Auditory I-III - Tollin Flashcards

1
Q

What is the human range of hearing (Hz)?

At what dB level does hearing damage occur?

dB SPL = (formula)

A sound with 100x the reference pressure (Pref) would be how many dB?

A

20 - 20,000 Hz

120dB

dB SPL = 20log10(P1/Pref) **Pref = 20 uPa (micropascal)

100x Pref = 40 dB [20log10(100)]

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2
Q

What is seen with a deficit in Broca’s area? Wernicke’s? Which Broadmann area is associated with each of these?

A

Broca - can’t speak properly (44, 45)

Wernicke - can’t understand speech (Broadmann 22)

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3
Q

From the inferior colliculus, excitatory projections proceed ___ (ipsilaterally/contralaterally) to which structure?

Where do they go from there?

A

ipsilaterally to the auditory portions of the thalamus, the medial geniculate body (MGB)

From the MGB, fibers are sent to the amygdala and the primary auditory cortex (Broadmann’s area 41)

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4
Q

Describe the tonotopic organization of the primary auditory cortex.

Where is the primary auditory cortex located? The secondary auditory cortex?

A

Lower frequencies are located anteriorly, higher frequencies posteriorly.

The primary auditory cortex is located in the lateral sulcus. The secondary auditory cortex surrounds it, and includes Wernicke’s and Broca’s areas.

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5
Q

What are ITDs? What information do they provide?

A

Interaural Time Delays. Spacial separation of the ears allows localization of sound based on time difference between the ears.

Good for localization of low frequency sounds (below 1500 Hz, where “phase locking works best”).

[The maximum ITD in humans is ~800 μs, but differences as small as 10μs can be detected (eg the width of a thumbnail at arm’s length)]

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6
Q

What are ILDs? What information do they provide?

A

Interaural Level Delays. These are primarily useful in spatial localization of high frequency sounds.

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7
Q

What are monaural shape cues? What information do they provide?

A

Primarily useful for vertical localization of sound. Basically the brain learns how the pinna reflect sound, allowing up/down and front/back localization.

[Most effective for high-frequency sound whose wavelength is similar in amplitude to the size of the pinna. People with hearing loss (esp presbycusis) struggle with elevation-based sound localization]

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8
Q

ITDs are processed in the ______.

A

MSO (Medial Superior Olive)

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9
Q

ILDs are processed in the ______.

A

LSO (Lateral Superior Olive)

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10
Q

What is the break point (in Hz) between high frequency and low frequency sounds (for the purpose of this exam)?

A

Below 1000 Hz (1 kHz) is considered low-frequency.

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11
Q

Describe the pathway by which low-frequency sounds are localized and communicated through the cochlea to the cerebral cortex.

A

From the cochlea, axons reach the AVCN (medulla) and synapse. From the AVCN, axons project to the MSO (this is where the time delay processing occurs, based on the time delay from the contralateral side). From the MSO, axons proceed rostrally to the IC and the DNLL. The IC sends ipsilateral axons to the MGB, which relays them to the cortex (or the amygdala).

MGB (Medial Geniculate Body)
DNLL (Dorsal Nucleus of the Lateral Lemniscus)
IC (Inferior Colliculus)
MSO (Medial Superior Olive)
AVCN (Anteroventral cochlear nucleus)
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12
Q

Describe the pathway by which high frequency sounds are localized (360, not vertically), and communicated through the cochlea to the cerebral cortex.

A

From the cochlea, axons enter the AVCN (medulla) and synapse. From the ipsilateral AVCN, axons project directly to the LSO. From the contralateral AVCN, axons project first to the MNTB (Trapezoid body, the “synapse of Held”), where they synapse and become an inhibitory signal. From MNTB these inhibitory axons reach the LSO. Because the signal is received ipsilaterally, the axons must immediately cross midline (for the simple reason that basically the entire brain processes contralateral information) and send projections to the contralateral IC and DNLL. The IC sends ipsilateral axons to the MGB, which relays them to the cortex (or the amygdala).

MGB (Medial Geniculate Body)
DNLL (Dorsal Nucleus of the Lateral Lemniscus)
IC (Inferior Colliculus)
AVCN (Anteroventral cochlear nucleus)
LSO (Lateral Superior Olive)
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13
Q

Unilateral lesions in the IC or above result in deficits in sound source localization for sources (ipsilateral or contralateral) to the lesion?

The IC is heavily innervated by neurons from both ears. Will unilateral lesions at the IC or more central result in unilateral deafness?

A

Contralateral

No.

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14
Q

What is the pathway for localization of elevation cues?

A

Cochlea–> Dorsal Cochlear Nucleus (DCN, right next to the AVCN)–> IC

[only discussed briefly in lecture, not addressed in the handout]

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15
Q

The response of spiral ganglion cells to high frequency sound is determined by ______, while for low frequency sounds (below 1 kHz) it is determined by the ______.

A

which spiral ganglion cells respond maximally

temporal pattern of action potential firing.

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16
Q

What is the phenomenon of “phase locking”? What cells are responsible?

A

Hair cell receptors depolarize at peak displacement, which creates regular (ie non-erratic) APs. This allows differentiation of low-frequency sounds based on rate.

[Note: the hair cell may not depolarize with each oscillation, based on the chart in the lecture slide, but it won’t depolarize faster than the Hz rate of oscillation]

17
Q

What is the “characteristic frequency” as it relates to an auditory nerve fiber (ANF)?

Low yield.

A

The frequency at which a particular cell is responding maximally. Can be plotted on a “frequency tuning curve.”

[16kHz was the example given in lecture]

18
Q

Which is more richly innervated, IHC or OHC? Why?

