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PHGY 314 > Auditory (Vollrath) > Flashcards

Auditory (Vollrath) Flashcards

1
Q

Why is it important to study the auditory system?

A
  • 4-6/1000 newborns have hearing disorders
  • Hearing is critical for development of speech
  • Hearing loss increases with age and is irreversible (through loss of hair cells, is associated with a decrease cognitive function)
  • 40% of adults of 75yo are hearing impaired
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2
Q

What are the names of both tests that are made on newborns to test if they can hear?

A
  1. Otoacoustic emissions (1st test, if not passed, do the 2nd) → hair cells send sounds waves back and measure these reponse waves to given stimuli
  2. Auditory brainstem response → record from auditory brain cells with electrodes in response to stimuli
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3
Q

What is the stimulus of the auditory system?

A

Sounds waves → vibration of the air molecules (pressure waves)

Each sound can be broken-down into a series of sinusoidal waveforms

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4
Q

What 2 parameters can be measured to get information on a specific sound wave?
What are the audible ranges?

A
  1. Pitch → frequency of the sound
    - Audible frequencies: 20-20,000Hz
  2. Loudness → amplitude
    - Range: 0.0002 - 2000 dynes/cm2 (force/surface area)
    *7 orders of magnitude
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5
Q

Is the ear equally sensitive to all frequencies?

A

NO
It is less sensitive to lower frequencies (have to be played much louder to be heard)

Max sensitivity range = 500 - 5000 Hz (sounds produce sensation at the lowest amplitude)
- Also the range used for communication

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6
Q

What determines the functional the frequency response?
*What frequencies we are most sensitive to

A

Th functional anatomy of the ear:
- Shape and size of the pinna and meatus allow sounds between 2000-5000Hz to pass betters/lose less energy bouncing off

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7
Q

What is Weber-Fechners Law for the auditory system specifically?

A

Converst Dynes/cm2 to dB to represent sound intensity in a way that corresponds to perceived loudness

L = 20 x log10 (P/Pstd)
→ Pstd = lowest possible pressure, when not sound wave = 0.0002 dynes/cm2

10-fold increase in loudness = +20dB (percieved increment of loudness)

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8
Q

What is the human hearing range of dB?

A

0 - 120 dB SPL

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9
Q

What are the 3 main part of the ear and their main function?

A

External ear → collection of mechanical energy (sound waves)

Middle ear → Transmission of mechanical energy, Amplification

Inner ear → Site of auditory mechanoeletrical transduction

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10
Q

Which ear compartements are air-filled/fluid-filled?

A

External ear → air-filled
Middle ear → air-filled
Internal ear → fluid-filled

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11
Q

What are the components of the external ear?

A

Pinna → funnels the sound waves into the meatus
- not an amplifier, just a funnel
- It’s orientation/shape explains why we hear sounds behind our head less well than beside us

Meatus (auditory canal) → acts as a resonator
- 2,000-5,000 Hz are resonant frequencies → ensure reliable transmission of speech by creating resonance in the meatus

*Sounds waves travel through the meatus and impinge on the thympanic membrane (ear drum)

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12
Q

What the the names of the 3 ossicles of the middle ear? What is their role?

A
  1. Malleus
  2. Incus
  3. Stapes

*They transfer sound from the air to more dense liquid media of the inner ear → Amplification
*Smallest bones in the body

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13
Q

What is the Eustachian tube?

A

In the middle ear
Normally closed to the outside world, connect to the pharynx
- During yawning, the Eustachian tube can open to equilibrate pressure
- If the tube is blocked, it can lead to a middle ear infection (otitis media)

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14
Q

What happens during otitis media?

A

Fluid accumulate in the Eustachian tube → accumulation of fluid in the middle ear → makes it harder for the ossicles to move

*Thympanic membrane can bulge out/appear read

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15
Q

What 2 mechanisms allow the middle ear to amplify sound pressure?
What is the total amplification?

