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NE > Auditory Pathways (Dennis/Brian) > Flashcards

Auditory Pathways (Dennis/Brian) Flashcards

1
Q
  • fibers of cochlear nerve arise from central processes of: _____ _______
  • auditory info is received by ______ _____ by fibers in the cochlear nerve that pass through the internal acoustic meatus
A
  • fibers of cochlear nerve arise from central processes of: spiral ganglion
  • auditory info is received by cochlear nucleus by fibers in the cochlear nerve that pass through the internal acoustic meatus
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2
Q

Where do the fibers of the cochlear nerve enter the brainstem and where do they synapse?

A
  • fibers enter at the cerebellopontine angle
  • fibers split into ascending and descending bundles
  • ascending bundle: fibers synapse at anterior part of anterior cochlear nucleus (anterior ACN)
  • descending bundle: fibers synapse at posterior ACN and posterior part of posterior cochlear nucleus (posterior PCN)

(cochlear nuclei is located in the pons medulla junction, aka the upper medulla)

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3
Q

What types of cells are present in the:

  • anterior ACN:
  • posterior ACN:
  • posterior PCN:
A
  • anterior ACN: bushy cells (globular and spherical)
  • posterior ACN: octopus cells
  • posterior PCN: pyramidal cells
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4
Q

What is the function and general pathway of the monaural tract?

A
  • function: info about sounds at a single ear (routed to contralat side)

Pathway

hair cell >

spiral ganglion cell >

fibers from cochlear nerve synapse at posterior PCN and posterior ACN >

fibers decussate via posterior acoustic stria (medulla to pons) >

lateral lemniscus (some fibers synapse here at the anterior nucleus, but most continue to ascend) >

inferior colliculus (fibers synapse on central nucleus, then continue to ascend through brachium) >

medial geniculate nucleus >

primary auditory cortex

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5
Q

What is the function and general pathway of the binaural tract?

A
  • function: manages info about differences between sounds at both ears; handled by central pathways that receive, compare, and transmit this input; localization

Pathway

anterior ACN >

some fibers decussate to trapezoid body of medial lemniscus >

these fibers then travel to superior olivary complex >

some fibers from anterior ACN travel remain ipsilateral and travel directly to SOC >

(fibers in medial superior olivary nucleus (MSO) are related to time)

(fibers in lateral superior olivary nucleus (LSO) are related to intensity)

fibers from SOC project to lateral lemniscus: posterior nucleus receives fibers from LSO, also sends fibers across to contralat inferior colliculus >

inferior colliculus: central nucleus also sends inputs to the contralateral IC via the commissure of the inferior colliculus >

medial geniculate nucleus >

primary auditory cortex

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6
Q
  • deafness that occurs due to damage of central pathways
  • rarely results in ipsilateral deafness
  • usually results in difficulty processing where sound is coming from and differentiating it
A

central deafness

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7
Q
  • deafness due to damage of the cochlea or cochlear root of CN VIII
  • caused by: antibiotics, tumors, repeated loud noise exposure
  • causes ipsilateral deafness of structure affected
A

sensorineural deafness

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8
Q
  • deafness due to obstructed or altered transmission of sound to tympanic membrane or through ossicle chain of middle ear
  • caused by: damage to pinna (cannot conduct sound properly), excess ear wax, damage to TM
A

conduction deafness

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9
Q

cochlea and auditory nuclei of pons and medulla blood supply

A

basilar artery

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10
Q

inner ear and cochlear nuclei blood supply

A

internal auditory artery

(aka internal labyrinthine A., usually branch of AICA)

(occlusion results in monaural hearing loss; can also damage fibers of CN VII and pontine gaze center (horizontal gaze) > monaural hearing loss w/ ipsilateral facial paralysis and inability to look toward side of lesion)

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11
Q

superior olivary complex and lateral lemniscus blood supply

A

short circumferential branches of the basilar A.

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12
Q

inferior colliculus blood supply

A

superior cerebellar and quadrigeminal As.

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13
Q

medial geniculate bodies blood supply

A

thalamogeniculate As.

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14
Q

primary auditory and association cortices blood supply

A

branches of M2 segment of middle cerebral A.

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15
Q

What are the areas involved w/ the dominant language hemisphere?