A

IHC are much, much more heavily innervated. They carry the afferent impulses from the cochlea (sound transducers). There are many because louder sounds can recruit more neurons (kind of analagous to muscle).

19
Q

Which end of the cochlea is defined as the base? What frequency sound does the base sense? The apex?

What is the fancy-pants term for this setup?

A

Base = end near the oval and round windows. Here, the basilar membrane is thinner, narrower, and more tightly strung, so it senses higher frequencies.

The apex is opposite, and is wider, thicker, and floppier.

This is termed the “tonotopic map.”

20
Q

Which cells are responsible for turning physical vibrations into electrical impulses?

A

The IHCs. There are ~3500 of them.

21
Q

What is the major cause for congenital deafness? Is this considered sensorineural or conductive deafness?

A

Deafness is caused by an inability of the body to maintain the endocochlear potential (not enough K+ in the endolymph).

[Notes: A mutation in the gap junction subunit connexin 32, which is important in active transport of potassium in the stria vascularis, is the major cause of congenital deafness.]

22
Q

Which compartment(s) of the cochlea contain endolymph vs perilymph? What is the orientation of the IHC relative to these compartments?

A

The scala media contains endolymph.

The scala vestibuli and scala tympani contain perilymph.

IHC cells have their apical (ciliated) side facing the endolymph, and the basal side facing the perilymph.

23
Q

Are the cation channels on IHCs ligand gated?

A

NO! They are mechanically-gated channels.

24
Q

While the term “tip links” sounds like something Phil Mickelson would ask his caddy for, it turns out they are a real feature of your cochlea. Wtf are they?

A

Tip links connect the mechanical gate of the cation channel on one cilia to the top of the next cilia. When the cilia sway towards the tall side, the channels open (depolarize), and when they sway towards the short side, channels shut (hyperpolarize).

An analogy might be that at a football game, every time the crowd does the “wave” the clown behind you grabs your hat. You can’t reach it because he’s taller than you. When he sits down, he puts the hat back on your head.

25
Q

Does the hair cell membrane potential follow the rate of the basilar membrane vibration (ie does a 700 Hz sound result in a 700 Hz oscillation of the membrane potential)?

A

Yes, to a point. Above 3000 Hz, you simply get a “large depolarization.”

26
Q

At its basal end, the hair cell is contacted by afferent, auditory nerve fibers (part of the cranial VIIIth nerve), whose cell bodies are located in the _____. These send an axon centrally to terminate on cells in the cochlear nucleus of the brainstem.

A

spiral ganglion

27
Q

There are 2 types of ANF (Auditory Nerve Fibers), Type I and Type II. Of the 30,000 nerves, what percent constitute each type?

What differentiates the fiber types in terms of location and function?

Which are myelinated?

A

Type I contact IHCs, and comprise 95% of the ANFs. They are myelinated.

Type II contact OHCs, and comprise the remaining 5%. They are unmyelinated.

IHCs act as sound transducers - that’s why there are so many of them.
OHCs are thought to respond to efferent stimuli from the central auditory system.

28
Q

What is the function of the OHCs?

A

When you think OHC, think “cochlear amplifier.”

OHCs respond to efferent stimuli (rather than sound transduction). In response to voltage changes, these cells increase/decrease in length, which increases the cochlea’s sensitivity to sound by moving the BM.

They are also innervated by MOC (Medial Olivocochlear neurons), which serve to “tune” the BM. Recall that each OHC responds maximally to a given frequency. The MOC stimulates the OHC such that resonance in the BM is maximized. (Not sure how this differs from the first “efferent” stimulus, but it’s in the notes).

[In lecture he used the example that cadavers can’t hear, (ie the mechanics of the BM can’t explain the exquisite sensitivity of the ear, particularly to low frequency sound).]

29
Q

Why is the cochlear amplifier important clinically?

A

Loss of OHCs is a major source of sensorineural deafness.

This can be measured by the presence/absence of Otoacoustic Emissions (OAE), which are produced when the tympanic membrane acts as a speaker. These can be spontaneous sounds or “echos” of sound stimulus.

Used to test for sensorineural deafness in infants.

30
Q

What things mentioned in class can damage the OHCs? (4 categories)

A

Gentamycin, Streptomycin

Cisplatin, Carboplatin

Aspirin

LOUD NOISES!

31
Q

Do IHCs fire action potentials?

A

Nope. Remember they depolarize/hyperpolarize, which sends a regular series of impulses through a given ANF (Auditory Nerve Fiber).

This is the concept of “characteristic frequency” which can be plotted on a frequency tuning curve.

32
Q

Describe the concepts of “rate coding of intensity” and “temporal coding of timing (ie phase lock)”.

A

Intensity of sound is communicated by increased rate of firing.

Temporal coding is how pitch is communicated (phase lock, fires only at a certain point during the waveform).

This is plenty confusing because both intensity and pitch are coded by the rate of APs. However at a given frequency of sound, you will have more frequent APs from a louder stimulus than from a quiet stimulus at the same pitch. (SO at a frequency of 1000 Hz, with low intensity, you will fire maybe 100 AP/sec, but at high intensity you might fire 150 AP/sec, but all “in rhythm” with the pitch.)

This is maximized if the stimulated ANF is operating at its characteristic frequency.

33
Q

How can a loss of phase locking lead to an inability to understand speech? What is this called?

Low yield

A

This is mentioned in the notes as a “rare type of sensorineural hearing disorder, not necessarily accompanied by hearing loss: auditory neuropathy.”

The audiogram and OAE would be normal in this case.

34
Q

Where are the Ventral Cochlear Nucleus (VCN) and the Dorsal Cochlear Nucleus (DCN) found?

A

Dorsal and lateral aspects of the inferior cerebellar peduncle.