week 5- Vestibular system Flashcards
are vestibular cells unipolar or bipolar?
bipolar
what 2 types of information does the vestibular system provide?
How head is oriented in space Whether the head is moving
What saccade and what smooth pursuit does the left hemisphere control
Left controls smooth pursuits to the Left via the parietal occipital region, and saccades to the Right via the FEF
What would result with damage to the right FEF
right gaze preference since the left FEF is unopposed… The eyes CAN move left as part of smooth pursuit/tracking maneuver. Can also move left as part of brainstem mediated reflexive response. It is only the voluntary actions that require the FEF to be affected
compare OKN to VOR
OKN uses visual processing while VOR does not, it is a brainstem reflex and only responds to rapid input such as a jerky head reflex
in the vOR the brainstem is the slow movement while the FEF saccade is the fast return to center
Outline what would happen when a cold caloric test is applied to the R ear from the vestibular nuclei to the MLF
also indicate what caloric test could be used for
Cold water in R ear
tells brain head turned to L so eyes look right
L vestibular nuclei activated
R abducens activated to pull R eye right
L MLF to activate L oculomotor and pull medial rectus
eyes look RIGHT with left beating nystagmus
(COWS cold opposite, warm same nystagmus)
this can be used in uncouncious PTs to determine if they are brain dead, but also in concious PTs to determine if there is dysfunction at any of the above mentioned levels
In the VOR cold caloric test what would happen cerebral cortex was damaged
Brainstem ok: VOR towards cold ear is intact
Cerebral cortex impairment: Saccade back to center is impaired
Final result:VOR causes deviation of eyes towards cold ear and they stay there
Cold caloric result to right ear if brainstem is ok but right abducens axon is impaired
Brainstem ok: VOR towards right cold ear is intact BUT…
Right abducens axon impairment: right lateral rectus is impaired, right eye cannot abduct right, but left eye medial rectus is fine and left eye adducts rightwards
what axons enter at ther cerebellopontine angle
VII and VIII into the internal aucoustic canal
differentiate the Static labyrinth vs the kinetic
Static labyrinth: utricle and saccule detect linear acceleration(gravity)
- macula of the utricle is horizontal, while the saccule if verticle
Kinetic labyrinth: semicircular canals detect angular acceleration
There are 3 pairs of semi-circular canals
- Horizontal left + horizontal right
- Anterior left + posterior right
- Anterior right + posterior left
Outline the process of stereocillia activation
detect movement of endolymph –> movement toward taller one ( kinocilium ) –> increase K form the K high endolymph into the inside of the hair –> K sent out to the perilymph and ca enters to facillitate the SNARE vesicle release of GLU–> increased firing rate of CN VIII sensory (afferent) axons
there is some GLU leakage at rest
Outline some peripheral causes of vertigo
outline some central causes
outline some systemic causes
peripheral: Labyrinthitis, acoustic neuroma, BPPV, Meniere’s disease (inner ear labyrinth or vestibular nerve)
central: brainstem, cerebellum, cerebral cortex
systemic: metabolic or CV
what are some general differences that you may see in a central versus a peripheral cause of vertigo
Peripheral:
spontaneous horizontal nystagmus that occurs after 3-10 secs
doesn’t change direction
and is fatigable
auditory involvement (tinnitus, deafness), nausea, vommitting
Central:
spontaneous IMMEDIATE nystagmus
that changes direction
and in NOT fatigable
vertical nystagmus (lesion to midbrain likely due to location of vertical gaze center)
rotary nystagmus
no nausea
what is benign paroxysmal peripheral vertigo BBPV caused by
clinical indications
how do you test it
how do you fix it
Problem is that otolith have shaken loose from the static labyrinth and ended up in the semicircular canal which becomes over-stimulated –> vertigo
clinical indications: episodic vertigo
test: Dix-Hallpike: provocative maneuver
fix: Epley maneuver
what is menieres disease
cause and the clinical hallmarks
cause:
increased endolymph pressure
clinical hallmarks
violent, sudden attack, vertigo lasting 1 - several hours, tinnitus, deafness, Nausea, vomiting, Nystagmus lasting 1-2 hours per attack
what is the cause and the hallmarks of vestibular schwannoma
cause:
Schwann cell tumor originating on vestibular portion of CN 8
hallmarks:
vertigo/dizziness, nausea, nystagmus, ipsilateral facial paresis/paralysis,
loss of corneal reflex,
loss of taste (front 2/3 of tongue),
loss of salivation, tearing
hyperacusis with facial nerve nerve damage? No! overridden by deafness!