A
  • hemisphere that controls language is the dominant hemisphere (about 95% of cases are left dominant, handedness does not equal dominance b/c it is not black and white)
  • Broca’s area
  • Wernicke’s area
  • arcuate fasciculus
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16
Q
  • Brodmann areas 44 and 45
  • production of language (spoken, written, signed)
  • also works w/ the frontal lobe which adds syntax, grammar, and higher order motor aspects of speech
A

Broca’s area

17
Q
  • Brodmann areas 39, 40, and small part of 22
  • comprehension of language (spoken and signed)
  • works along w/ parietal and temporal lobe, which add lexicon (vocab) and attach sounds to their meaning
A

Wernicke’s area

18
Q
  • connecting network between Broca’s and Wernicke’s areas
  • allows combo of speaking coherently, understanding what is being said, and responding appropriately
A

arcuate fasciculus

19
Q

What is the function and structures involved w/ the non-dominant language hemisphere?

A
  • non-dominant is typically the right hemisphere
  • responsible for non-verbal communication: tone of voice, prosody (nml melodious intonation of speech that helps convey meaning), imparting emotional sig to language
  • area analogous to Broca’s
  • area analogous to Wernicke’s
20
Q
  • responsible for producing non-verbal communication (one’s own prosody of speech)
  • allows for the ability to change tone of voice to relay emotion in speech (aka sarcasm)
  • lesion > motor aprosodia
A

area analogous to Broca’s

21
Q
  • responsible for comprehending non-verbal communication (other’s prosody of speech)
  • ability to understand sarcasm and body movements as an aspect of language
  • lesion > sensory aprosodia
A

area analogous to Wernicke’s

22
Q

What is the general pathway for language comprehension and speech?

A
  1. primary auditory cortex: differentiates where and when of sound
  2. auditory association cortex: classifies sound (w/ assistance from primary auditory cortex and visual/somesthetic info) as what it is
  3. Wernicke’s area: comprehends what is being said
  4. arcuate fasciculus: connects Wernicke’s and Broca’s areas
  5. Broca’s area: instructions for speech output
  6. motor cortices: sends info to speech muscles to move accordingly
23
Q
  • inability to identify something, but still can perceive it
  • caused by bilateral lesions to anterior superior temporal lobes of the auditory association cortex
  • individual can perceive sound, but cannot describe the sound
  • example: similar to someone talking in another language that you do not understand
A

auditory agnosia

24
Q
  • expressive aphasia: difficulty turning concept/thought into meaningful sounds, difficulty writing, no repitition
  • caused by tumors and occlusions of frontal M4 branches of middle cerebral A.
  • patients are often frustrated b/c comprehension of speech is intact
  • severe forms of condition are mute, but can swallow/breath nml
  • patients typically use short phrases and leave out nonessential words
A

Broca’s aphasia

25
Q
  • comprehension of speech aphasia: unable to understand what is said, unable to read (alexia), unable to write comprehensible language (agraphia), display fluent paraphasic speech (fluent aphasia), no repitition
  • caused by occlusion of temporal and parietal M4 branches of middle cerebral A., also by hemorrhages into thalamus (extends lateral and caudally to invade subcortical white matter)
A

Wernicke’s aphasia

26
Q
  • virtually complete loss of language
  • caused by occlusion of left internal carotid or proximal portion of middle cerebral A. (M1) > results in damage to both Broca’s and Wernicke’s
A

global aphasia

27
Q
  • aphasia caused by interruptions of the arcuate fasciculus
  • comprehension is nml, speech is fluent, patients have difficulty translating what someone said to him/her into an appropriate reply, no repetition
A

conduction aphasia

28
Q
  • mild aphasia that results in contralat paresis and expressive language deficits similar to Broca’s, except repetition is maintained
  • caused by anterior watershed infarct (anterior cerebral A. and middle cerebral A.)
A

transcortical motor (pericentral) aphasia

29
Q
  • mild aphasia that results in partial visual field deficit and receptive language deficit similar to Wernicke’s, except repetition is maintained
  • caused by posterior watershed infarct (middle cerebral A. and posterior cerebral A.)
A

transcortical sensory (pericentral) aphasia

30
Q
  • similar to global aphasia > some expressive and some comprehension deficits
  • repetition is maintained
A

mixed transcortical aphasia

31
Q

aphasia flow chart

A

NE (36 decks)

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