ocular motor control: brainstem generators Flashcards
what is the main purpose for slow eye movements
maintaining gaze in the presence of motion
what is the main purpose for fast eye movements
shifting gaze/change fixation
name the two types of binocularly coordinated eye movements
- conjugate: same direction/versions
- dysjunctive: opposite direction
list the 4 types of conjugate eye movements
- vestibular-ocular reflex (VOR)
- optokinetic reflex (OKR)
- smooth persuit
- saccades
what are the two reflex type of conjugate eye movements
- vestibular-ocular reflex (VOR)
- optokinetic reflex (OKR)
both associated with self motion, particularly they stabilise the image of the world on our two retinas when we’re moving our heads
what are the two voluntary types of conjugate eye movements
- smooth persuit
- saccades
what is the maximum speed of a slow eye movement
~50 deg/sec
what does a slow eye movement compensate for and therefore what is it’s function
self or object movement (which will cause blur and reduce acuity)
therefore function of slow eye movements reduce blur and improve acuity
list all the coordinated eye movements involved in slow eye movements and state their purpose
- VOR and OKR: head motion (self motion)
- smooth pursuit: tracking a target
- vergence: tracking a target in depth
what is the maximum speed of fast eye movements
~1000 deg/sec
what is the coordinated eye movement involved in fast eye movements and state their purpose
saccades: looking at novel stimuli, scanning objects of interest, searching for information, allows to shift gaze rapidly from one point to another function is to redirect the line of sight i.e. the fovea, quickly from one place to another
what is the function of brainstem nuclei generators
send particular patterns of impulses to the motor neurons in the trochlear, abducens and oculo-motor complex which fire to the muscles to get them to move in a particular way
name the three ocular motor neurons found in the brainstem
abducens, oculomotor and trochlear
which system are the extra-ocular muscles innervated by
infra-nuclear system, which are the cranial nerves which innervate them
which type of movements (name three) does the brainstem generator nuclei, the medial vestibular nucleus (MVN) innervate
slow conjugate eye movements: both reflex and voluntary
- vestibular ocular reflex VOR
- optokinetic reflex OKR
- smooth pursuit
how many medial vestibular nucleus (MVN) are there in the brainstem
2, one on each side of brainstem
which brainstem generator nuclei innervates, slow dysjunctive (convergence, divergence) eye movements
mesencephilic reticular formation MRF
which type of eye movement does the paramedian pontine reticular formation PPRF innervate
fast conjugate horizontal saccades
which brainstem generator nuclei innervates, fast conjugate vertical saccades
rostral interstitial nucleus of medial longitudinal fasciculus riMLF
which two brainstem generator nuclei are located very high up in the midbrain
- riMLF
- MRF
where in the brainstem is the MVN brainstem generator nuuclei for slow conjugate eye movements located
lower pons and partially in medulla
what is the basic requirement for conjugate eye movements in the horizontal direction
to simultaneously contract the synergistic lateral rectus muscle on one eye and medial rectus muscle of the opposite eye
and relax their antagonists in each eye
what is the basic requirement for conjugate eye movements in the vertical direction
to simultaneously contract the elevator muscles (superior rectus, inferior oblique) or depressor muscles (inferior rectus, superior oblique) of both eyes
and relax their antagonists in each eye
which pathway is keys for innervating eye movements binocularly
inter-nuclear pathways via the medial longitudinal fasciculus (MLF)
what does the inter-nuclear pathways via the medial longitudinal fasciculus (MLF) coordinate the activity of
ocular motor neurons that innervate binocularly synergistic muscles
what does the medial longitudinal fasciculus (MLF) contain, and what do they form connections between
contains numerous, separate tracts of heavily myelinated (fast conducting) axons
forming direct connections between oculomotor, trochlear and abducens nuclei and the brainstem generator nuclei
from where to where does the medial longitudinal fasciculus (MLF) extend
from the medulla, through the pons, to the upper midbrain
i.e. runs through the length of the midbrain
what are the two neuron types of the abducens nucleus and what do they innervate
- motor neurons (60%) innervates: the ipsilateral (same side) lateral rectus muscle
- interneurons (40%) innervates: neurons in the opposite oculomotor nucleus supplying the synergistic medial recuts via a crossed projection in the MLF
name the classic disorder caused by damage to the crossed pathways of the interneurons
inter-nuclear opthalmoplegia (INO)
manifest by weakness (paresis) of adduction of the MR ipsilateral to the lesion on attempted gaze shifts
list 6 main causes of inter-nuclear opthalmoplegia (INO)
- vascular infarcts
- brainstem tumours
- demyelinating diseases (e.g. multiple sclerosis)
- drug toxicity
- viral infection
- trauma
describe what occurs in the brainstem in order to make conjugate eye movements slow and saccades towards the left