A

*Need amplification to go from air wave → fluid wave

  1. Mechanical amplification:
    The ossicles move together on an axis and act as a lever arm
    - Amplifies by 1.3X (not a lot)
  2. Pressure amplification:
    *Pressure = Force/Area
    Thympanic membrane → Oval window
    50 mm2 → 3 mm2
    So a given force applied to the thympanic membrane would result in 17X pressure at the oval window

Total → 17 x 1.3 = 22x amplification

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16
Q

What are the middle ear mechanisms that protect the inner ear from loud sounds?

A

The motion of ossicular chain is limited by 2 muscles:
1. Tensor Tympani → attached to the malleus
2. Stapedius → attachde to the stapes

These muscles are reflexively activated (feedback from inner ear) for sounds > 80 dB
When activated, they limit the movement of the ossicles to transmit less energy to the cochlea
*Only about 20dB decrease

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17
Q

What is the general structure of the cochlea?

A

Coiled structure 2.5 turns → 33mm long in human
3 fluid-filled compartments:
- Scala Vestibuli, Scala media (cochlear duct, organ of Corti in there), Scala tympani
Comprises the Organ of Corti → site of sensory transduction
- Receptor cells (hair cells) sit on the basilar membrane
- Stereocilia extend in to the tectorial membrane

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18
Q

What are the names of the 2 membranes separating the cochlear compartements?

A

Between Scala vestibuli and Scala media → Reissner’s membrane (vestibular membrane)
*top one

Between Scala media and Scala tympani → Basilar membrane
*Bottom one, hair cells sit on it

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19
Q

What are the different fluids in the cochlea?

A
  1. Endolymph:
    - Similar to intracellular fluid
    - Found in scala media (middle)
    - High K+
    - Produced by cells in stria vascularis (external wall of scala media)
    - +80mV compared to perilymph
  2. Perilymph:
    - Similar to extracellular fluid
    - Found in scala vestibuli (top) and scala tympani (bottom)
    - High Na+
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20
Q

How many hair cells are present in each ear?

A

16,00 cell/ear total:
- 3,500 Inner hair cells
- 12,000 Outer hair cells

*Very few and they don’t regenerate

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21
Q

What is the Traveling wave?

A

The wave motion along the Basilar membrane → max 150nm in height

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22
Q

What is the mechanism of receptor cell (hair cell) activation?

A
  1. Stapes pushes no Oval window → produces a wave in Scala vestibuli
  2. The pressure wave is transmitted to the basilar membrane
  3. The Round window acts as a pressure release
  4. The motion along the Basilar membrane is a “Traveling Wave”
  5. At the location the basilar membrane is excited → shearing force → hair cell stimulation
    *Happens because the pivot points of Basilar vs Tectorial membranes are not the same (geometry of the system)
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23
Q

What is the importance of the Round Window?

A

It allows for the liquid to move when pushed by the Oval Window (every thing else is solid bone so without it, the liquid would be able to move and produce a wave)

Oval Window → waves in Scala vestibuli → all the way around →transmitted by the membranes to the Scala tympani (wave coming back) → Round Window (releases pressure)

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24
Q

What are the mechanical properties of the basilar membrane like?

A

Not uniform along the basilar membrane:
Apex → elastic (20Hz needed to generate movement of the basilar membrane)

Base → stiffer (20kHz needed, closer to Oval Window)

The basilar membrane acts as a mechanical frequency analyzer → pattern of motion begins the encoding of sound frequency and intensity → TONOTOPY

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25
Q

What is tonotopy?

A

Spatial arrangement of where different sound frequencies are processed → start by moving the basilar membrane at different spots depending on frequencies

Higher frequencies closer to Oval Window, lower frequencies more at the apex

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26
Q

What is the effect of an upward vs downward deflection of the basilar membrane?

A

Upward deflection → Excitation
Downward deflection → Inhibition

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27
Q

What is the Kinocilium?

