Auditory Sytem

Front 1

Epidemiology of hearing loss

Back 1

1 in 1500 born death
Last decade of most australian lives will be spent in silence
Social isolation (hearing aids arent good enough to understand the task of hearing and understanding)
Conitive and language delay

Front 2

Terminology

Back 2

1 cycle per second = 1Hz
amplitude relates to loudness
The greater the Fq the higher the perception of pitch.

Front 3

Normal hearing

Back 3

20-20,000Hz

Front 4

Loudness

Back 4

Loudness is a second component of sound; its perception represents the energy or level of sound pressure. We can hear over a range of 7 orders of magnitude of loudness. This ability requires a system for reducing the brain response to really loud sounds and for amplifying the brain response to really soft sounds

Front 5

Physical Attributes of Sound

Back 5

1. frequency
2. loudness (energy)
3. timing (onset, duration, change)

Front 6

Ascending Auditory Pathway

Back 6

descending pathway (not shown) modulates what ascends

Front 7

Eustachian tube and infections

Back 7

In normal adults, fluid caused by inflammation of the middle ear can be drained through the eustachian tube. In children younger than 7-8 years of age, however, the eustachian tube is often the problem. It is horizontal and narrower in children. An infection can cause swelling of the adenoids, lympth tissue, and the swelling can impinge upon the eustachian tube and prevent drainage and/or ventilation. Fluid build up in the middle ear can cause a 30-40 dB hearing loss, where sounds appear muffled, as if the speaker was under water. If the fluid build up is sufficiently bad, the ear drum can rupture and the fluids ooze. This condition is called otitis media with effusion or suppurative otitis media.

Front 8

Inner Ear Schemmatic

Back 8

4 rows of hair cells
3 outer and 1 inner

Front 9

Type I and Type II ganglion cells

Back 9

1. type I; large IHC
2. type II: small; OHCs

30,000 spiral ganglion cells on each side. 90-95% of these cells are type I and innervate inner hair cells. The remaining 5-10% are type II and innervate outer hair cells. Type I ganglion cells convey information about sound rapidly into the brain; little is known about the function of type II cells.

Front 10

What happens when the ear is exposed to loud noise??

Back 10

Acoustic overexposure: the acoustic overexposure stimulus was an octave band of noise (8-16 kHz) at 100 dB SPL for 2 hours.

Front 11

Acute Effects of loud noise

Back 11

Front 12

What really happens after loud noise?

Back 12

there is a delayed loss of spiral ganglion cells. The loss of synapses results in an absence of neurotranmitter and some other trophic factor that causes the auditory nerve fiber to degenerate. This degeneration engulfs the cell body, and eventually the entire neuron dies.

Front 13

Ratio of nerves to Hair cells

Back 13

Each inner hair cell is innervated by 20-30 type I ganglion cells; each ganglion cell innervates only a single IHC. Do the fibers differ in any way or are they homogeneous? Do they all project into the brain in the same manner?

In contrast, a single type II cell innervates multiple outer hair cells. We know nothing of their response properties.

NORMALLY we get HD sound (lots of detail with loss, like pixelation)

Front 14

Does the auditory nerve spontaneously fire?

Back 14

60% of the fibers exhibit high rates of spontaneous activity, up to 100 spikes per second. The other 40% have low rates of spontaneous activity, usually near zero.

THUS 2 different thresholds

Front 15

Arrangement in the Cochlear nucleus, brainstem...

Back 15

Enters v.orderly, layered

Black high spont
Red opposite

can implant a device directly here to bypass the cochlear nerve

Front 16

Endbulbs

Back 16

found in all vertebrates and the largest synpatic endings

secure synapses, no gitter or delay, links neuroacoustic activity (thus when audio is out of sync in amovie it drives us crazy)

Front 17

Why do we need timing precision? (answer: sound localization, speech comprehension).

Back 17

It is thought that these large synaptic endings ensure that neural activity is tightly coupled to sound. When depolarization invades the endbulb, a small prepotential can be recorded. A half millisecond later, a postsynaptic spike occurs. When the oscilloscope trace is triggered by the prepotential, there is never a failure of the postsynaptic spike. As a result, it has been concluded that this synapse is a high fidelity structure, key to preserving the precise timing of auditory events within CNS activity

Front 18

Auditory brainstem response

Back 18

Children screened with ABRs (in america screening babies)
Electrodes on the forehead and ear to imit an average response)

Front 19

Deaf cats

Back 19

- auditory nerve synpases changed
- end bulbs atrophy
- Reissner's membrane and tectorial membrane collapse

Front 20

inhibitory input to spherical bushy cells

Back 20

DEC. in deafness
- excitatory terminals remain relatively similar
- HOWEVER the inhibitory inputs are released and so we think thats why tinnutus starts up

Front 21

Synpase recovery from deafness

Back 21

The normal synapses go back to normal
Thus need to give an implant much earlier, the child becomes normal
-after 3 the synapses cant recover
Implanted these in cats after puberty and no recovery still

Front 22

HEaring loss and amplification of sound

Back 22

Hearing loss and deafness cause the brain to change. Thus, strategies to repair
hearing cannot simply rely on amplification.

Front 23

Disadvantages of Cochlear implants

Back 23

Hearing aids and cochlear implants can never replace our natural hearing. They
work best in quiet circumstances and are challenged by background noise