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LCRS Neuro > Vestibular Pathophysiology > Flashcards

Vestibular Pathophysiology Flashcards

1
Q

what are the two labyrinth organs

A

1) semicircular canals

2) otolith organs

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2
Q

what stimulates the semicircular canals?

A

stimulated by angular acceleration (dynamic equilibrium)

- gives signal of approx angular velocity

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3
Q

what stimulates the otolith organs?

A

stimulated by linear acceleration and gravity force

gives signal of head acceleration and tilt

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4
Q

what are 5 uses of the signals produced by the labyrinth organs?

A
  • control balance
  • provide spatial reference for other motor actions
  • provide compensatory reflexes
  • provide proprioception
  • tune CVS for re-orientations
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5
Q

what is the result of dysfunctional control of balance and spatial reference ?

A

ataxia

“instability of gait and posture”

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6
Q

what is the result of a loss of compensatory reflex production?

total loss and unilateral loss

A

a total loss leads to oscillopsia (objects oscillate)

unilateral loss leads to nystagmus (involuntary eye movement)

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7
Q

what is the result of proprioception dysfunction”

A

dizziness

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8
Q

what is the result of not tuning the CVS to re-orientations?

A

hypotension

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9
Q

3 types of vestibular disorders?

A

structural- destructive or irritative disease

functional- misinterpretation of sensory input, maladaptation, loss of rules of correspondence

both- structural disorder provoking chronic dysfunction

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10
Q

6 types of disruption to the vestibular system

A

1) vertigo
2) vestibular ataxia: instability of gait and posture
3) vestibular nystagmus
4) oscillopsia
5) motion sickness
6) acute phase of vestibular loss

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11
Q

what is vertigo?

time scales of vertigo

A

false perception of movement in space.

  • Can last anywhere between seconds and minutes
  • most common possibly due to vertebrobasilar insufficiency (migraine)
  • Seconds due to BPPV
  • Hours of vertigo caused by Meniere’s syndrome.
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12
Q

how would you differentiate the causes of vestibular nystagmus and oscillopsia?

A

VN: caused by unilateral vestibular lesions

Osc: caused by Bilateral vestibular lesions

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13
Q

what is motion sickness?

A

loss of co-ordination on directional reorientation, oversensitivity to visual motion in the environment.

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14
Q

what is acute phase of vestibular loss?

A

slight impairment of orthostatic control –> severe nausea and vomiting.

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15
Q

what are the two components of the otolith organs?

A

utricle (horizontal)
saccule (vertical)

omnidirectional organs
used in static equilibrium i.e. linear acceleration

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16
Q

what is the function of the utricle

A

senses movement in the horizontal plane

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17
Q

what is the function of the saccule

A

senses movement in the vertical plane

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18
Q

what features of the otolith leads to the pulling of hair cells?

A

otoconia (layer of calcium carbonate) sits on a gelatinous layer
this is heavy so movements of the head displace the otoconia and therefore pulls hair

linear acceleration all moves the heavy otoconia layer

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19
Q

movement in reaction to kinocillium

A

movements towards it leads to stimulation of the hair cells (there is one per hair cell)

when there is movement away from it, the cell is not stimulated

20
Q

what do the 3 semi-circular canals link to?

what does this structure contain?

A

they connect to an ampulla

the ampulla contains a capulla full of hair bundles

21
Q

what needs to happen to the ampulla to fire off APs in from the hair cells?

A

endolymph needs to be displaced in the canals

this moves the ampulla and fires of the APs

22
Q

what is the effect of linear acceleration on the ampulla in terms of net movement?

A

there is an equal force on each side of the ampulla

so there is no net movement

23
Q

how does depolarisation occur in the ear in the direction which the head turns into?
what happens in the opposite ear?

A

with a left turn, the movement is towards the kinocilium in the left ear, but it is away from the kinocilium in the right ear.

There will be depolarisation in the left ear as hair cells are stimulated.
There will be hyperpolarisation (inhibition) in the right ear

24
Q

process of AP firing at rest

A

constant tonic firing at rest

25
Q

pathway of vestibular projections

A

via the thalamus into tempera-parietal cortex

26
Q

what is the role of the vestibular projections

A

regulate perception of motion in space

27
Q

what happens to signalling in an unilateral lesion?

A

the tonus of the intact canal gives a signal as if the head is rotating to the intact side

the other side has lost its intrinsic tone

28
Q

Benign, Paroxysmal Positional Vertigo (BPPV)

A

Debris causing false stimulations:
Accounts for a 1/3rd of all incidences of vertigo and is caused by otoconial debris in the canals.

