cochlea
Primary degeneration of auditory nerve as indicated by loss and shrinkage of spiral ganglion

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15
Q

Neural presbycusis

A

supported by subsequent research in human temporal bone
- Annual decline of around 100 spiral ganglion cell bodies
- Human temporal bones @50-60 years 250-4000Hz remained normal, loss of 20% spiral ganglion cells over entire cochlear partition

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16
Q

T/F Damage in stria vascularis does not cause damage

A

true
No evidence to show a metabolic component
SV does not affect hearing loss

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17
Q

Central presbycusis

A
  • Age related changes in brain include CANS
  • Deprivation induced brain plasticity peripheral damage may exacerbate central dysfunction
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18
Q

Auditory periphery:

A
  • Sensitivity loss
  • Spectral processing disrupted
  • Reduced speech in noise perception
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19
Q

CANS

A
  • Decreased temporal & frequency resolution
  • Decreased inter-hemispheric communication/binaural integration
  • Reduced speech in noise perception
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20
Q

Cognitive changes

A
  • Speed of information processing slows
  • Working memory poorer
  • Attentional difficulties (noise, distraction, executive control)
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21
Q

statistics risk of HL and dementia

A

Hearing impairment independently associated with 30-30% acceleration in cognitive decline
Over 10 year period:
Mild hearing impairment increases risk of dementia by twofold
Moderate hearing impairment increases risk of dementia by threefold
Severe hearing impairment increases risk of dementia fivefold

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22
Q

Potential mechanisms of presbycusis

A
  1. Common causes
  2. Cascade hypotheses
  3. Cognitive load
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23
Q

Audiological management of presbycusis

A
  • Aural rehab
  • Hearing technologies (ALD, CI, HA)
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24
Q

Endolymphatic Hydrops

A

any causes for build-up of fluid
Menier’s disease is endolymphatic hydrops but not all endolymphatic hydrops is Menier’s

