Auditory and vestibular systems Flashcards

1
Q

Auditory pathway N1

A
  • Neuron 1 are bipolar neurons located in the spiral cochlear ganglion of the inner ear
  • Dendrites contact hair cells in organ of Corti in the cochlea and axons converge to form the cochlear part of CN VIII
  • Cochlear and vestibular parts of VIII joint and travel thru petrous part of temporal bone to the internal auditory meatus to enter the brain stem at the pontomedullary junction (cerebellopontine angle) lateral to VII
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2
Q

Auditory pathway N2

A
  • N2 is in the dorsal and ventral cochlear nuclei in the medulla at the pontomedullary junction, the nuclei are wrapped around the inferior cerebellar peduncle
  • Most of the axons from the ventral and dorsal cochlear nuclei decussate in the lower part of the pons to the contralateral side as the trapezoid body
  • Contralateral axons ascend in the lateral lemniscus (LL) to the inferior colliculus in midbrain
  • There are a number of nuclei along this pathway which contribute axons to LL to make the pathway to the inferior colliculus a bilateral system
  • Therefore innervation from N2 to inferior colliculus is bilateral, but predominantly contralateral
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3
Q

Auditory pathway N3

A
  • The multisynaptic and bilateral aspects of the pathway result in spatial mapping of the auditory input by detecting differences in intensity and time delay
  • After synapsing in inferior colliculus, axons enter the brachium of the inferior colliculus to reach the medial geniculate nucleus of the thalamus (MGN- N3)
  • Axons from MGN form auditory radiations that pass thru the sublentiform part of the posterior limb of internal capsule to end in primary auditory cortex of superior gyrus of temporal lobe
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4
Q

Association cortices of audition

A
  • From the primary auditory cortex in superior gyrus of temporal lobe, neurons project to adjacent areas of the superior temporal gyrus (lateral aspects) which are the auditory association areas
  • These areas interpret, discriminate, and localize sounds
  • From the association areas, axons project to multimodal association cortex (primarily the inferior parietal lobule)
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5
Q

Summary of auditory pathway

A
  • Auditory pathway is multisynaptic, and bilateral beyond the cochlear nuclei (in upper medulla)
  • Each auditory cortex receives info from both ears (bilateral innervation), with greater input from the contralateral ear
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6
Q

Lesions in auditory pathway

A
  • Unilateral CNS lesions beyond cochlear nuclei do not result in significant hearing loss, except for some decreased hearing in contralateral ear
  • Most significant hearing loss is due to problems in middle or external ear (conduction deafness), organ of corti, or CN VIII anywhere along its path before entering the brainstem (sensorineural deafness)
  • Both conduction deafness and sensorineural deafness will always be ipsilateral to lesion (b/c happens before cochlear nucleus)
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7
Q

Conduction deafness

A
  • Can be due to wax in external ear, ruptured tympanic membrane, fluid in middle ear and otosclerosis
  • Causes ipsilateral substantial/complete loss of hearing
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8
Q

Sensorineural deafness

A
  • Can be due to aging, from ototoxicity of drugs, exposure to chronic loud sounds, or compression of VIII
  • Ex: vestibular schwannoma, which can occur at the internal auditory meatus and compress VIII, can lead to tinnitus, vertigo, and nystagmus on top of progressive hearing loss
  • Sensorineural deafness produces ipsilateral significant/complete hearing loss
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9
Q

CNS auditory lesion

A
  • Does not result in significant hearing loss, only slight decrease in hearing for contralateral ear
  • Occurs after the cochlear nucleus and thus the pathways for both ears are bilateral, with more info to auditory cortex from contralateral ear
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10
Q

Vestibular pathway 1

A
  • N1 is bipolar neurons of vestibular ganglion, their dendrites contact vestibular receptors in membranous labyrinth and axon converge to form vestibular part of CN VIII
  • VIII enters brainstem at pontomedullary junction after leaving the internal auditory meatus
  • Axons synapse in the vestibular nuclei, and some enter the vestibulocerebellum (flocculonodular lobe) via ICP
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11
Q

Vestibular pathway 2

A
  • N2 is in the vestibular nuclei (floor of fourth ventricle) which is just inferior and medial to the cochlear nucleus
  • Axons from vestibular nuclei primarily connect w/ EOM, LMN, via vestibuocerebellar tracts
  • Axons from vestibular nucleus (after going thru vestibulocerebellar tract) enter the medial longitudinal fasciculus (MLF) to control eye movements relative to head movements
  • Vestibulospinal tracts (lateral and medial) arising from vestibular nuclei synapse on LMNs
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12
Q

Vestibular pathway 3

A
  • Lateral tract extend throughout the SC, whereas medial tract is present in cervical SC only
  • These tracts maintain balance during change in head position by adjusting tone in neck, trunk and limbs
  • Inferior cerebellar peduncle (ICP) contains bidirectional axons that connect the vestibular nucleus and the flocculonodular lobe to coordinate eye movements and balance in response to changes in head position and movement
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13
Q

Vestibulo-ocular reflex (VOR) 1

A
  • Mediates ocular responses to head movements
  • Keeps eyes focused on a target while the head turns by turning out eyes in the opposite direction of head rotation
  • This movement of the eye is the slow movement (one of the components of nystagmus)
  • Turning head to one side (left) stimulates the ipsilateral (left) vestibular nuclei
  • Vestibular nuclei send axons to each other, so activation of one vestibular nucleus results in inhibition of the other vestibular nucleus (so the activated muscles are not opposed by activation of the opposite vestibular nucleus)
  • Axons from the left vestibular nuclei synapse on the contralateral (right) nucleus of VI to activate the lateral rectus on the opposite (right) side of head turning
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14
Q

