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Neuro III > Auditory > Flashcards

Auditory Flashcards

1
Q

Describe sound pressure waves

A

alternating compression and rarefaction of air

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2
Q

What causes amplitude/intensity to increase?

A

more forceful air compression

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3
Q

What is the equation for determining amplitude?

A

dB SPL = 20 log [P1/P2]

P2 = standard reference pressure
P1 = pressure of tested sound
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4
Q

what is the sound amplitude threshold associated with permanent hearing loss?

A

> 120 dB

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5
Q

What is frequency range compatible with human hearing?

A

20-20,000 Hz

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6
Q

What are the units of frequency?

A

measured in Hz = cycles/sec

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7
Q

Describe presbycusis

A

loss of HIGH frequency hearing, trouble hearing fricative consonants (t, p, s, f)

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8
Q

Describe auditory threshold

A

smallest amplitude (dB SPL) a person can just detect

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9
Q

How does the middle ear alleviate acoustic impedance mismatch?

A

P = F/A
Surface area of ossicles = 1/20 surface area of tympanic membrane.
Ossicle orientation –> levering action –> larger force

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10
Q

What is sensorineural hearing loss?

A

Damaged/lost hair cells and/or nerve fibers.

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11
Q

List some causes of sensorineural hearing loss

A

Excessive loud sounds, ototoxic drugs, age (presbycusis)

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12
Q

What is conductive hearing loss?

A

degraded mechanical transmission of sound energy through the middle ear

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13
Q

List some causes of conductive hearing loss

A

otitis media, otosclerosis (impeded movement of ossicles), atresia, perforated tympanic membrane, static pressure in middle ear

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14
Q

How would you distinguish conductive vs sensorineural hearing loss on exam?

A

Compare audibility of 512Hz tuning fork heard in air vs against skull.
Positive result for conductive loss: tuning fork held against bone –> sound transduction via bone –> overcome conductive hearing loss

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15
Q

Describe the physical setting of the basilar membrane

A

spans the length of the cochlea; direct contact with CN VIII axons; sandwiched between scala media and scala tympani

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16
Q

How does sound affect the basilar membrane

A

sound –> oval window compression –> oval window bulges into scala vestibuli –> fluid compression –> downward movement of basilar membrane –> bulging round window into middle ear

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17
Q

The basilar membrane has a tonotopic map. Where is it sensitive to HIGHER frequencies?

A

Near the round and oval windows. (thinner, more rigid BM)

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18
Q

The basilar membrane has a tonotopic map. Where is it sensitive to LOWER frequencies?

A

Apex of the cochlea. (Flexible, wide, thick BM)

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19
Q

What is the primary stimulus attribute mapped along the cochlea?

A

sound frequency and intensity

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20
Q

How are we able to discriminate among different frequencies?

A

Each hair cell responds best to a certain frequency

21
Q

What is the relationship between BM tonotopic map and hair cell frequency sensitivity?

A

Low frequency-sensitive BM contains low frequency-sensitive hair cells; high frequency-sensitive BM contains high frequency-sensitive hair cells

22
Q

what is the normal membrane potential of a hair cell?

A

-50 mV

23
Q

What is the hair cell response to bending of stereocilia?

A

change in membrane potential (mechanosensitive ion channels).

24
Q

What happens when stereocilia are bent in the direction of LONGEST stereocilia?

A

“tip links” pull the tops of stereocilia –> mechanical opening of ion channels –> depolarization

25
Q

What happens when stereocilia are bent in the direction of the SHORTEST stereocilia?

A

“tip links” push tops of stereocilia –> mechanical closing of ion channels –> hyperpolarization

26
Q

Describe the physical environment of stereocilia

A

Apical: bathed in endolymph from scala media (High K, low Na; maintained by active pumps on scala media)

Basal: bathed in perilymph (similar ionic composition to blood)

27
Q

What ion is responsible for deoplarization of hair cells?

A

K+ influx

28
Q

What is the endocochlear potential?

A

+80 mV (leads to K influx driving force of -130 mV)

29
Q

What happens with collapse of endocochlear potential?