A

It is a part of the hair bundle (~additionnal hair) located at the tall end of the hair bundle (beside the tallest stereocilia)

Only found in vestibular hair cells, NOT in auditory hair cells

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28
Q

What are the characteristics of the hair bundle of the hair cells?

A
  • 10-100s of stereocilia (depending on the organ/specie)
  • Staircase arrangement (shortest → tallest)
  • Filled with cross-linked actin filaments (to prevent bending and allow stereocilia to move as a whole)
  • Tapered base allows stereocilia to pivot in response to mechanical force
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29
Q

How are hair cells connected to neighbouring cells?

A

By thight junctions (connected to supporting cells, not direclty to other hair cells)
Important to separate the endolymph (on the side of hair/apical side of cells) from the perilymph (in scala tympani/basolateral side of cells)

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30
Q

How do hair cells send signals?

A

They synapse on the basolateral surface → produce a GRADED response (not an AP) by releasing glutamate onto afferent nerves

The afferent nerve will itself, when sufficient glutamate levels, fire an AP

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31
Q

What type of cells are hair cells?

A

Neuro-epithelial cells
Like all epithelial cells, they have POLARITY (have a basolateral and apical side)

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32
Q

What are the different components of the hair cell?

A
  • Stereocilia
  • Kinocilium (vestibular cells)
  • Cuticular plate (dense network of actin filaments at the apical cytoplasm)
  • Basal body
  • Nucleus
  • LOTS of mitochondrias (to release lots of glutamate)
  • Synaptic Ribbons (doc for a pool of readily releasible glutamate vesicles)

On the basal side, the cell is connected to afferent nerves on which it sinapses and efferent nerves that modulate the activity of the hair cell

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33
Q

How can the hair cell be stimulated?
What happens when the cell is stimulated?

A

Excited by horizontal (only) mechanical movement towards the tall stereocilia (towards short one inhibits)

  1. Deflection (not bending) of the stereocilia opens ion channels
  2. Hair cell depolarizes (Ca2+, mostly K+ influx)
  3. Ca2+ influx and transmitter release onto the afferent nerve (no AP)
  4. Afferent VIII nerve firing sends signal to the brain

*In the experiments to know how to excit the cell, record from the apical surface of the cell, at the basis of the hair bundle because large surface allows in bull frog hair cells

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34
Q

How are hair cells arranged in the cochlea (for auditory input)?

A

1 row of inner hair cells → actual sensory cells
3 rows of outer hair cells → rafine sensory selectivity and sensitivity
All separated by supporting cells

35
Q

What 3 areas of the ear has hair cells?
What differs in these 3 areas?

A

They differ in the way the hair bundle is deflected
1. Cochlea → basilar membrane move up while tectorial membrane moves towards the tall ends of hair bundles (horizontally)

  1. Semicircular canal (sensitive to angular rotation) → hair bundle are in a plate, that plate is deflected/bent by movement of a gel when rotation
  2. Utricle and Saccule (sensitive to linear acceleration and gravity) → when linear accelerators, the epithelium move following the body, but the gel that rest on the bundles move in delayed time which creates deflection
36
Q

What is the resting potential of hair cells at rest?
When maximally depolarized? (saturated excitation)
When maximally repolarized? (saturated inhibition)

A

Hair Bundle Displacement causes a change in Receptor Potential:
Rest = -57mV
Max Excitation = -40mV
Max Depolarization = -60mV
*Signmoidal relationship between hair bundle displacement and receptor potential (not linear)

37
Q

What does Receptor (cell) Potential rely on?
What are the characteristic of the channels?

A

It relies on mechanoelectrical transduction channels for changes in membrane potential

  • non-selective cation channels (mostly K+ because of endolymph, some Ca2+)
  • ~100 ion channel/cell
  • Some are open at rest (always want % open for sensitivity)
  • +80mV standing potential (ouside cells → increases current flow into hair cells)
  • narrow operating range of deflection
38
Q

What was seen in the recorded current recorded under patch clamp, when the hair bundle was pulled for a longer period and then relaxed?

