B7.039 Vestibular System Flashcards
bony labyrinth
space within the temporal bone of the skull base which contains the vestibular apparatus
membranous labyrinth
area filled with endolymph and surrounded by perilymph that lies within the bony labyrinth
gives input to auditory (cochlea) and vestibular (remainder of membranous labyrinth) systems
two types of vestibular receptors
- semicircular canals (kinetic labyrinth)
2. otolith organs (static labyrinth)
stimulus of semicircular canals
- dynamic stimuli (rotational forces)
2. head acceleration of deceleration
stimulus of otolith organs
- static stimuli; maintained head position (tilt)
2. translational forces; horizontal displacement
what are the otolith organs
saccule
utricle
functional pairs of semicircular canals
2 canals, one on each side of the head, that have their planes parallel
give dynamic information about rotation of the head by acting together
1. horizontal on R and L
2. anterior on R, posterior on L
3. posterior on R, anterior on L
structure of a semicircular canal
- attached to the utricle
- filled with endolymph (which is continuous from the utricle through the canal)
- ampulla on one end is an enlargement where vestibular hair cell receptors are located
- cilia of hair cells insert into a gelatinous mass called cupulla
ultimate function of hair cells
synapse with terminals of afferent axons from CN VIII
glutamate transmission
structure of vestibular hair cells
cauldron like shape with hair cells on top and synaptic vesicles at the base
1 long cilium - kinocilium
multiple smaller cilia - sterocilia
tonic discharge of hair cells
50-100 Hz
response to motion which bends cilia toward kinocilium
depolarization
increased firing rate of CN VIII afferent
response to motion which bends cilia away from kinocilium
hyperpolarization
decreased firing rate of CN VIII
adequate stimulus for semicircular canal receptors
head rotation > inertial movement of endolymph > bends cupulla and cilia of hair cell
effect of clockwise rotation on endolymph flow
counterclockwise endolymph flow
effect of cessation of clockwise rotation on endolymph flow
reversal of flow (clockwise)
effect of rightward rotation on horizontal canals of vestibular system
due to inertia, endolymph will move in opposite direction of rotation
- in the R canal: endolymph will bend the cilia toward the kinocilium > excitation
- in the L canal: endolymph will bend cilia away from the kinocilium > inhibition
barany chair test
clinical test of brainstem and vestibular function
subject rotated in a chair
chair is stopped and vestibular function is examined via VOR and vestibulo-postural reflexes
effects of deceleration (post-rotational component) are examined
3 phases in barany chair test
- acceleration to the R (rotational phase)
- increase in R CN VIII activity
- decrease in L CN VIII activity - rotation at constant angular velocity
- no effect after 30 s, endolymph has equilibrated - deceleration (post rotational phase)
- decrease in R CN VIII activity
- increase in L CN VIII activity
effect of rotation on vestibulospinal neurons
rotation to the R > increased R CN VIII firing > extensors on the R are activated
i.e. rotation to a side increases activation of extensors on that side and decreases activation of extensors on the opposing side
which direction will a patient fall after a barany chair test?
in direction of rotation
in post-rotational phase, activation switches due to shifting of equilibrium during rotation
SO if youre spinning R, youre activating your R side extensors, BUT when you stop, you start activating your L side extensors
thus, when you get up post-spinning, your L side extensors are activated and your R side are not, so you fall R
what is the vestibulo-ocular reflex (VOR)
when a subject is rotated to the right, the eyes move to the left
for this to happen, the activity of the L lateral rectus and R medial rectus must increase while the opposite muscles activity will decrease
nystagmus
slow movements opposing rotation, followed by fast reset movements
ie when turning R, slow movement to the L with a fast reset to the R
pathways of the VOR
increased CN VIII firing > increased medial vestibular nucleus firing > decreased abducens nucleus firing rate > decreased contraction of LR
AND
decreased 3rd nerve nucleus firing rate on opposite side > decreased contraction of medial rectus
internuclear ophthalmoplegia
lesions to the medial longitudinal fasciculus prevent eye from rotating medially in response to lateral rotation of opposite eye (fibers which connect abducens to oculomotor travel in MLF)
results in nystagmus
phases of nystagmus
- direction of nystagmus is names by direction of the fast phase
- slow phase is the VOR
- fast phase is non vestibular
what is a caloric test
irrigation of the canal with warm/cold water to induce physiologic nystagmus
water creates a convection current in the endolymph
warm water caloric test
produces nystagmus to the same side (fast movement toward same side)
cold water caloric test
produces nystagmus to the opposite side (fast movement toward opposite side)
vertigo
illusory feeling of spinning, falling, or giddiness with disorientation in space that usually results in a disturbance of equilibrium
what happens to balance when vestibular damage occurs
still good if you have vision
visual info can compensate for loss of both labyrinths
characterize unilateral lesions of the vestibular nerve
- CN VIII afferents have a high background firing rate
- anything that produces an imbalance of input from semicircular canals on each side will elicit vestibulo-ocular and vestibulo-postural reflexes
- a lesion on one side sets up an imbalance in favor of the opposite side
- subject tends to fall toward the side of the lesion and has nystagmus to opposite side
lesions to the L CN VIII
produces same effect as rotation to the R
imbalance in L and R CN VIII input can be more disabling than no input at all