A

Sensorineural deafness (due to loss of driving force for transduction)

30
Q

Name a major cause of congenital deafness

A

mutation of gap junction connexin 26. (leads to collapse of endocochlear potential due to loss of active K pump on scala media)

31
Q

What is a major difference between outer and inner hair cells?

A

OHCs = poorly innervated by auditory nerve fibers (ANFs), therefore they are not transducers

32
Q

What is the role of outer hair cells?

A

Cochlear amplifiers. OHCs attach to basilar membrane. Efferent neurons –> change in OHC length –> BM pulled toward/away from tectorial membrane –> changed mechanical frequency selectivity of BM

33
Q

What is the intensity contribution of OHCs?

A

50 dB. Damage –> sensorineural deafness

34
Q

How do ototoxic antibiotics lead to deafness?

A

blockage of transduction channels –> loss of cochlear amplifier

35
Q

How do spiral ganglion cells respond to high frequency sounds?

A

high frequency sounds activate fibers sensitive to specific frequency. Greatest sensitivity –> maximal action potential firing rate

36
Q

How do spiral ganglion cells respond to low frequency “pure tones”?

A

Auditory nerve fiber AP phase lock (APs only fire at compression OR rarefaction of sound wave) –> temporal pattern of action potential firing

37
Q

Describe the auditory pathway

A

cochlea –> spiral ganglion –> auditory nerve –> rostral medulla –> cochlear nuclei on dorsal/lateral aspects of ICP –> trapezoid body in mid pons (some decussation) –> superior olivary complex –> ascend in lateral lemniscus –> inferior colliculus (some decussation) –> medial geniculate of thalamus –> primary auditory cortex at sup temporal gyrus

38
Q

Why would a unilateral lesion rostral to the cochlear nuclei NOT lead to unilateral deafness?

A

Some axons decussate, joining the contralateral lateral lemniscus, while the rest remain at the ipsilateral lateral lemniscus

39
Q

What are the main mechanisms involved in sound localization?

A

Interaural time delays (physical separation of ears),
Interaural level differences (high frequency sound –> head creates “acoustic shadow” for far ear)
Monaural spectral shape (pinna -> localization of elevation and front/behind)

40
Q

Where and how are ITDs encoded?

A

Medial superior olive (MSO). ANFs –> excitatory input to anteroventral cochlear nucleus (AVCN) –> excitatory inputs to MSO. Differences in neural path lengths to MSO from L/R ears –> differences in conduction times –> offset by physical ITD cue

41
Q

MSO neurons are also known as:

A

coincidence detectors. Respond maximally when they receive simultaneous, bilateral AVCN stimulation

42
Q

MSO neurons encode ITDs produced by sounds from which side of the body?

A

Contralateral. ITD can compensate for longer conduction time from contralateral ear

43
Q

Where and how are ILDs encoded?

A

Lateral superior olive (LSO)

Ipsilateral ear –> ANF –> AVCN –> excitatory projection to ipsilateral LSO

Contralateral ear –> ANF –> AVCN –> decussation –> medial nucleus of the trapezoid body (MNTB) –> glycinergic calyx of Held –> inhibitory effects at LSO

44
Q

From what side of the body is sound represented in the inferior colliculus?

A

Contralateral

45
Q

How would a unilateral lesion to the inferior colliculus present?

A

contralateral deficit of sound source localization (MSO, LSO, DCN cues re-converge at inferior colliculus)

46
Q

Would a unilateral lesion to the inferior colliculus result in unilateral deafness?

A

No! IC is heavily innervated by neurons from both ears

47
Q

After passing the inferior colliculus, where do auditory fibers travel next?

A

medial geniculate body –> amygdala (auditory fear conditioning) or auditory cortex in sup temporal gyrus

48
Q

Describe the tonotopic cortical map

A

Brodmann’s area 41 (primary auditory cortex): Low frequency = anterior; high frequency = posterior

49
Q

Describe Wernicke’s area

A

Within secondary auditory cortex (surrounding primary auditory cortex). responsible for comprehension/processing of spoken language

Neuro III (17 decks)

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