A

Pulled toward tall end → strong increase in negative current followed by a decay

Pulled towards the short end → decrease in current, when relax → big increase in negative current followed by decay

*shows some adaptation of the receptor

39
Q

What stimulating experiment/protocole was done to study adaption of the stimulus response function?

A
  1. Start with no stimulus
  2. Give short pulse of different current amplitudes (patch clamped so current depolarizes)
  3. Let down to 0
  4. Give adapting step stimulus (background)
  5. Give another short pulse

*If the reason for the decay of the current was because of inactivation, the second pulse would not allow greater current because of the inactivation from the adapting step
→ Means the system has rearranged it self to be sensitive even when there is a long lasting stimulus

40
Q

What mechanism underlies transduction?

A

Mechanically-Gated Channels:
1. Gating done by elastic structures in hair bundle
2. Channel opening and closing is controlled by tension in the elastic gating spring
3. Bundle displacement towards the tallest cilia increases tension → open channel → hair cell depolarization
Bundle displacement towards the shorted end → decrease tension → closes channel → hair cell hyperpolarization

41
Q

What is the effect of Calcium un the mechanically-gated channels underlying transduction?

A

Myosin motor molecules at the end of the tip link attach temselves to the actin core of the next taller stereocilia

Channels open → High Ca entry → Myosin motors slipping down the actin filaments (release tension to allow some channels to close)
*Too much sound → less sensitivity

Channels closed → low Ca entry → myosin motors climb up the actin filament (increase tension to allow some channels to open more readily)
*Very little sound → more sensitivity

42
Q

Why is mechanical gating required for auditory transduction?

A
  1. No need for 2nd messenger → much faster
    - 10s of microsec for hair mechanotransduction vs 10s of millisec for phototransduction (requires 2nd messengers)
  2. Speed is critical for hearing:
    - Respond to sounds up to 100kHz → hair bundle moves to quickly → channels open/close to quickly for 2nd messenger system
    - Sound localization base on small temporal delays (10 microseconds)
43
Q

How do hair cells vary from the base to the apex of the cochlea?

A

Hair cells are tuned to respond best to certain frequencies

1) mechanical Properties of Bundle → shorter + stiffer = higher frequency (base of cochlea)
- 2x difference between base and apex in humans

2) Ion channel properties → faster mechanically-gated channels in high frequency cells

44
Q

What is the hair cell Tuning Curve?

A

1) Play a tone at a given frequency, increase the amplitude until hair cell response is 1mV
*Take different hair cells along the cochlea → different characteristics frequencies

We see cells are much more sensitive at lower amplitudes (only respond to their characteristic frequency and not other) → called Sharp Tuning
*Cells that respond to higher frequencies are more sharply tuned?

45
Q

What could be responsible for the sharp tuning of the hair cell at lower frequencies?

A

Outer hair cells act as Cochlear Amplifiers
*LOCAL effect

46
Q

What are the evidences for the existence of the Cochlear Amplifier?

A
  1. Tuning and Sensitivity of the cochlea is greater than predicted by its passive mechanical properties → much of the stimulus energy is needed to overcome damping by the cochlear fluids
  2. Tuning is sharpest for low dBs → for low amplitude stimuli basilar membrane movement is amplified x100 relative excepted passive properties
  3. Evoked and spontaneous otoacoustic emissions → in quiet envrionment, human ears spontaneously emit pure tones

→There has to be an Active means of Amplification

47
Q

What is the cellular mechanism behind Cochlear Amplification?

A

Prestin → motor protein in OHC responsible for cochlear amplification
*Electromotility (change in potential → change in size)

  1. OHC rapidly shorten when depolarized and lengthen when hyperpolarized
  2. The motion of OHC → augments the motion of basilar membrane → further amplifies the receptor potentials in both IHC and OHC

Reducing OHC function with efferent activation, drugs, ablation decreases cochlear sensitivity and frequency discrimination
Without functional OHCs → no otoacoustic emissions

hair bundle motion may also contribute to cochlear amplification

48
Q

How can hypoxia be an evidence for the cochlear amplifier?