- the axons of the motor neurons of the abducens nucleus travel straight to the left (same side) lateral rectus and activate and innervate their motor neurons, causing the left eye to look towards the left
- the axons of the interneurons cross the midline and travel to the opposite side of the brainstem through the MLF to activate and innervate motor neurons in the oculomotor complex which activate the medial rectus on the right hand side
so if you can get the motor neuron supplying the same side and interneuron supplying the motor neurons on the opposite side at the same time = conjugate eye movements for slow and saccade eye movements
what symptoms will a patient with inter-nuclear ophthalmoplegia (INO) caused by a unilateral lesion of the right MLF have
- px can move both eyes normally to the right
- shows full abduction of the left eye on leftward gaze but weakness (paresis) of adduction of the right (ipsi-lesional) eye
left eye may show instability (nystagmus) when moved outward in abduction, along with paresis of the inward eye = NO PIE (nystagmus of outward eye and paresis of inward eye)
what symptoms will a bilateral MLF damage cause
it will affect the ability of both eyes to adduct on attempted saccades
what is the name of a disorder of saccades
gaze palsy (usually make head saccades instead)
manifest by inability (reflex or voluntary) to shift bi-foveal fixation either horizontally or vertically (not both together)
why is a gaze palsy of horizontal and vertical direction both together a very rare occurrence
because the generator nuclei are in different brainstem locations (one is in the pons and one in the medulla) so rarely both get damaged together
what particular population of neurons does the PPRF and riMLF contain and what do they do
contain excitatory burst cells (EBCs)
which fire at very high frequency of up to 1000Hz just before a saccade towards the SAME side/direction
where do excitatory burst cells of the PPRF project to
project to the ipsilateral abducens nucleus
activating motor neurons to the LR and interneurons to the opposite oculomotor nucleus to the medial rectus pool
what does a unilateral lesion to the PPRF result in
loss of saccades towards the lesioned side (paralysis of ipsi-versive gaze/conjugate eye movement)
and patients make whole head saccades instead
e.g. lesion to left PPRF = can’t make left side saccades
what is the role on inhibitory burst cells (IBCs) during saccades towards the left
a separate nucleus that sits in the medulla
sends axons across the midline to inhibit the abducens nucleus on the opposite side, so that inhibitory signals are sent to the antagonistic MR and LR muscles so eye movement occurs in correct precision
what does the medial riMLF mediate
down-gaze via projections in the MLF to the ipsilateral trochlear and oculomotor nuclei
what does the lateral riMLF mediate
up-gaze via MLF projections to the contralateral oculomotor (IO, SR) nucleus, which cross the midline in the posterior commissure (PC)
what symptom can a large bilateral lesion to the riMLF in the upper midbrain cause
abolishment of all vertical saccades
what symptoms can small bilateral lesions to the riMLF in the upper midbrain cause
selectively impair up or down gaze
what lesions affects upward saccades
lesions of the lateral riMLF or posterior commisure in the upper midbrain
what pathology can cause a lesion to the posterior commisure
pineal tumour
what three (triad) conditions can occur due to lesions to the lateral riMLF or posterior commissure in the upper midbrain
= dorsal midbrain or parinaud’s syndrome
- up-gaze palsy and down-gaze is still intact
and
- convergence-retraction on attempted up-gaze: instead of looking up, the eyes converge and contract
and
- near-light dissociation: pupil constriction is absent on attempted convergence and absent in response to light
what do lesions to the medial riMLF in the upper midbrain cause
inability to make downward saccades
describe what occurs in the brainstem in order to make bilateral upward saccades
- the excitatory burst cells axons of the lateral riMLF come out and cross up the midline towards the posterior commissure (located just above the riMLF)
- those axons then run down to the opposite side of the brainstem in the medial longitudinal fasciculus and innervates the neurons in the oculomotor complex
- this innervates the elevator muscles: SR and IO
- the pathway is bilateral to get perfectly vertical saccades
describe what occurs in the brainstem in order to make bilateral downward saccades
- the excitatory burst cells axons of the medial half of the riMLF come down and travel DOWN the brainstem in the MLF
- and innervates the motor neurons that supply the IR in the oculomotor complex and the SO in the trochlear nucleus
- the two muscles are responsible for depressing the eye
what condition and characteristic symptoms will a patient with a lesion to their medial riMLF in the upper midbrain cause
a supra nuclear gaze palsy:
- horizontal saccades are intact (right and left)
- vertical downward saccades are selectively impaired
- upward saccades are intact
- only saccades i.e. fast downward eye movements are affected
- VOR (dolls eye reflex): down is spared (as VOR lower down in the midbrain is still intact) so can make slow downward saccades
