vestib - dysfunction: peripheral vs central

Question 1

what is VOR gain

Answer 1

eyes move opposite direction to head at same speed
- 1:1

Question 2

what is the mechanism that triggers 1:1 VOR gain

Answer 2

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

Question 3

if something is wrong w vestib system how does this impact the VOR gain

Answer 3

<1:1
- aka eye velocity < head

Question 4

what would dysfunction in the VOR present as if the head wasn’t moving

Answer 4

eyes moving to opposite side of dysfunction and then bounce back bc realize head isn’t moving bc lost object
==> results in nystagmus

Question 5

what is spontaneous nystagmus and what path is this seen in

Answer 5

eyes going into VOR and then tries to find object again

see in central path, and initially in peripheral path

Question 6

what is the purpose of a tonic firing rate and what is unique ab this vestibular system characteristic

Answer 6

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

Question 7

SCC orientation and complimentary pairs

Answer 7

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

Question 8

how does head rotation impact complimentary canal pairs

Answer 8

ipsilateral post excited
contra ant inhibited

ipsi lat excited
contra lat inhibited

Question 9

what is the push and pull arrangement

Answer 9

equal and opposite response of complimentary canals
- ipsi inc firing, contra dec firing

Question 10

what role do the stereocilia and kinocilium play in the push and pull mechansim

Answer 10

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

Question 11

what happens at head velocities >100deg/sec and what does this mean

Answer 11

inhibited nerve driven to zero at head velocities >100deg/sec

1/2 of vestib system unable to quantify head mvmt velocities >100deg/sec

Question 12

why is there an inhibitory cut-off and what does this mean in a healthy vestibular system

Answer 12

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.

Question 13

inhibitory cut-off impact in a healthy vestibular system

Answer 13

still getting input from excitatory side
- how brain knows the stim CN8 is excited
- brain perceives asymmetry and knows head is moving

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

what is a strategy to treat spontaneous nystagmus d/t unilateral vestib hypofunction from virus and when can this resolve

Answer 16

gaze fixation

occurs in absence of head mvmt and persists until CNS compensates for peripheral

Question 17

what is nystagmus, what are the types, and how is it named

Answer 17

involuntary rhythmic conjugate eye mvmt

spontaneous (no head mvmt)
gaze-evoked (end ranges)
positional (ie BPPV)

named for fast phase

Question 18

peripheral vs central nystagmus: location of lesion, presentation, trigger

Answer 18

p = end organs or nerves

c = brainstem & central connection

Question 19

peripheral vs central nystagmus: plane

Answer 19

p = mixed plane
- torsional, combined w horizontal or vertical

c = pure persistent vertical, torsional, or horizontal

Question 20

peripheral vs central nystagmus: presentation

Answer 20

p = slow phase eye mvmt (VOR) in one direction and fast phase saccadic “reset” back towards primary position

c = pendular (oscillate at equal speeds)

Question 21

peripheral vs central nystagmus: trigger

Answer 21

p = perceived head mvmt

c = disruption of central VOR pathways which are consistent w directions of head mvmt

Question 22

peripheral vs central nystagmus: impact of gaze fixation

Answer 22

p = dec w fixation

c = doesn’t dec w fixation

Question 23

peripheral vs central nystagmus: impact of gaze direction

Answer 23

p = non-direction changing w gaze direction, will always beat away from affected side

c = usually direction changing toward gaze direction

Question 24

peripheral vs central nystagmus: duration of sx

Answer 24

p = spontaneous horizontal nystagmus usually resolves w/i 3-7 days once CNS compensates or peripheral path resolves/quiets down

c = spontaneous nystagmus typically chronic and may not resolve

Question 25

what are the slow vs fast phases of nystagmus

Answer 25

slow = VOR fast = saccadic reset

Question 26

what is central adaptation secondary to peripheral vestib dysfunction

Answer 26

CNS recognizes peripheral issue and adapts via compensatory mechanisms - not dependent on therapy, resolves spontaneously

Question 27

how long can it take for central adaptation secondary to peripheral vestib dysfunction

Answer 27

up to 72hrs

Question 28

how is the CNS able to compensate for peripheral vestib dysfunction

Answer 28

utilizes other sensory inputs as reference point - inc somatosensory and visual input likely changes in levels in vestib nuclei to give input to rebalance cerebellum

Question 29

what is a consideration about components contributing to VOR function

Answer 29

secondary reflexes contribute to VOR

Question 30

vertigo = sx or dx

Answer 30

sx

Question 31

what is vertigo and how is it often described

Answer 31

illusory sensation of motion rotational, translational, tilting of self/environment "room spinning"

Question 32

what is dizziness and sx, and what can it be attributed to

Answer 32

nonspecific term that describes altered orientaiton in space sx: lightheadedness, flainting, floating, waving, imbalance vestib, CV, cerebrovascular, metabolic, meds

Question 33

what is dysequilibrium and what can it be associated with

Answer 33

inability to maintain upright posture -> can result in phenomenon known as lateropulsion or retropulsion can be associated w non-vestib problems/CNS such as dec somatosensation or weakness

Question 34

what are 9 common vestib disorders /conditions

Answer 34

BPPV** peripheral vestib hypo uni** vestib loss (B) meniere's dz central vestib disorders head trauma cervicogenic dizziness migranous vertigo vertebro basilar insufficiency