A

Record frequency x Sound pressure level (amplitude)

In hair cell and in afferent nerve → both have characteristic frequencies
*Hair cells are very energy-dependent as they release lots of glutamate (lots of mitochondrias)

Hypoxia reversibly eliminates OHC, eliminates sharp tuning and shows passive response (lack of OHC) → Auditory nerve fiber recording shows this
*Are IHC affected?

49
Q

In the Evoked otoacoustic emission test, do all healthy patients react exactly the same?

A

NO
Everyone has different frequencies evoked by OHC depending on many factors, we only measure the presence of some frequency (750 Hz - 3.6 kHz)

50
Q

How are afferents distributed in the cochlea?

A

Total 30,000 afferents/cochlea

Inner hair cells receive 95% of connections ~10/cell
- Sharp pitch discimination → sets up the tonotopic map

Outer hair cells receive 5% of connections → single afferent fiber contacts many cells
- More broadly tuned sensation, information on cochlear activity and amplitude, but not specific frequencies
→ OHC receive 95% of efferent input

51
Q

Where do the Auditory afferents project to?

A

Auditory afferents project via the VIII nerve → Cochlear Nucleus

Type 1 Neurons input info from IHC
Type II Neurons input info from OHC

52
Q

Where do auditory efferents come from?

A

Efferent cell bodies are located in the Superior Olivary Complex:

Lateral Olivary Complex Neuorns → inner hair cells (5%)

Mediul OC Neurons → outer hair cells (95%) (→ shut of the OHC)

53
Q

What type of sound do (Type 1) Afferents adapt for?

A

Type 1 = from IHC → Cochlear nucleus
Adapt for louder, sustained sounds

When subjected to a tone burst, show high peak at first which declines over time

54
Q

How does the firing rate change as a function of sound levels? (Afferent response properties)
*With and without noise

A

A) Response to pure tone → Firing rate increases with sound level (starts at specific frequency → increases linearly → saturates as specific amplitude)

B) Response to pure tone + noise → Changes the working range of the neuron → due to adaptation, neuron responds less in noise
(higher background firing rate → start increasing at higher amplitude → saturates around the same amplitude)

55
Q

What is the effect of efferent stimulation on afferent responses?
*With and without noise

A

Done by Stimulation of medial olivocochlear neurons (of the Superior Olive Complex) → reduces cochlear amplification

1) Response to pure tone → shift to the right compared to no stimulation → change the dynamic range (start increasing at higher amplitudes and saturates at higher amplitudes)

2) Response to pure tone + noise → no adaptation/same as without noise → greater response for increasing levels of tone intensity

*Efferent stimulation is used everyday such as speech comprehension in background noise (dim down OHC)

56
Q

What information is included in Type 1 auditory afferents for the brain?

A
  1. Which nerve fiber is activated → tonotopic arrangement
  2. Rate of spiking → more spiking = louder sound for ex
  3. Temporal pattern of spiking → Low frequency sounds could cause every deflection to spike which gives info on the frequency
57
Q

What is the Place Code?

A

Frequency coding of sound as it is tonotopically Arranged

58
Q

What is the importance of having ~10 afferents synpasing from 1 IHC?
How does it convert to information about loudness?

A

*Afferent information is NOT redundant
- Each type 1 afferent has a sensitivity range of about 30dB (not the same for each)
- Afferent contacting 1 IHC have different thresholds for activation (amplitude → more/less glutamate release)
- Afferents can respond over the range of hearing sensitivity 0-120 dB

Loudness is code by increasing the firing rate of 1 afferent + recruiting additional afferent fibers

59
Q

What are the differences in sensitivity of different afferents synapsing onto a single IHC due to?

