Week 11: NIHL and Hidden Hearing Loss Flashcards
temporary threshold shift (TTS)
changes in hearing/fullness/ ringing after loud sounds, then improves (warning sign of permanent hearing loss)
permanent threshold shift (PTS)
underlying mechanisms of TTS and PTS are different, so affected OAEs w/ PTS, but back to normal w/ TTS
damage location with NIHL
- stria vascularis, OHCs, STEREocilia, IHCs (synapses of), pillar nad supporting cells of reticular lamina
- –if endolymph mixed with chordalymph, then the hair cells can’t get rid of potassium in them because of the increased concentration of K+ around them
- when ion concentration in the cell increases (such as K+) and it just keeps accumulating, then the cell dies
- –it swells to a point where it can’t return to normal and basically it explodes
- –as in the right pic, it can be so significant that the reticular lamina and basically the organ of corti is damaged
OAEs and detecting NIHL
- can detect subtle changes in the cochlea through (preclinical):
- –regular monitoring of OAE changes
- –screening for absent or reduced OAEs
- early detection allows for early intervention
- predict susceptibility for developing NIHL allow for extra measures, susceptibility can be enhanced by many factors such as genetics or ototoxic drugs
OAE mechanisms and the effect of noise
- OAES are generated by distortions, reflections, or a combo of the two
- reflection OAEs are more sensitive to gain changes in the cochlear amplifier
- TEs and SFOAEs:
- –at low levels: are primarily reflection components
- –at high levels: become a mix of both reflection and distortion components
three reasons studying the process of NIHL is difficult
- noise exposure in the field is uncontrolled (unlike in lab studies on animals)
- difficult to gain access to large noise exposed population and monitor them for adequate time span
- difficulty to gain access to demographically matched control groups
two ways studying the process of NIHL
- cross-sectional studies= different groups of people that represent different points in time
- longitudinal studies= group of people followed over a long time
efferent strength with NIHL
- animal research shows variations in efferent strength are predictive of PTS
- –de-efferented animals show larger PTS after noise exposure
four reasons OAEs are more sensitive to NIHL than the audiogram
1) OHC redundancy
- –we have more OHCs than we need (12000-15000)
- –when a critical # is affected hearing loss appears
- –some damage is easily picked up because OAEs measure OHC for example TEs decreased by 80% before hearing threshold in a study
2) OAE intermodulation and distortion
- –diminished OAE amplitudes can be associated with high frequency HL, so TEs may just be more sensitive to HL because the HL is undetected on the normal audiogram (off-frequency instead of on-frequency HL)
3) aging
- –some studies show OAEs dimish with age, and with control for hearing thresholds, age-related changes in OAEs may be due to unmeasured high frequency HL
- –or it could be metabolic factors
4) test re-test
- –for audio is 5 dB because of the step size, OAEs have smaller test-retest reliability
- –this means a small change will be considered real with OAEs where it could be interpreted as just test, re-test for audio
what type of synapse do IHCs have
ribbon synapse
what is a ribbon synapse
- a large organelle anchored to the plasma membrane
- has a number of glutamate-filled vesicles tethered to it to be released (up to 100 vesicles could be tethered)
- additional glutamate in the synaptic cleft is regulated by transporting it to neighboring supporting cells by glutamate transporters
- –it needs to be removed because if it stays in there it will keep the channels open and there will be stimulation when there is no stimulus
- —-synapse becomes desensitized and will cause excitotoxicity and the nerve will die
how many auditory nerve fibers and what percent are type 1
32,000 to 37,000 nerve fibers and 90-95% are type one
*there are 10-30 type 1 fibers synapsing with each IHC
hidden hearing loss
- cochlear synaptopathy
- loss of nerual output at the ribbon synapse of the IHC and the type 1 auditory fibers
- neural damage without permanent threshold shift and without any hair cell loss
- –starts with loss of synapse then moves to loss of neuron because if the neuron is not stimulated then it dies
- —-affects mainly low spontaneous rate neurons and remember that the lows are important for encoding speech because they saturate around 60 dB SPL
causes of hidden hearing loss (3)
- aging=loss of neural fibers/synapses
- ototoxicity-carboplatin induced= loss of IHCs, auditory nerve fibers, and synapses
- –also demyelination of the nerves
- noise exposure= ribbons do not come back after damage
underlying mechanisms to hidden hearing loss (HHL)
targets the slow spontaneous rate neurons which arre important for encoding moderate sounds such as speech and high frequency auditory nerve fibers
- –don’t really know why, but maybe because they have fewer mitochondria and smaller available pools of Ca2+ ions
- —-limited ability to manage glutamate excitotoxicity
- —-fewer glutamate transporters in the synaptic cleft to export excessive glutamate