Vestibulo-ocular reflex (VOR) 2

A
  • The VI nucleus by way of MLF activates the nucleus of III on the side ipsilateral to head turning (left)
  • Together, these nuclei contract the muscles in the eye responsible for keeping both eyes stationary while the head rotates
  • The lateral rectus contralateral to direction of rotation contracts, causing the contralateral eye to move against the direction of rotation (remain in place)
  • The medial rectus ipsilateral to direction of head rotation contracts, causing the ipsilateral eye to move against the direction of rotation (remain in place)
  • Overall effect: slow horizontal conjugate eye movement to side opposite of head turning (eyes go right when head goes left)
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15
Q

Nystagmus

A
  • Normally VOR is suppressed at rest, but can be activated by a number of ways (rapidly spinning, using cold/warm water in vestibule
  • Doing these things will cause nystagmus, which has 2 components: fast and slow movements
  • The direction of nystagmus is defined by the direction of the fast movements (slow movement to the left followed by fast movement to the right: right nystagmus)
  • The slow movements are induced by the vestibular system (as described above) due to movement of endolymph in the semicircular canals
  • The fast movements are due to the FEF/PPRF correcting the slow movements since it recognizes the head is not turning
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16
Q

Anatomy of semicircular canals 1

A
  • 3 semicircular canals are attached to the central vestibule roughly 90 degrees from each other
  • Bulges in each canal near the vestibule are called the cupula
  • The hair cells have one long kinocilium at the end of the hair cell and small cilia of different heights adjacent to the kinocilium
  • When cilia bend toward the kinocilium the hair cells depolarize, when cilia bend away from kinocilium the hair cells hyperpolarize
17
Q

Anatomy of semicircular canals 2

A
  • The cilia bend based on the direction of flow of the endolymph, which always flows in the same direction (either clockwise or counterclockwise) for both ears depending on the rotation of the head (endolymph in both ears flows opposite to direction of head rotation)
  • The kinocilium/cilia are oriented in opposite directions in the two ears, meaning that when rotating in any given direction, one vestibule will be activated (the one on the side ipsilateral to direction of rotation) and one vestibule will be deactivated (the one on the side contralateral to direction of rotation)
18
Q

VOR/nystagmus based on spinning (rotary nystagmus)

A
  • By rotating the head to the right, the right vestibule is activated and the left one is inhibited, therefore activating the right vestibular nuclei
  • This causes the eyes to move (slow movements) to the left (opposite to direction of rotation) via activation of the left VI nucleus (left lateral rectus contracts) followed by activation of the right III nucleus (right medial rectus contracts)
  • The FEF/PPRF then correct this by initiating fast movements to the right (same side as direction of rotation)
  • Therefore: rotation to one direction (right) will cause nystagmus in that same direction (right)
19
Q

VOR/nystagmus based on hot/cold water (caloric nystagmus) 1

A
  • Allows for testing the right and left semicircular canals separately: water (hot or cold) is placed into the canals and the effect is observed (only the horizontal canal is activated)
  • Warm water (warmer than body temp) creates convection currents in the horizontal canal causing endolymph to move towards the ampula (similar to being spun in that direction) in that ear and activating it
20
Q

VOR/nystagmus based on hot/cold water (caloric nystagmus) 2

A
  • Cooler water (cooler than body temp) has the opposite current, and moves endolymph away from the ampula (similar to being spun in the opposite direction) in that ear and thus inhibiting it
  • The result is hot water in one ear activates the vestibule there, causing nystagmus in that direction
  • Cold water in one ear inhibits the vestibule there, allowing the other vestibule to dominate and there is nystagmus in the direction opposite to the inhibited ear
  • Pneumonic for direction of caloric nystagmus: COWS (cold opposite warm same)
21
Q

Sensations accompanied by nystagmus 1

A
  • When under the influence of nystagmus of any kind, there is a sensation of rotation, past-pointing, and falling to the side opposite of nystagmus
  • If there is nystagmus to the right (fast movements to right and slow to left), the right vestibule has been activated (or left was inhibited)
  • This is equal to being spun to the right, and being spun to the right means everything looks like it is moving to the left
22
Q

Sensations accompanied by nystagmus 2

A
  • So with a right nystagmus there is a feeling of the room spinning to the left
  • There is also a tendency to past-point to things to the left and fall to the left while there is right nystagmus
  • Sensation of spinning, past-pointing direction, and falling direction always opposite to the direction of nystagmus (and thus the side of relative vestibule activation)
23
Q

Nystagmus in unconscious pts

A
  • Conscious pts exhibit slow movements to the opposite side and rapid movement to the same side of rotation
  • In an unconscious pts w/ an intact brain stem, turning the head to one side (w/ eyes open) will produce slow eye movements to the opposite side. This is called doll’s eyes
  • Doll’s eyes indicates an intact lower brainstem, but there is no fast response b/c the FEF is not active
  • In the unconscious pt w/ a completely damage brainstem there will by no VOR and the eyes will fail to turn in the direction opposite to head rotation (doll’s eyes absent)
  • Loss of doll’s eyes suggests lower brainstem damage and ensuing loss of respiratory and CV function