A
  • Due to properties of the hair cell-to-afferent synapse
  • Due to preperties of the afferent themselves
60
Q

What is the role of most efferent fibers?

A

Efferent control the gain of the cochlear amplifier → efferent activation decreases their sensitivity

*In noise, efferents protect the hair cells

61
Q

What is the concept of Phase Locking?

A

*Temporal code
Preferential firing of certain phase of a sound waveform (not necessarily at each cycle, but as a pattern and in the same phase of the cycle)

It gives information about the frequency of the sound < 4000 Hz

62
Q

How are place code and phase locking complementary?

A

Place code (tonotopy) is very precise and efficient for higher frequencies → a more narrow section of the basilar membrane moves

At lower frequencies, a larger part of the basilar membrane moves (more hair cells activated) → phase locking allows for better frequency discrimination

At intermediate frequencies, both are used

63
Q

How is loudness encoded in afferents for high vs low frequencies?

A

Higher frequencies → number of spkies increases with loudness (the few tonotopically corresponding hair cells spike at a higher cste frequency)

Lower frequencies → The number of spiked in a burst increases (afferents spike with a pattern dependent on frequency and within that pattern, each burst has more spike when louder)

64
Q

What are the steps of the Auditory pathway from the ear to the cortex?
(And some key aspects)

A
  1. Afferents
  2. Cochlear Nucleus
  3. Superior Olivary Nucleus
  4. Inferior Colliculus
  5. Medial Geniculate Nucleus
  6. Auditory Cortex (A1)

*Information is processed in parallel pathways → binaural processing
*Tonotopy is preserved to the cortex

65
Q

What is the site of the first synapse in the brain stem ?

A

Cochlear nucleus → Extensive crossing from right to left and vice verse at this level and later

*This partial crossing of the auditory information is good because the only way to 100% of the information from 1 ear is to have a lesion at the level of the cochlear nucleus

66
Q

What is the structure of the cochlear nucleus?

A

Has 3 subnuclei → one for higher frequencies, one for intermediat frequencies, one for lower frequencies (from cochlea tonotopic mapping)
Each as an orderly tonotopic map
Dorsal, Anteroventral, Posteroventral

Different cell types differ in their response properties:
Sperical bushy cells → mimic the afferent input
Octopus cells → only pass information from the onset

67
Q

Which part of the Auditory pathway is responsible for sound localization?

A

Superior Olivary Nucleus → 1st part fo the brain where we ahve input from both ears together → allows to compare both inputs

*Also were the efferent come from

68
Q

What are the different cues used in processing for sounds localization?

A

1) Difference in arrival time → at level of the medial Superior Olive
- 1ms to travel from one ear to the other
- For frequencies below 1,500 Hz (less chances of having 2 wavefronts at the exact same time)

2) Intensity difference → Lateral Superior Olive
- Head absorbs high-frequency sounds → Intensity difference depends on the frequency
2:1 at 1,000 Hz
100:1 at 10,000 Hz
→ for frequencies > 3,000 Hz

3) Miniature Echoes
Curvature of pinnae helps differentiate sound coming from top vs bottom → brain uses miniature echoes produced by complex curves of pinnae
(Straws is ears cancels out that)

*1 and 2 to determine left vs right

69
Q

At the neuronal level, how is the medial superior olive (subnuclei in the Superior Olive Complex) able to differentiate sound coming from the right vs left?

A

*Used for interaural time differences < 1500 Hz → Sets up a map of sound location
Longer axon = longer Delay
Neurons = coincidence detectors → They fire only when they get input from both side at the same time (meaning the contralateral side started travelling 1st)

Each neuron signals a different interaural time difference:
Ipsilateral inputs from CN → MSO neurons (output place code) ← Contralateral inputs from CN

70
Q

What are the characteristics of the neurons of the Lateral Superior Olive?

A

Each neuron is sensitive to different interaural level difference:
- Input from ipsilateral side is excitatory
- Input from contralateral side synapses on inhitory neuron before → is inhibitory
The input is summed up → gives info on which side is louder

71
Q

Which cells are responsible for preserving timing information?
What happens with this information?

