9/14 Eye Movements - Glendinning Flashcards
purpose of extraocular system
categories of functions plus specifics
optimize vision through movement and focusing
two categories of functions:
1. extraocular muscle control
- enables eyes to position objects on fovea
2. intrinsic muscle control
- pupillary reflexes to optimise light input to retina (hi light constriction; lo light dilation)
- ciliary muscle controls lens shape → allows lens to focus light when obj closer to eye
- unaccomodated: ciliary m relaxed, zonules tense → lens thinner and flatter for viewing distant obj
- accomodated: ciliary m contracted, zonules disengaged → lens thicker for viewing objects nearby
extraocular muscles and actions
III - superior rectus = elevation_supraduction
III - inferior rectus = depression_infraduction
VI - lateral rectus = abduction
III - medial rectus = adduction
IV - superior oblique = intorsion & depression when adducted
III - inferior oblique = extorsion & elevation when adducted
diplopia
double vision
typically R and L eyes work together
- extraocular muscle weakness means they cant → inability to position image on macula of both eyes → diplopia
*one image may be hazy bc its positioned off macula (on rods!)
*usually occurs due to LMN problem
tropism
deviation of eyes inward or outward
- esotropia (eye inwards)
- exotropia (eye outwards)
- hypertropia (eye upwards)
- hypotropia (eye downwards)
portions of eye exam and what they test
- looking forward: requires balanced tone
* look for: tropism, diplopia - looking up/down in “H”: tests muscles, conjugate gaze
- movement requires activation of agonists, inhibition of antagonists
- conjugate gaze = movement of eyes together
***when eye is ADducted, inf/sup oblique move eye UP/DOWN respectively
***when eye is ABducted, inf/sup rectus move eye DOWN/UP respectively
- follow obj moving closer/further: tests vergence
- convergence = eyes adduct
- divergence = eyes abduct
oculomotor nucleus and nerve
source of CN III (GSE and GVE)
- GSE to: 4 extraocular muscles, levator palpebrae superioris
- GVE_Edinger-Westphal: pregang PSNS to pupillary constrictor and ciliary muscle of lens
responsible for…
- extraocular actions (GSE)
- moving eye up and down
- adduction
- external rotation (plus elevation when adducted)
- lifting eyelid (GSE)
- LPS works with superior tarsus (SNS innerv)
- pupillary constriction (GVE)
deficits caused by damage to single CN III nerve/nucleus : GSE components
exotropia: ipsilateral eye deviates “down and out” when looking straight ahead
- due to unopposed action of lateral rectus m
inability to move ipsilateral eye vertically or medially
diplopia
ptosis (eyelid droop)
SNS, PSNS innervation to pupillary muscles
dilator m receives SNS innerv
- lesions cause miosis in Horner’s syndrome
E-W innervates ciliary m and constrictor mm, receive PSNS innerv
- lesions cause mydriasis (dilated pupil), loss of accomodation
explain the light reflex
direct and consensual constriction due to light
- light sensed via afferent limb (CN II), travels bilaterally to R/L pretectal nucleus → R/L E-W nucleus → efferent CN III fibers
- CN III fibers travel to both eyes to elicit pupillary response (constriction)
light reflex response to…
complete optic nerve lesion
partial optic nerve lesion
complete:
- no constriction of either eye when light shined on affected side pupil
- direct consensual constriction when light shined on unaffected side pupil
partial: “relative afferent pupillary defect”, Marcus Gunn pupil
- v slight constriction (direct, consensual) on illumination of affected side
- direct consensual constriction when light shined on unaffected side pupil
detect via…swinging flashlight test!
light reflex response to…
lesion to CN III
would affect direct light reflex on shining light in affected eye
- could still expect to see indirect!
