Eye Movements Flashcards
Saccades
- Goal = fixate new target for optimal visual processing
- 200 ms delay (slower than VOR) - position b/n fovea and target is being computed —> motor command SO if target moves during this time the motor command cannot be changed and target is missed (ballistic)
- Velocity of saccade depends on amplitude of eye movement (max is about 20 degrees)
- Faster movements for larger amp
Smooth Pursuit Movements
- Goal = keep moving target on fovea (target must be moving or else you will have multiple saccades NOT smooth pursuit)
- Also slow
- Require visual feedback
- Voluntary pursuit movement
Optokinetic
- Reflexive pursuit movement
- Does not require visual processing by cortex (even occurs in those that are cortically blind)
- Eyes automatically follow slow-moving broad visual field (ex - train)
- Optokinetic nystagmus - (not pathological) - when eye reaches end of orbit during pursuit, saccade occurs in opposite direction
VOR
- Goal = move eyes at same velocity as moving head but in opposite direction to maintain target on fovea (ideally VOR gain = 1 b/c velocity of eye / velocity of head = 1)
- VERY rapid (7-15 ms delay)
Gaze
- Goal = combo of eye and head movements for lager changes in eye position (» 20 degrees)
- 1- eyes move first (VOR suppressed at this time so saccade can occur)
- 2- head then turns and eyes move back in opposite direction so that they do not overshoot target (VOR is turned back on and helps this response)
- Vestibular lesion —> do not make reverse eye movements so overshoot target
Where are frontal eye fields located?
- Brodman area 8
- Motor area right in front of area 6 in cortex
Intraparietal Sulcus
involved in decision making about what target to choose
Temporal Visual Fields
- involved in smooth pursuit
- Damage to temporal regions —> deficit in smooth pursuit eye movements
Role of Superior Colliculus
- Gets info from frontal eye fields and passes along to PPRF for saccades AND gives rise to tectospinal tract which controls neck motoneurons
- SO… superior colliculus coordinates small changes in eye position from extra-ocular muscles alone AND large changes in eye position for combined eye and head movements
Superior Oblique v. Inferior Oblique
- Superior Oblique -
- Wraps around fibrocartilaginous trochlea then inserts on superior eyeball
- Depress & intort (turn in)
- When straight on it does both
- When already facing in - mainly causes depression
- When facing out - mainly causes eye to turn medially
- Inferior Oblique-
- From maxillary bone in medial wall of orbit —> travels underneath eye ball and inserts on lateral side of eyeball
- Elevate & extort eye
How do saccades work? Circuits of Jump & Maintenance
- JUMP (“burst signal”)
- R frontal eye field —> R superior colliculus (or directly from R frontal eye field to L PPRF) —> L PPRF (paramedic pontine reticular formation) —> L eye movements (L lateral rectus and R medial rectus contract)
- PPRF both excites the ipsilateral abducens (so ipsilateral lateral rectus and contralateral medial rectus) AND inhibits the contralateral abducens (inhibits contralateral lateral rectus)
- Then maintain eyes in this new location (“step signal”)
- PPRF tonic excitation of ipsilateral abducens to MAINTAIN (“direct path”)
- Also PPRF —> prepositus hypoglossi (PH) —> ipsilateral abducens (“indirect path”)
- PH integrates burst from PPRF and turns it into step signal
How do smooth pursuit movements work?
- Circuit involved higher order temporal cortex + cerebellum
- Middle superior temporal area (V5) —> pontine nuclei + flocculus + vestibular nuclei
Diploplia + Some Causes
- dbl vision
- Often caused by strabismus - when movement of 1 eye is messed up (leads to image being projected to different areas on ea retina)
- Can be due to damage to extra ocular muscles, neurons or fibers- Can be extropia (lateral deviation) OR esotropia (medial deviation)
- Esotropia more common b/c caused by damage to abducens
- Amblyopia - lack of visual perception in 1 eye due
- If strabismus in child during critical period in visual development; loss of input becomes permanent
- Can be extropia (lateral deviation) OR esotropia (medial deviation)
CN III Damage
- Likely due to aneurysm in PCA or posterior communicating artery
- Eye down and out, ptosis, mydriasis (pupil dilation)
CN IV Damage
- Likely due to trauma
- Trochlear is the only one that activates contralateral muscle
- Superior oblique damage SO…weak downward gaze of opposite eye so contralateral eye faces up —> vertical dbl vision (characteristic head tilt to compensate)
CN VI Damage
- Likely due to trauma (inc ICP or head trauma) OR tumor at base of skull
- If damage R CN VI…
- Normal when gaze L
- R eye devices medially when gaze straight
- R lateral rectus does not work when try to gaze R (stays centered)
What happens when there are lesions to abducens nucleus?
- So both the abducens motoneuron & interneuron to oculomotor are damaged
- Result = ipsilateral lateral rectus & contralateral medial rectus damaged; normal gaze to opposite side BUT neither eye works when gazing to side of lesion
- Some estropia
What happens when there are lesions to PPRF?
- Blocks info from getting from L frontal eye field/superior colliculus —> R oculomotor nucleus and R abducens nucleus
- Result = L eye gaze fine BUT neither eye works for R eye gaze
- NO estropia (distinguished it from abducens nucleus lesion) **B/c abducens nucleus itself is intact
What happens when there are lesions to MLF?
- If L MLF damage… blocks L oculomotor nucleus BUT R abducens is FINE
- Result = when looking R the R lateral rectus works but L medial rectus does not work so L eye stays straight AND R eye shows nystagmus when R eye movement (do not know why); L eye movement is normal
- Most common cause = MS (de-myelinate MLF)
1 1/2 Syndrome
- Damage to L CN VI nucleus + L MLF
- If L side damage… no movement to L; when looking R - R eye moves R but L eye stays midline + R eye nystagmus when looking R
- Called 1 1/2 because 1 full gaze and 1/2 other gaze affected