25
inner ear homeostasis
equilibrium between vestibule, cochlea and endolymphatic sac
26
cochlear homeostasis
- Tight control of ion movement & fluid volume across cell membranes of membranous labyrinth - Ion homeostasis depends on complex transport systems - Regulation of cochlear endolymph & perilymph electrolyte composition critical for: o Maintenance of endoccochlear potential o Hair cell and nerve function - Stria vascularis & spiral ligament (specialized molecules, cells and tissues) - Ion regulation: numerous ion channels and transporters in the plasma membranes of cells lining scala media
27
Cochlear homeostasis: Ion regulation
- Epithelial complex: o Spiral ligament: fibrocytes o Stria vascularis: basal and intermediate cells, stria capillary cells - Molecules: o Gap junctions: facilitate transport of K+ between cells and into the intrastrial space o tight junctions: limit intercellular leakage of ions o ion exchange: specialized ion channels and Na+ K+ ATPase system o numerous genes regulate their expression
28
Reissner’s Membrane
Job to separate perilymph from endolymph If rupture lose ion homeostasis and development of clinical hearing loss and symptoms like vestibular issues
29
Endolymph Duct system (EDS)
cochlea and vestibular organs contain separate compartments filled with endolymph fluid - interconnected by narrow channels forming an endolymphatic duct system o cochlea linked to the vestibular system via the reunion duct o saccule to the ED via the saccular duct o utricle to the ED via the utricular duct
30
Inner ear homeostasis: aquaporins
- Active water transport involves aquaporin channels in cells of membranous labyrinth - Hearing loss resulting from aquaporin dysfunction (knockout of AQP4 leads to HL)
31
Site of lesion endolymphatic hydrops
Site of lesion: cochlear and vestibular membranous labyrinths - Condition involves distortion/ruptures of membranous labyrinth
32
EH pathology
- Regulation of endolymphatic fluid homeostasis disturbed - Underlying mechanisms (mostly unknown) - Leads to: excess endolymphatic volume & distension= hydropic state - altered endolymph composition - Underlying mechanisms, altered endolymph and/or hydropic condition>cascade of additional problems - Causes poorly understood, likely that various mechanisms lead to: o Overproduction of endolymph o Under absorption of endolymph o Both of the above
33
possible mechanisms & pathophysiology EH
Abnormal homeostasis (local regulation) - Disruption of aquaporin channels>inappropriate fluid balances - Disruption of ion channels & transporters can lead to inadequate ion transport>disrupt fluid volume - Damage to other specialized molecules/cells/tissues lining the membranous labyrinth disrupt endolymph volume and composition (genetic mutations, infection) - Inner ear environmental factors may contribute (inflammation, circulating hormones)
34
Further consequences of EH
Altered cell biochemistry and/or excess volume trigger a cascade of additional problems: - Disruption of ion transport > affects endolymph - Ruptured membranes> affects endolymph - Cochlear nerve degeneration possibly due to constant excitation at IHC-spiral ganglion synapse o Glutamate excitotoxicity> degeneration of spiral ganglion cells
35
EH Associated with different diseases or conditions:
- Meniere’s disease - Infection - Trauma - Vascular etc.,
36
Menier’s syndrome & disease:
vertigo & hearing loss in series of cases, due to inner ear rather than brain (pathophysiology and management remains controversial)
37
Meniere’s Disease Idiopathic Endolymphatic Hydrops symptoms
intermittent attacks of vertigo, tinnitus, aural fullness or pressure, SNHL
38
Meniere’s Disease Idiopathic Endolymphatic Hydrops etiology
Etiology: unknown (idiopathic), genetic predisposition in 2.6-12%, no causative genes identified
39
Familial meniers disease:
autosomal dominant inheritance pattern (only need 1 copy of affected allele from mother or father, if inherit 60% chance of showing)
40
Meniere’s Disease Idiopathic Endolymphatic Hydrops prevalence
4-15/ 100 000
41
Meniere’s Disease Idiopathic Endolymphatic Hydrops sex distribution
Sex: 1.3 F to 1 M
42
Meniere’s Disease Idiopathic Endolymphatic Hydrops Course of disease
Onset: 20-60 years,4th decade typical Acute and quiescent phases Unilateral diseases can progress to bilateral disease: in 33% cases (after 8 yrs) 50% (after 20 yrs)
43
Symptoms amplified during acute episodes (Meniere’s Disease Idiopathic Endolymphatic Hydrops) :
- Episodes often occur in “clusters” - Acute episode associated with vertigo - Increased HL and/or tinnitus - Aural fullness - Nausea & vomiting
44
early stages of MD idiopathic endolymphatic hydrops
Rupture of membranes in endolymphatic system, hair cells generally intact
45
late stages of MD idiopathic endolymphatic hydrops
Degeneration of hair cells and cochlear neurons (particularly in cochlear apex) - Distortion rupture and/or atrophy of tectorial and reisseners membrane - Herniation into scala tympani via helicotrema - Atrophy of stria vascularis - Abnormal tissue growth in cochlear duct and vestibule
46
Biochemical disruption
altered biochemistry may affect transduction processes causing hearing threshold loss - Perilymph & endolymph mix: toxicity damages cells & tissues
47
medical assessment MD idiopathic endolymphatic hydrops
Clinical diagnosis (based on clinical features alone): can be a challenge for non-specialists, no definitive diagnostic test or procedure Usually based on patient history & symptoms: careful documentation of symptoms is basis of diagnosis and categorization of MD Radiographic imgaging and laboratory tests may be used to exclude other underlying causes of EH - ABR/ MRI/ CT for differential diagnosis: rule out retrocochlear & other mass lesions etc
48
audiologic assessment of MD idiopathic endolymphatic hydrops
- To confirm SNHL, monitor fluctuating HL Glycerol test may be ordered: monitor hearing thresholds which are expected to improve with glycerol ingestion Physiological tests: electrocochleography SP/AP Vestibular assessment: ENG.VNG &VEMP PT audiometry: initially fluctuating, low freq SNHL, progress to flat moderate-severe to severe SNHL, progression to bilateral loss, vertiginous episodes cease (Enough damage occurring to vestibular organs that they become non-functioning- this is why they cease) - Speech testing: poor WRS relative to PT audiometry: If traditionally normal SNHL you would expect 90-100% WRS but for someone with Menier’s may get 70-80%
49
Medical management Goal: control symptoms, especially vertigo what is treatment
varies - Acute vs dormant phase - Severity and duration of symptoms - Conservative approach used initially to control symptoms - If disabling & chronic: ablation of vestibular end-organ - No therapy can prevent progression of hearing deterioration
50
Medical management: conservative
Goal: manage symptoms during acute phase (vertigo) using pharmacological approach: vestibular suppressants & antiemetics (nausea), steroids (reduce inflammation)
51
When conservative options fail
Goal: manage chronic & disabling symptoms (vertigo) Vestibular ablation: pharmacology Vestibular treatment or ablation: surgical
52
Vestibular ablation: pharmacology
- Vestibulotoxic aminoglycosides - Oral (systemic & bilateral effect) - Intratympanic (higher does & ear specific)
53
Vestibular treatment or ablation: surgical
Endolymphatic sac decompression - Vestibular neurectomy- hearing preserved - Transmastoid labyrinthectomy- drill away SCC
54
Endolymphatic sac surgery: decompress or shunt
Goal is to decrease endolymphatic pressure - Remove some of mastoid bone surrounding endolymphatic sac, drain or insert valve - Lower risk surgery, hearing preserved, varying success rates in controlling vertigo and stabilizing hearing (up to 80% success reported)
55
Vestibular neurectomy-
section of vestibular nerve removed, hearing preserved, prevents signals from vestibular nerve from stimulating the brain, neurosurgery has higher risk: anesthesia, CSF leak, facial nerve damage
56
Labyrinthectomy
ablation of the vestibular end organ, destroys cochlea, hearing not preserved, appropriate for those with no useful hearing on diseased side
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Audiologic management early phase
fluctuating hearing sensitivity & poor speech recognition accompanied by episodic vertigo - Amplification, ALD, aural rehab (communication strategies, tinnitus, vocational rehab)
58
Audiologic management late phase
progressive HL and bilateral burnout of hearing sensitivity - Severe HL with poor WRS bilaterally - Cochlear implantation

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