Auditory Pathways Flashcards
Where do the cochlear nerve fibers go when reaching the cochlear nucleus?
- The fibers enter @ cerebellopontine angle and split into ascending and descending bundles:
a. Ascending bundle –> synapse at anterior part of anterior cochlear nucleus
b. Descending bundle –> synapse at posterior part of anterior cochlear nucleus and posterior part of posterior cochlear nucleus
Monaural Tract
- Information about sounds at a single ear
- Fibers from the posterior cochlear nucleus travel contralaterally via the posterior acoustic stria to the lateral lemniscus –> inferior colliculus –> brachium of inferior colliculus –> medial geniculate nucleus in thalamus –> primary auditory cortex
Binaural Tract
- Manages info about differences b/w sounds @ both ears by central pathways that receive, compare and transmit input
1. Fibers from anterior cochlear nucleus travel either:
a. directly to the ipsilateral superior olivary complex
b. to contralateral superior olivary complex via trapezoid body
2. Superior olivary complex
a. Medial superior olivary nucleus - interaural time differences
b. Lateral superior olivary nucleus - interaural intensity differences
3. Superior olivary complex –> lateral lemniscus:
a. Posterior nucleus of lateral lemniscus - receive fibers from lateral superior olivary nucleus and also sends fibers to central nucleus of contralateral inferior colliculus
4. Lateral lemniscus –> inferior colliculus
a. Central nucleus of inferior colliculus - also sends inputs to contralateral inferior colliculus via commissure of inferior colliculus
5. Inferior colliculus –> brachium of inferior colliculus –> medial geniculate nucleus in thalamus –> primary auditory cortex
Central deafness
- Caused by damage to central pathways (e.g. nuclei) which disrupts the crossing fibers
- Can hear sound but unable to process specifics about the sound (e.g. difficulty processing where sound coming from and differentiating it)
- Rarely results in ipsilateral deafness
Sensorineural deafness
- Caused by damage to cochlea or cochlear root of CN VIII –> antibiotics (MC aminoglycosides), tumors, repeated exposure to loud noises
- Ipsilateral deafness of structure affected
Conduction deafness
-Caused by obstructed, or altered, transmission of sound to tympanic membrane or through ossicle chain of middle ear (more anatomic causes) –> damage to pinna (cannot conduct sound properly), excess ear wax, damage to tympanic membrane
Blood supply to: cochlea and auditory nuclei of pons and medulla
Basilar artery
Blood supply to: inner ear and cochlear nuclei
Internal auditory (labyrinthine) artery (typically branch of AICA)
Occlusion of internal auditory (labyrinthine) artery results in
- Monaural hearing loss
- Can damage fibers of CN VII and pontine gaze center
- Pt presents w/ monaural hearing loss w/ ipsilateral facial paralysis and inability to look toward side of lesion
Blood supply to: superior olivary complex and lateral lemniscus
Short circumferential branches of basilar artery
Blood supply to: inferior colliculus
Superior cerebellar and quadrigeminal arteries
Blood supply to: medial geniculate bodies
Thalamogeniculate arteries
Blood supply to: primary auditory and association cortices
Branches of M2 segment
Motor aprosodia
- Due to lesion of the non-dominant hemisphere (typically RT) in area analogous to Broca’s (area allowing us to add non-verbal meaning to speech such as sarcasm or emotional significance)
- Pt still able to feel the emotions that they want to add to their speech but can’t verbally express it (teacher who can’t yell at students when angry)
Sensory aprosodia
- Due to lesion of the non-dominant hemisphere (typically RT) in area analogous to Wernicke’s (area allowing us to comprehend non-verbal meaning to speech such as sarcasm or emotional significance)
- Pt unable to understand non-verbal cues in speech
Language Pathway
- Primary auditory cortex - differentiates where sound is coming from and when sound is being heard (transverse temporal gyrus)
- Auditory association cortex - classifies what the sound is w/ visual and somesthetic info via assistance from primary auditory cortex (superior temporal gyrus)
- Wernicke’s area - comprehending what is being said
- Arcuate fasciculus - connects Wernicke’s to Broca’s area
- Broca’s area - instructions for speech output based on info received from Wernicke’s, determines how you want to respond to information received
- Motor cortices - send information to speech muscles to move accordingly
Auditory agnosia
- Inability to describe a sound but pt can still perceive they are hearing a sound (e.g. Pt may hear instrument played but describe it as a car horn to you. However, they still cannot confidently say it is a car horn they heard)
- Caused by b/l lesions to anterior superior temporal lobes (predominantly the auditory association cortex)
Broca’s Aphasia
- Expressive aphasia in which the pt experiences difficulty in turning concept/thought into meaningful sounds (feeling of word at tip of their tongue), difficulty writing and cannot repeat words back to you
- Frustrating b/c comprehension of speech is intact
- Typically use short phrases and leave out nonessential words, responding w/ “um”, “yes”, “no”
- Caused by tumors and occlusions of frontal M4 branches
Wernicke’s Aphasia
- Defect in comprehension of speech, unable to understand what is said to them, unable to read (alexia), unable to write comprehensible language (agraphia), display fluent paraphasic speech (lots of words w/o meaning) and unable to repeat words back to you
- Caused by occlusion of temporal and parietal M4, as well as, hemorrhages into thalamus that extend lateral and caudally, invading the subcortical white matter
Global Aphasia
- Virtually complete loss of language comprehension and speech
- Caused by occlusion of LT ICA or proximal M1, damaging Broca’s and Wernicke’s areas
Conduction Aphasia
- Normal comprehension, fluent speech but pt struggles translating what someone has said to him/her in appropriate reply (unable to repeat words back to you)
- Caused by interruptions of the arcuate fasciculus which links Broca’s to Wernicke’s area
Transcortical (pericentral) motor aphasia
- Contralateral paresis and expressive language deficits similar to Broca’s BUT ability to REPEAT is maintained (mild Broca’s aphasia)
- Caused by anterior watershed infarct (ACA and MCA region)
Transcortical (pericentral) sensory aphasia
- Partial visual field deficit and receptive language deficit similar to Wernicke’s BUT ability to REPEAT is maintained (mild Wernicke’s aphasia)
- Caused by posterior watershed infarct (MCA and PCA region)
Mixed transcortical aphasia
-Similar to global aphasia but more mild in that there is some expressive and some comprehension deficits BUT ability to REPEAT is maintained
Function of Broca’s area
- Brodmann areas 44 and 45
- Production of language (spoken, written, signed)
- Works w/ frontal lobe which adds syntax, grammar and higher order motor aspects of speech
Function of Wernicke’s area
- Brodmann areas 39 and 40
- Comprehension of language (spoken and signed)
- Works w/ parietal and temporal lobe which add lexicon (vocab) and attaching sounds to their meaning
Function of the Arcuate fasciculus
- Connecting network b/w Broca’s and Wernicke’s areas
- Allows combination of speaking coherently, understanding what is being said to us and then responding appropriately
Function of the area analogous to Broca’s (non-dominant hemisphere)
- Producing non-verbal communication (our own prosody of speech)
- Tone of voice, normal melodious intonation of speech that helps convey meaning, imparting significance to language
Function of the area analogous to Wernicke’s (non-dominant hemisphere)
-Comprehending non-verbal communication (someone else’s prosody of speech - e.g. Tone of voice, normal melodious intonation of speech that helps convey meaning, imparting significance to language)