Horner’s syndrome sx
potential lesion sites
messed up SNS innervation to eye
- miosis
- ptosis
- anhydrosis
brainstem, hypothalamus, spinal cord (C, upper T), T1-T2 spinal nerves, carotid plexus, orbit
deficits due to CN III damage (E-W specific)
ipsilateral mydriasis : “blown” pupil
ipsilateral loss of pupillary constriction
ipsilateral loss of accomodation : cant view near obj
CN III clinical keys
- risks to CN III
- order of sx seen and WHY
CN III susceptible to compression from aneurysms & increased ICP
- esp true bc they are very close to tentorial notch!
often see pupillary changes first
- GSE fibers on inside, GVE fibers on outside (first affected by compression)
uncal herniation
transtentorial herniation, often due to supratentorial mass/bleeding
clinical triad:
- “blown pupil” → ipsi CN III signs
- hemiplegia → cerebral peduncles
- coma → reticular formation affects consciousness/coma
trochlear nerve and nucleus
functions
CN IV (GSE to superior oblique m)
- intorsion & depression in adducted position\abduction
nucleus located near periaqueductal gray and cerebral aqueduct at approx level of inferior colliculus
lesion of CN IV
sx: extorsion with hypertropia!
abducent nerve and nucleus
effect of lesion
CN VI (GSE to lateral rectus muscle)
nucleus located in caudal pons
- abduction of eye
lesions result in esotropia
- can occur with incr ICP pushing brainstem downward and stretching CN VI
red glass test
used to determine cause of diplopia
put red glass in front of affected eye → diplopia most pronounced in direction of eye that cant move
voluntary eye movement system
6 systems, huge card
six systems whose job it is to control eye movement → keep eyes on target so IMAGE is focused on FOVEA and stays there
- part voluntary, part reflexive
1. Active Fixation on object of interest
- works best if eyes are still
2. Saccadic System to point eyes to an object
- v fast saccades (900deg/s) initiated in response to visual targets, tactile stimuli, verbal commands, remembered locations
3. Smooth-Pursuit Eye Movement (SPEM) system for follwoing objects
- holds MOVING image on fovea in case of moving target
- max velocity of 100deg/s
4. Vergence System to align eyes to targets at diff depths
- “disconjugate eye movements”
- activated by retinal disparity
- mediated entirely by medial and lateral rectus mm
5. Vestibulo-ocular Reflexes that hold images still on retina during brief head movements
- elicited by vestibular inputs
6. Optokinetic Movements that hold images still on retina during translation or sustained rotation
- elicited by visual field movements
how are CN nuclei controlling eye systems coordinated/communicating?
all eye movements systems involve all 3 CN nuclei (III, IV, VI)
major pathway coordinating: medial longitudinal fasciculus (MLF) aka ascending medial vestibulospinal tract
how are eye movements generated?
amplitude and velocity of eye movements depends on activity of motor nuclei
lateral saccades produced by bursts of activity (saccadic pulses)
position is held by tonic activity
- without tonic activity, eyes would drift back to center following elastic forces
brainstem gaze centers
- horizontal gaze center
- vertical gaze center
- vergence gaze center
horizontal gaze center: PPRF
paramedian pontine reticular formation
right PPRF → right conjugate gaze
left PPRF → left conjugate gaze
- located next to nucleus of VI
- produces excitatory burst to CN VI LMN to ipsi lat rectus and interneurons
- interneurons then project to CN III to innervate contralat medial rectus
ex. right PPRF sends out 2 projection neurons to R abducens nucleus
- R abducens nucleus → sends neuron to R lateral rectus m
- R abducens nucleus → decussates, ascends through MLF, synapses at left oculomotor nucleus → L medial rectus m
lesion 1: R abducens nerve
CN VI palsy (LMN issue)
- tropism when looking straight ahead: R esotropia
- failiure of R eye to move to R on right gaze (won’t go past midline)
* left gaze unaffected
lesion 2: R abducens nucleus
R lateral gaze palsy
- R gaze for BOTH R and L eyes affected
1. R esotropia when looking ahead
2. failiure of right gaze (won’t move past midline)
lesion 3: right PPRF
right lateral gaze palsy
- no signal for rightward gaze coming from PPRF → failure of rightward gaze (doesn’t go past midline)
HOWEVER, no esotropia! bc not LMN lesion
- no disconnection between abducens nucleus and lat rectus m
lesion 4: left MLF
internuclear opthalmoplegia (INO)
- might seen in people with MS (myelinated pathway)
recall: left MLF refers to POST-DECUSSATION MLF coming from R PPRF (→ R abducens nucleus → MLF)
- affects connection from R PPRF to L oculomotor nucleus → L medial rectus
1. failure of L eye during right gaze
2. also see nystagmus in R eye! not sure why
should see normal convergence (don’t need MLF for convergence!)
lesion 5: left MLF and left abducens nucleus
- 5 syndrome
- failure of whole leftward gaze (left abducens nucleus affected)
- failure of L eye (medial rectus m from L MLF) during R gaze + R eye nystagmus
- L esotropia when looking forward (L abducens affecting LMN to lat rectus)
brainstem control of vertical and vergence eye movements
nuclei involved need to project to oculomotor nucleus (sup/inf rectus)
upward gaze
- rostral interstitial nucleus of Cajal → fibers decussate through posterior commissure
- connection: compression of these fibers (EX. IN HYDROCEPHALUS!!!!) leads to downward gaze!!!!