what is a disorder of the vestibular ocular reflex VOR
oscillopsia
what system allows the image to stay on the fovea when moving the head
VOR - compensates for head motion
what symptoms does oscillopsia cause
blurred vision and illusionary movement of the environment during self motion e.g. locomotion
which 2 vestibular and inner ear organs does head position and motion activate and what is their function
vestibular organs = otoliths: utricle and saccule - tells you where your head is statically with respect to gravity
and
ear organs = 3 semi circular canals - tells you where your head is dynamically i.e. in motion
where in the head does the semi-circular canals sit
in the temporal portion of the petrous bone, either side of the head
what excites the semi-circular canals with horizontal eye motion
it is excited by lateral head motion towards that side
what excites the semi-circular canals with anterior eye motion
excited by forward (down) head motion
what excites the semi-circular canals with posterior eye motion
excited by backward (up) head motion
what does a ‘resting’ potential of vestibular hair cells result in
results in constant transmitter release, so vestibular afferents are tonically active
what is bi-directional signalling of vestibular hair cells
it is increased activity when cells are bent towards the kinocilium (becomes depolarised, increases firing frequency) and decreased activity when bent away from the kinocilium (becomes hyperpolarised, decreases firing frequency)
which hair cells are activated with rightward head motion
hair cells in the horizontal semi circular canal in the right inner ear
describe what occurs in the brainstem in order to make slow conjugate VOR eye movements to the left (i.e. rightward head motion)
- activates hair cells in the horizontal semi circular canal in the right inner ear
- this excites the vestibular ganglion cells of the 8th CN
- this is then relayed onto the brainstem of the same side which activates the ipsilateral MVN, which contains brainstem generator nuclei for slow conjugate movements
- the MVN activates axons which cross the midline
- and this activates two neurons of the left (opposite side) abducens nucleus
- activation of the left LR and right MR (via internuclear pathway) to the oculomotor nucleus
= compensatory leftward eye movements for the rightward head position
how does the vestibular system make sure the VOR is of the correct amplitude and that the antagonists are relaxed to conform to sherringtons law of equal innervation, when moving the head towards the right
inhibitory input from opposite SCC:
the semi circular canal of the right ear vestibular system becomes stimulated but the horizontal semi circular canal in the left (opposite) ear vestibular input is inhibitory to the MVN of the left side via the mirror image pathways, causes relaxation of the antagonistic MR of the left eye and LR of right eye = eyes move properly and conjugately towards the left and this improves precision
what occurs in the brainstem during a down VOR
a backward (up) head motion activates the posterior semi circular canals in both inner ears
- excites vestibular ganglion cells of the 8th CN of both inner ears
- this is then relayed to the MVN at the brainstem which has crossed inputs to the trochlear which innervates the SO and oculomotor nuclei which innervates the IR
- this pathway is bilateral so both eyes move down to compensate for the head motion
how can stimulation of one inner ear lead to e.g. downward contraction of both eyes
because the SO trochlear axons are crossed and IR oculomotor axons are uncrossed to produce conjugacy
which semi circular canals are inhibited by backward head motion
anterior semi circular canals
resulting in relaxation of antagonistic elevator muscles
what occurs in the brainstem during a upward VOR
a forward (down) head motion activates the anterior semi circular canals in both inner ears
- excites vestibular ganglion cells of the 8th CN of both inner ears
- this is then relayed to the MVN at the brainstem which has crossed inputs to the oculomotor nuclei which innervates the opposite SR and IO
- this pathway is bilateral so both eyes move up to compensate for the head motion
which semi circular canals are inhibited by forward head motion
posterior semi circular canals
resulting in relaxation of antagonistic depressor muscles
what can cause damage to head movement dependent oscillopsia (HDMO)
damage to:
- vestibular apparatus e.g. inner ear viral infection
- vestibular nuclei (and problems with balance/posture as some send axons down to spinal chord)
- MLF damage (and other eye disorders)
explain why head movement dependent oscillopsia (HDMO) may not be affected in internuclear ophthalmoplegia (INO)
so can’t make saccadic eye movements in INO but can still make a VOR because of an alternative pathways which spares people with a lesion to the MLF, that is:
the lateral vestibular nucleus also receives direct input from the semi circular canal which have axons that travel up the brainstem and activates the oculomotor nucleus on the same side which innervates the MR muscle = an alternative pathway that causes contraction of the MR muscle to compensate for damage to the internuclear pathway of the INO = VOR spared
