Eye Movements Flashcards

1
Q

Saccades

A
  • 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
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2
Q

Smooth Pursuit Movements

A
  • 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
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3
Q

Optokinetic

A
  • 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
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4
Q

VOR

A
  • 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)
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5
Q

Gaze

A
  • 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
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6
Q

Where are frontal eye fields located?

A
  • Brodman area 8

- Motor area right in front of area 6 in cortex

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7
Q

Intraparietal Sulcus

A

involved in decision making about what target to choose

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8
Q

Temporal Visual Fields

A
  • involved in smooth pursuit

- Damage to temporal regions —> deficit in smooth pursuit eye movements

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9
Q

Role of Superior Colliculus

A
  • 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
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10
Q

Superior Oblique v. Inferior Oblique

A
  • 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
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11
Q

How do saccades work? Circuits of Jump & Maintenance

A
  • 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
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12
Q

How do smooth pursuit movements work?

A
  • Circuit involved higher order temporal cortex + cerebellum

- Middle superior temporal area (V5) —> pontine nuclei + flocculus + vestibular nuclei

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13
Q

Diploplia + Some Causes

A
  • 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
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14
Q

CN III Damage

A
  • Likely due to aneurysm in PCA or posterior communicating artery
  • Eye down and out, ptosis, mydriasis (pupil dilation)
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15
Q

CN IV Damage

A
  • 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)
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16
Q

CN VI Damage

A
  • 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)
17
Q

What happens when there are lesions to abducens nucleus?

A
  • 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
18
Q

What happens when there are lesions to PPRF?

A
  • 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
19
Q

What happens when there are lesions to MLF?

A
  • 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)
20
Q

1 1/2 Syndrome

A
  • 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