- vertical movements require input from both Frontal Eye Fields
Parinaud’s Syndrome
increased pressure on dorsal, rostral midbrain
ex. pineal tumor, cerebellar upward herniation, hydrocephalus
1. paralysis of upward gaze
2. hydrocephalus (cerebral aqueduct), headaches (ICP), nystagmus (MLF)
2. large, irreg pupils (post commissure fibers to E-W nucleus interrupted)
two stabilizing reflexes:
1. vestibulo-ocular reflex
2.
1. vetibulo-ocular reflex (VOR): gaze stabilization
- detects head movments through vestibular system (heel strike, head turning)
- generates eye movements in opp directio to stabilize eyes
- for BRIEF movements
if head turns left, right gaze muscles contract, eyes turn right to keep gaze fixed on whatever’s being focused on
VERY SIMILAR to PPRF gaze control except input is from vestibular nuclei in Scarpa’s ganglion via CN VIII (instead of PPRF)
-
difference: each vestibular nucleus heads to contralateral abducens nucleus
- L Scarpa’s ganglion → R abducens nucleus → two projections to…
- R lat rectus
- decussate, ascend L MLF, hit L oculomotor nucleus → L medial rectus
- L Scarpa’s ganglion → R abducens nucleus → two projections to…
- difference: each vestibular nucleus ALSO sends inhibitory signals to ipsi abducens nucleus
sx of abnormal VOR
conditions that affect VOR
- inability to see clearly (read) while walking, driving
- oscillopsia: sensation that environment is moving
conditions affecting VOR:
- injury to vestibular system (central/periph)
- cerebellar deficits
- vestibular cortex lesions (parietal lobe) → prevent suppression of VOR
- anxiety disorders
how to test brainstem fx in coma?
use oculocephalic reflex aka “doll’s eye maneuver” to test integrity of brainstem
- another name for VOR (under conditions of coma)
impaired reflex? brainstem dysfx :(
*NOTE: people who are healthy/awake will also suppress oculocephalic reflex!
optokinetic response
response to retinal slippage of image (ex. when moving)
- generates tracking to keep eyes focused on image
- imp for sustained movements and translation through space
- response to motion of an image across a visual field
pathway through vestibular nuclei via projections form visual system
cortical control of gaze
lesions to…FEF? PPRF?
similarities and diffs
FEF projects to contralateral PPRF and through superior colliculus
- L FEF used for voluntary movements to R and vice versa
FEF lesion: transient loss of horizontal gaze to contralat side
PPRF lesion: long lasting deficits in horiz gaze to ipsilat side
superior colliculus
lesions
major visuomotor center fir direction and amplitude of eye movement
- superficial layers: inputs from retina
- deeper layers: oculomotor fx
- inputs from visual, auditory, somatosensory cortices → enables eye movements to be directed towards specific location
ex. seeing a person, hearing voice enables direction of eyes/head to speaker
lesions
- transient deficit in accuracy, freq, velocity of saccades
- permanent loss of reflexive saccades
eye direction in…
cortical lesions vs. brainstem lesions
cortical lesions (involve FEF, UMN)
- eyes point towards lesion
brainstem lesions (involve PPRF, UMNs)
- eyes point away from lesion
cortical gaze centers
- FEF for contralateral saccades; bilateral for vertical
???
- parieto-occipito-temporal association cortex and visual cortex participate in SPEMs (smooth pursuit eye movements) with FEF
- SPEMs generated from FEF and lat post parietal cortical regions w superior colliculus and cerebellum
- project to same brainstem centers
convergence eye movements
near response triad
convergence/divergence controlled by neurons in midbrain near oculomotor nucleus
convergence: moving eyes from something far to something near
- convergence (medial rectus being activated)
- accomodation (incr curvature of lens)
- pupillary constriction (incr depth of field)
