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Measuring the inner ear
Extremely difficult and dangerous
Little improvement
Only way to measure is the cochlear implant
Menuere’s disease
Sensorineural hearing loss
Causes fluctuating hearing loss and balance, not sure why it happens
Conductive hearing loss
Means no sound is getting from the outside to the inner ear
Sensorineural hearing loss
Caused by damage to the inner ear
What is used to test air-conducted thresholds
Headphones
What is used to test bone-conducted thresholds (by-passing any middle-ear problems)
Bone vibrator
Bone vibrator
Used to test bone-conducted thresholds
Bypasses outer and middle ear, straight through skull
By comparing against normal thresholds for air and bone audiometry, can find the air-bone gap
The difference in discrepancy with normal hearing
What are the two types of pure-tone audiology
Headphones and Bone vibrator
If there is a larger discrepancy in normal hearing with the headphones than with the bone vibrator, what kind of hearing loss does this suggest?
Conductive loss
If there is a larger discrepancy in normal hearing with the bone vibrator than with the headphones, what kind of hearing loss does this suggest?
Sensori-neural loss
What are the two things outer hair cells do physiologically
Amplify sound
Improve the frequency selectively (only amplify sounds of the right frequency)
What can temporarily reduce the response of the basilar membrane
Furosemide
Loss of OHCs: Deactivation with furosemide (Ruggero & Rich, 1991)
Measures motion of the membrane (through shining laser light through round window)
Means can ONLY look at very high frequencies
Furosemide
Affects how the ear operates
14 minutes after administration, can see reduction in basilar membrane activity
They are being suppressed by this drug
Results
No amplification occurring
When given a different frequency that the basilar membrane is not tuned to, there is no change in response due to the furosemide
THEREFORE, the outer hair cells don’t make any difference away from the correct frequency
Amplification reduces as sound level increases
Conclusion
Support that OHCs used in amplification and are frequency selective
Loss of OHCs: Loudness magnitude estimation
P’s with hearing impairment
Magnitude estimation
Give someone sound, say it is 100, give them another sound and as how much is that worth?
From before, the amount by which loudness goes up is much smaller than the amount the sound has increased in intensity
Results
Don’t hear very low sound levels
Loudness curve goes up very fast until it is quite similar to a normal hearing person
Very sensitive to small increments in intensity
Conclusion
Hearing impaired individuals lack normal “compressive” growth in loudness, instead experience “loudness recruitment”
Loss of outer hair cells: Frequency selectivity (Glasberg & Moore, 1986)
Used the noise notch technique
P’s had hearing impairment on only one side, so within-subject design as compared normal hearing on one side to impaired on the other
Results
Frequency selection was poor regardless of width for hearing impaired side (broad filter)
What is the noise notch technique
Psychophysical technique
One low noise and one high noise, in between is a notch
Part of the sound spectrum where there’s no noise, just a tone
Measure the lowest intensity of that tone that people can detect with that noise
If tone close to noise, high threshold
If far away, lower threshold
Manipulate the width of the notch
What is a bigger issue: Loss of OHCs or IHCs?
OHCs
IHCs more physiologically robust
Why do you not go completely deaf in a frequency region from loss of some IHCs
You don’t go completely deaf in a frequency region from loss of some IHCs
BECAUSE each IHC has a range of response, so just less responsive
If you don’t go completely deaf from loss of IHCs, how do you tell you have loss of IHCs?
Dead regions
Excitation in the dead region would NOT reach of threshold for detectable movement in a basilar membrane
Even if the tone is increased enough so that the sound is detected outside of its preferred frequency range (despite this being in the dead zone), adding noise prevents the hair cell from picking it up
Noise it at preferred tone so trumps the sound
Conclusion
If tone is in dead zone can still be picked up but need really intense frequency
Threshold Equalising Noise (TEN)
In a normal hearing listener, tone thresholds in TEN should all be the same
Called threshold equalising as tend to get the same threshold regardless of frequency of tone
TEN and Dead Zone
All the thresholds suddenly become the same regardless of what level of threshold equalising noise being used
What area pumps loads of K+ ions into the Scala media
Stria vascularis
Loss of endocochlear potential (EP)
Might suppress both inner and outer hair cells
Why might we think loss of endocochlear potential (EP) is something that happens?
The stria vascularis degrades with age
Don’t know how much it drops in humans, can only get animal models
Some individuals with known hearing loss have intact hair cells at post-mortem
Hearing loss can’t be due to hair cells
The endocochlear potential is known to fall with age in animal models
Why is loss of EP hard to distinguish from IHC and OHC loss
Loss of EP affects both IHC and OHC function
Does age-related hearing loss mainly affect high or low frequencies?
High frequencies
What might be evidence against loss of EP as an age-related hearing loss?
As it affects whole cochlea, would expect its effects are fairly uniform across frequency
BUT most age-related hearing loss mainly affects high frequencies so not uniform
BUT we can’t measure inner ear so knowledge is limited
Cochlear synaptopathy: The evidence from noise-exposed mouse histology
Measured mouse hearing through two objective measures (DPOAEs and ABRs)
Exposed mouse to very loud sound
Found noise threshold increased for a few days after before returning to baseline
BUT if you take out the cochlears of exposed mice and count the synapses on the IHCs
Compared to control mice down about 2/3 rds
Does this happen in humans?
Why is cochlear synaptopathy sometimes referred to as “hidden hearing loss”
It only takes a few synapses to detect a sound, so may be invisible audiologically
Cochlear synaptopathy: The evidence from human histology
The number of IHC synapses in human cadaver temporal bones declines with age at death
Cochlear synaptopathy: The evidence from human psychophysics
IPD = Interaural phase difference detection
Sound localisation skill, can detect time it takes for sound to hit first ear then the second
Found no decline in IPD tasks across ages
AMD = Amplitude modulation detection
Ability to detect variations in sound level, thought to be dependent on the survival of audiotry nerve fibres and synpases
BUT again found no significant different in AMD tasks across ages
Summary of things that can go wrong with hearing