A

Cochlear Nucleus octupus cells → project to the Superior Olive where maps of sound location are created

*Superior Olive Nucleus = first site of binaural interaction

72
Q

What are the characteristics of the Primary Auditory Cortex (A1)?

A
  • Tonotopic map in kHz
  • Information is organized in columns
  • Extensive crossing of pathways
  • Neurons can have receptive fields for location in space → some are broadly tuned unit, other have narrowly tuned unit

*A1 is small but flankde by up to 9 other areas, many with tonotopic organization → specialized for speech processing or multimodal processing

73
Q

What is the main general question of the paper for this section?
What method was used?

A

How does noise exposure affect development of the auditory cortex?
Wanted to deprive the rat of all sounds, but not possible (sounds can get in by bone stimulation), so exposed them to a 70dB broadband noise (all frequencies) to cover all other sound stimulation

74
Q

What was seen in response to the broadband noise exposure?
*In the paper

A

P16 control → disorganized tonotopic arragement of the brain
P50 control → organized tonotopic map

P50 noise → disorganized tonotopic arrangement

Question:
Has noise exposure change the mature pattern of A1 (defenitive) or has it extended the critical period?

75
Q

How did they check if A1 was definitively altered or if is was immature after broadband noise?
*In the paper
What where the results?

A

After 70dB Broadband noise, at P50, add 7kHz Tone

After 50-90 days of broadband noise, A1 remains plastic → 7kHz noise leads to overrepresentation of 7kHz sensitivity in tonotopic arrangement of A1

For control after P50 + 7kHz noise → no change because the critical period has ended

76
Q

What is the critical period for the auditory cortex development in humans?

A

6-7 years → need coherent auditory inputs in that period for development of language

Perception of word sounds + syllables matures between 8-10 months
Perception of word meaning matures between 2-4 years

*Environmental noise could contribute to auditory and language-related delays in children → chronic otitis media, cleft palate (closes the eustachian tube)

77
Q

What is the frequency and causes of congenital deafness?

A

Incidence ~ 0.1%
~1/2 is genetic

78
Q

What are the causes of Age-related (progressive) hearing loss?

A

~40% by age 75

  • Most due to cochlear damage (loss of hair cells) → OHC > IHC > Auditory nerves
  • Some genetic
  • Bacterial meningitis
  • Noise (genetic predisposition?)
  • Ototoxic drugs (aminoglycoside antibiotics, cisplatin)
    *They all kill the hair cells
79
Q

What are the average max frequencies heard in newborns vs age 20 vs retirement age?

A

Newborn → 20 - 20,000 Hz
Age 20 → 20 -16,000 Hz
Retirement age → 20 - 8,000 Hz

80
Q

What is presbycusis?

A

Age-related hearing loss

81
Q

What are the types of peripheral hearing disorders?

A

1) Conduction deafness → Inteference with the sound conduction of the external or middle ear
Causes: wax accumulation, otitis media (infection), otosclerosis

2) Sensorineural hearing loss → Damage to organ of Corti (hair cells) or VIII nerve
Causes: persistent loud noise, toxic drugs (streptomycin), old age, tumors of VIII nerve, infections

82
Q

What are some clinical tests that can be done to assess different types of hearing disorders?

A

1) Auditometry → test with pure tones → generate hearing threshold curve
2) Bone conduction (Rinne test) → with tunnning fork, tests if conductive or sensorineural hearing loss
3) Otoacoustic Emission → tests outer hair cells

83
Q

What is the mechanism of cochlear implant?

A

1) Implanted through round window
2) Electrode array placed withint the scala tympani
3) Electrodes are spaced along the cochlear spiral to stimulate groups of auditory nerve fibers that respond to different frequencies (~20 electrodes, enough to have tonotoppic mapping)

PHGY 314 (8 decks)

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