Cerebellar signs possible
Brainstem auditory evoked responses (BAER) are a very sensitive test
- You are rounding on patients during your Neurology clerkship. You meet a man who was admitted two days ago following a stroke. You note that he has paralysis of his left arm and weakness of his left leg. His tongue deviates to the left on protrusion. His eyes are deviated a bit to his right, but he can look over at you when you stand to his left and speak to him.
Occlusion of branches of which artery would best explain these findings?
Right MCA –> contra body
Right MCA –> right UMN for hypoglossal = contra tongue
Right MCA –> right FEF –> to move the eyes to the left. With this gone = remaining left FEF continues to drive the eyes to the right, resulting in a right gaze preference
You test your patient’s VOR by asking them to look at your finger that you hold directly in front of them. You then ask them to RAPIDLY turn their head to the right while continuing to focus on your finger. You then ask them to bring their head back to center and then to RAPIDLY turn their head to the left, while continuing to focus on your finger.
You observe the following:
On rapid head turn to the right, their left eye and right eye both shift left.
On rapid head turn to the left, their left eye shifts right but their right eye does not respond.
Damage involving which of the following locations would best explain these findings?
Damage to right abducens nucleus àno R LR. But the best answer would be damage to the R pontine BASE since the dorsal medial pons would include the nucleus = also MLF
what would lateral medullary syndrome result in
PICA occlusion – lateral medullary syndrome
Spinothalamic tract – contralateral
Spinal trigeminal- ipsilateral
Descending sympathetic fibers- ipsilateral horners syndrome
Nausea, vertigo limb ataxia- ipsilateral from cerebeleum inferior peduncle and vestibular nuclei
align each symptom with the correct area of dysfunction
Parkinson
ataxia
spastic gait
dystrophic
slapping
BG dysfunction- Parkinson
Cerebellar- ataxia
UMN- spastic (chronic), flaccid (acutely)
Muscle- dystrophic
Peripheral neuropathy- slapp
indicate the role of the rubrospinal tract
tectospinal tract
reticulospinal
vesticulospinal
rubrospinal tract: excites distal flexors
tectospinal tract :Turn head to a stimulus
reticulospinal: Feed forwardàPostural adjustments in anticipation of voluntary movements to maintain balance & stabilityby axial muscles and proximal limb extensors
vesticulospinal: Feed back àActivated by fast movements such as slipping, NOT star gazing
where are the cell bodies of the
rubrospinal tract
tectospinal tract
reticulospinal
vesticulospinal
rubrospinal tract: red nuclues of midbrain (right below STN and above SN
tectospinal tract: tectum of the midbrain
reticulospinal: pons and medulla
vesticulospinal: pons and medulla
where does the vestibulospinal tract send projections to and from
Receives projections from:
§ Flocculonodular lobe of cerebellum
§ Static and Kinetic labyrinths via CN VIII
§ Contralateral vestibular nucleus
§ Spinal cord (proprioception)
oProjects to
§ Cerebral cortex via thalamus
§ Flocculonodular lobe of cerebellum
§ Contralateral vestibular nucleus
§ Spinal cord
- Alpha and gamma MNs via MVST
- Ipsilateral limb extensors via LVST
Adjusts head, eye coordination and excites limb extensors
integrate informationabout the position of the head in space (via the labyrinth) AND the position of the body (via proprioception
Lean to the LEFT–>
Excite LEFT labyrinth –>
LEFT CN VIII –>
excites LEFT Vestibular nucleus –>
LEFT lateral VST –>
LEFT side extensors
describe Decorticate and decerebrate posturing
Decorticate and decerebrate posturing= both tell you that only the brainstem is working
Decorticate
Flexor bias in limbs because lesion is above the midbrain red nucleus so it cannot provide feedback
Decerebrate
Lesion between red nucleus and vestibular nucleus which means loss of flexor bias now BUT the vestibular nucleus can now do what it wants without overtone = extension of arms and legs