motor functions performed by the cerebellum
- oculomotor control
- adaptive control of eye movements
- eye stability control (VOR)
- eye blink conditioning - switching reflexes on and off
- modifying the strength of reflexes
- motor learning
overall function of cerebellum
add the fine tuning to make voluntary movements and a variety of different reflexes correct in terms of strength and timing
layers of the cerebellum
midline - vermis
2 lateral lobes - cerebellar hemispheres
contents of cerebellum
cerebellar cortex and underlying cerebellar white matter
white matter contains 4 paired deep cerebellar nuclei
cerebellar nuclei
from medial to lateral: fastigial globose emboliform dentate
vestibulo-cerebellum
small structure on the caudal end of cerebellum
has vestibular connections and is concerned with equilibrium and eye movements
vermis projections
brain stem area concerned with control of axial and proximal limb muscles
cerebellar hemisphere projections
control of distal limb muscles
cerebrocerebellum
lateral portions of hemispheres
interact w motor cortex in planning and programming movements
spinocerebellum
vermis + medial hemisphere portions
receives proprioceptive info from the body
motor execution, correction of movement errorspurkinje fiber
cerebellar peduncles
attach cerebellum to the brainstem and contain pathways to and from the brainstem
inferior cerebellar peduncle
contains fiber systems from spinal cord and lower brainstem (olivocerebellar fibers from inferior olivary nucleus)
vestibular inputs
middle cerebellar peduncle
fibers from contralateral pontine nuclei
superior cerebellar peduncle
efferent fibers that send impulses to thalamus and spinal cord, with relays in the red nuclei
purkinje cells
provide primary output from the cerebellar cortex
have cell bodies in purkinje cell layer and have dendrites that fan out in a single plane
axons project ipsilaterally to deep cerebellar nuclei, where they form inhibitory synapses (GABA)
granule cells
cell bodies in granular layer of cerebellar cortex
only excitatory neurons in cerebellar cortex
send axons upward into molecular layer where they bifurcate and become parallel fibers
run perpendicular through purkinje dendrites and form excitatory synapses on the dendrites (glutamate)
inputs to cerebellum
- climbing fibers
2. mossy fibers
climbing fibers
origin from interior olivary nucleus
powerful, obligatory synapses on a small number of (1-10) of purkinje cells
collaterals to deep cerebellar nuclei
mossy fibers
from pontine nuclei and spinocerebellar tracts
make excitatory synapses with granule cells
parallel fibers of granule cells make synapses with a large number (10,000) of purkinje cells, thus most fiber influence is widely distributes
cells in the deep cerebellar nuclei
project to the thalamus which then goes to the motor cortex
other projections go to descending pathways
pukinje cell response to inputs
climbing fibers lead to all or non response
climbing fibers elicit a complex spiking pattern
mossy fiber contribution is simple and graded
feedforward model of motor control
motor cortex > motor output > cutaneous/proprioceptive afferents > sensory cortex
in between these steps, there is input related to expected output vs actual output
between these two measurements, error correction is made and fed back through the system
how does info about actual movement travel to the cerebellum
spinocerebellar tract (mossy)
how does info about intended movement travel to the cerebellum
via pontine inputs (mossy)
how does error connection signal travel from cerebellum
out through deep cerebellar nuclei to both thalamus > motor cortex and red nucleus > spinal cord
neocerebellar functional circuit (initiation and programming of movement)
limbic system > frontal cortex > pontine nuclei > cerebrocerebellum (lateral hemisphere) > dentate nucleus > ventral lateral nucleus of thalamus > motor cortex > muscles > movement
somatotopic organization of the cerebellum
spinal input is somatotopically organized
organization maintained throughout interconnections with other brain structures
vermis = trunk
cerebellar hemispheres = ipsilateral motor coordination and muscle tone
cerebellar regulation of vestibulo-postural reflexes
adds fine tuning to ensure correct amplitude, strength, and range of movement
function of VOR
allows eyes to fixate on a stationary visual target in the presence of head movement
eye movements are equal and opposite to head movements
suppression of the VOR by vestibulo-cerebellum
inhibitory activity of purkinje fibers opposes typical excitatory activity from CN VIII afferents from head movement
two inputs cancel each other out allows for eyes to move with head and leaving the firing rate of vestibular nucleus cells unchanged
other examples of motor adaptation that depend on the cerebellum
- wearing reverse prisms
- compensation for unilateral destruction of the vestibular labyrinth or cutting the vestibular nerve
- adaptations in limb movements similar to the reversing prism experiment with eye movements
- adapting to unexpected changes in external load
lesions of the vestibulocerebellum
nystagmus and disequilibrium or wavering, ataxic gait
- example is medulloblastoma in children
- also can be damaged in chronic alcoholism
cerebellar syndrome
lesions of the cerebrocerebellum and spinocerebellum
hypotonia
loss of input to gamma system
ataxia/ asynergia
lack of coordinated movements
associated with errors in metrics of movement (velocity, force, direction) and difficulty terminating movements at the desired point (dysmetria)
intention tremor or action tremor
tremor associated with voluntary movement
irregular frequency but around 10-12 cycles per second
adiadochokinesis
inability to make rapid, alternating movements (rapid pronation/supination of the hands)
decomposition of movement
complex movements involving multiple joints are not made with continuous smooth trajectories
