vestib - dysfunction: peripheral vs central Flashcards
what is VOR gain
eyes move opposite direction to head at same speed
- 1:1
what is the mechanism that triggers 1:1 VOR gain
when move, canals polarized and CN 8 fires and velocity, direction, amp of head mvmt is transmitted and will correspond w ms pairs in eyes that will move opposite and proportional to head mvmt
if something is wrong w vestib system how does this impact the VOR gain
<1:1
- aka eye velocity < head
what would dysfunction in the VOR present as if the head wasn’t moving
eyes moving to opposite side of dysfunction and then bounce back bc realize head isn’t moving bc lost object
==> results in nystagmus
what is spontaneous nystagmus and what path is this seen in
eyes going into VOR and then tries to find object again
see in central path, and initially in peripheral path
what is the purpose of a tonic firing rate and what is unique ab this vestibular system characteristic
allows for equal and opposite signals on R and L and detects loss of function if something goes wrong
other sensory systems in body won’t be able to detect absence of input the way that vestib can d/t this
SCC orientation and complimentary pairs
ant & post canals
- vertical
- 90deg from each other
- 45 deg from sagittal
R post canal + L ant canal
R ant canal + L post canal
lateral canals
- horizontal
- 30deg inclined
R + L lateral canals
how does head rotation impact complimentary canal pairs
ipsilateral post excited
contra ant inhibited
ipsi lat excited
contra lat inhibited
what is the push and pull arrangement
equal and opposite response of complimentary canals
- ipsi inc firing, contra dec firing
what role do the stereocilia and kinocilium play in the push and pull mechansim
stereocilia arranged so that paired canals when one stim, ipsi CN excited and contra is inhibited
- happens bc of how kinocilium are moving away or toward stereocilium
what happens at head velocities >100deg/sec and what does this mean
inhibited nerve driven to zero at head velocities >100deg/sec
1/2 of vestib system unable to quantify head mvmt velocities >100deg/sec
why is there an inhibitory cut-off and what does this mean in a healthy vestibular system
The inhibited side can only decrease to zero from a resting firing rate of 70-100 spikes/second. Therefore, if movement is > than that, the inhibited side provides no additional information.
inhibitory cut-off impact in a healthy vestibular system
still getting input from excitatory side
- how brain knows the stim CN8 is excited
- brain perceives asymmetry and knows head is moving
inhibitory cut-off impact if R vestib side isn’t funtioning and what is the result and what has to potential to modulate that result
if turn head >100deg/sec to R, wouldn’t get excitatory firing
- still see inhibition in L driven down to cut-off
no signals are sent -> VOR not engaged and as head turns to R, eyes also drift to R
CNS has potential to recognize lost gaze and see corrective saccades
what is the effect on the inhibitory cut off if a virus attacking the peripheral vestib system resulting in a hypofunction at rest - describe specifically to a virus on L side
get asymmetry perceiving signals and CNS generates eye mvmt in response to perceived head mvmt
virus on L side -> tonic firing rate lower than normal -> asymmetry
- brain assumes head is turning to R when not
- see eyes move L and get spontaneous nystagmus R
- perceives head turning to be continuous so beaething occurs as trying to keep correcting i