BPPV is TRANSIENT and provoked by head movement.

Debris floating in the canals stimulates the ampulla causing false signals of head rotation – vertigo.

–> Treated by vigorous head rotation to flush debris.

29
Q

what is the mechanism in nystagmus

A

Acute UNILATERAL vestibular disorder:

  • the unopposed tone of the intact canal causes the eyes to be driven to the lesioned side (vestibular-ocular reflex).
  • The movement is detected by the brainstem which then corrects eye position with fast movements.
  • effect minimised by visual suppression mechanisms
30
Q

pathway of the vestibular-ocular reflex

A

Superior and medial vestibular neurons project to motor nuclei supplying the extraocular muscles:

1) Axons ascend in the MLF (Medial Longitudinal Fasciculus)
2) excite the contralateral abducens (CN VI) nucleus
3) excite ipsilateral oculomotor (CN III) nucleus
4) compensatory eye movement against the direction of movement

abducens nucleus in the pons
oculomotor nucleus in the midbrain

31
Q

what is the purpose of the vestibular-ocular reflex

A

acts to maintain gaze on a selected target

when the head rotates left, the eyes rotate right

therefore continuous head rotation causes a physiological vestibular nystagmus

32
Q

what is the mechanism of oscillopsia

A

Loss of vestibular function impairs eye stabilisation during rapid head movements as the VOR is the only mechanism to drive fast compensatory reflex.

33
Q

how is oscillopsia diagnosed?

A

head shaking test- so while the head oscillates, the eyes are monitored

34
Q

2 types of vestibular function loss in oscillopsia

A

attempt to correct with catch-up cascades

1) bilateral loss- eyes taken off target by head swing, multiple catch-up saccades made to regain target
2) unilateral loss- eyes remain on target on intact side, while multiple saccades occur in rotation towards lesioned side

35
Q

2 types of vestibular ataxia

A

1) Bilateral – mild gait ataxia that is worse at speed, when negotiating rough ground or when vision is reduced.
2) Unilateral – tendency for the body and head to lean and fall to the lesioned side which becomes pronounced in difficult balancing situations.

36
Q

lateral vestibulo-spinal tract pathway

A

descends ipsilaterally in ventral funiculus of spinal cord. Axons terminate in lateral ventral horn and influence motor neurons to the limbs.

37
Q

describe the medial vestibule-spinal tract pathway

A

descends bilaterally in medial longitudinal fasciculus to cervical and upper thoracic spinal cord.
Axons terminate in medial ventral horn and influence motor neurons to neck and back.

The lateral VS tract reaches lower parts of the spinal cord

38
Q

what happens in calorics?

A

Thermal stimulation of individual horizontal canals of the labyrinth.

Temperature differences between the liquid inserted and the temperature of the endolymph causes convection currents that stimulate the ampullary hair cells.

Warm water stimulates that side

39
Q

what are the caloric results?

A

o 30C (colder than BT)

  • stimulation of opposite ear
  • tonus of opposite canal drives eyes ipsilateral initially (slow phase)
  • nystagmus to opposite side (fast phase)

o 44C (warmer than BT)

  • stimulation of ipsilateral canals excited
  • eyes driven contralateral initially (slow phase opposite to direction of stimulation)
  • nystagmus to the ipsilateral side (fast phase towards stimulation)
40
Q

calorics measures

A

nystagmus duration, peak velocity and subjective sensation.

41
Q

how is calorics interpreted?

A

o Small amplitude, short duration to both hot and cold ipsilateral – canal paresis.
o Bilateral small short responses – bilateral hypofunction.
o Asymmetry of hot/cold responses – of little significance/normal.

42
Q

symptoms of acute vestibular lesions

A

Ipsilateral tilt

attempted compensation and/or an ipsilateral head tilt and skew

43
Q

treatment of acute vestibular lesions

A
  • Reassurance of patient
  • drugs (steroids, anti-virals etc)
  • treatment of associated anxiety e.g. cognitive behaviour therapy with desensitisation and physiotherapy, behavioural anxiolytic tactics
  • minimise risk factors
44
Q

primary symptoms of motion sickness

A

pallor
sweating
nausea
vomiting.

45
Q

associated symptoms of motion sickness

A 
headache
dizziness
nystagmus
instability
restlessness
drowsiness
feeling of eye strain.
46
Q

treatment of motion sickness

A

Cognitive behaviour therapy with desensitisation in SMALL doses

behavioural anti-emetic

anxiolytic (reduce anxiety) exercises.

LCRS Neuro (19 decks)

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