Eye movement Flashcards

1
Q

Muscles

A

Any movement up or down involves >= 2 muscles!

Adduct/converge = medial rectus
 - elevate = inferior oblique
 - depress = superior oblique
Abduct/diverge = lateral rectus
 - elevate = superior rectus
 - depress = inferior rectus

Direct

  • elevate = inferior oblique + superior rectus
  • depress = superior oblique + inferior rectus
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2
Q

Cranial nerves

A

All run through cavernous sinus, near internal carotid
Tonic activity -> inc or decrease for movement, new positions

Oculomotor (3)

  • midbrain ventral to periaqueductal grey -> interpeduncular fossa (near post cerebral and communicating arteries) -> all ipsi except LR, SO, also levator palpebrae
  • carries PNS from Edinger-Westphal -> ciliary ganglion -> pupil constrict and ciliary/lens

Trochlear (4)

  • trochlear nucleus -> decussates -> ponto-mesencephalic junction -> cavernous sinus -> contralateral SO
  • long and skinny -> traumatic damage

Abducens (6)
- abducens nucleus (facial colliculus) -> ponto-medullary junction -> ipsi LR

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3
Q

PNS eye control

A

lens accom, constrict (accom, converg, light)

Light reflex:
Optic nerve -> tract -> pre-tectal nuclei ->
Edinger-Westphal nucleus (bilateral) ->
outside of oculomotor (CN III) - susceptible to compression ->
ciliary ganglion -> sphincter pupillae (bilateral)

Can have isolated loss of light constriction with preserved accom, converge (ex pre-tectal or peripheral syphilis, DM)

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4
Q

Saccadic movement

A

Sudden “saccades” - no vision during movement (blurs)

  • new object or catch up with sudden change (ex face features)
  • must be accurate -> 200 ms lag to plan, check movement
  • head follows in 20-30 ms -> compensation via vestibulo-ocular

Generation - frontal eye cortex, superior colliculus

  • vertical via rostral interstitial nucleus
  • horizontal via PPRF -> CN VI -> MLF -> CNIII

vs microsaccades - use neighboring retina cells to avoid adaptation

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4
Q

Conjugate horizontal gaze

A

ex eyes to L visual field

R frontal eye field cortex -> R superior colliculus ->
L (contralateral) PPRF -> L ipsilateral abducens
- L lateral rectus
- MLF -> contralateral R oculomotor -> R medial rectus

Key locations

  • frontal eye center = premotor cortex -> movement away from active side
  • PPRF - para-median pontine reticular formation -> movement towards active side
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5
Q

Eye palsies

A

Loss of function -> drift away from that movement

  • > double vision (worse in weak position, bad eye is “further from center”)
  • > turn head to bring in line

CN III
- abducted, inadequate vertical

CN IV - extorts, medial
- tilt head away from bad eye (other eye intorts to compensate)

CN VI - adducted
- spin head towards bad eye

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6
Q

Superior colliculus

A
Input:
 - retina (visual) -> superficial layers
 - inferior colliculus (auditory)
 - spinal cord (proprioception, somatic)
 - cortex
Maps stimuli
Output -> from deep layers
 - PPRF, midbrain reticular formation, spinal cord (tectospinal)
 -> reflex eye and head movements
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7
Q

MLF

A

Medial longitudinal fasciculus

Input from vestibular, PPRF, CN III, CN IV, CN VI nuclei
- ex connects CN VI and contralateral CN III -> horizontal
(lesion -> internuclear ophthalmoplegia - lateral not followed by other eye)

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8
Q

PPRF

A

Paramedian pontine reticular formation
At level of facial colliculus, CN IV bisects

Critical for voluntary horizontal movements
- damage -> can’t look toward injured side
Multiple neurons type -> burst and tonic activity

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10
Q

Voluntary vertical gaze

A

Diffuse cortical areas -> rostral interstitial nucleus (midbrain) ->

  • > posterior commissure (dorsal midbrain)
  • > b/l CN III, CN IV

Damage (RIN or post commissure)
-> loss of voluntary but can still move with vestibular
Intact with pontine damage (ex “locked-in”)

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10
Q

Smooth tracking

A

Only if “locked” onto object
Shares vestibulo-ocular pathways

Occipital eye field = visual association area (locks in) ->
(frontal eye field ->) ipsilateral pontine nucleus (NOT PPRF) ->
middle peduncle -> contralateral flocculus -> inf peduncle ->
vestibular nucleus -> bilateral PPRF, CN VI -> MLF -> CN III, CN IV

Reflexes use same pathway!
Fixation - fixate on moving target
Optokinetic - involuntary fixation on moving target (relative to head…?) - ie looking out of moving car
- track -> saccade towards new object (optokinetic nystagmus)
- lost when object moving towards cortical lesion

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11
Q

Vestibulo-ocular reflex

A

Vestibular nerve -> (nucleus ->) flocculus -> vestibular nucleus ->
- bilateral PPRF, CN VI -> MLF -> CN III, CN IV

Damage to tract - drift (as if head were moving) -> saccadic (nystagmus)
Loss of cortical input -> static drift without saccadic

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12
Q

Vergence

A

Less well-understood:
- requires occipital lobe -> mesencephalic reticular
- probably superior colliculus
Coordinated movement, constriction, ciliary muscles

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13
Q

Nystagmus

A

Pendular - equal phases, not CNS or vestibular
Jerk - normal at edges of visual field
- vestibular system (inner ear, CN VIII, nucleus, flocculus, MLF)
- can also be from drugs, toxins
- slow phase - vestibulo-ocular reflex
- fast phase - compensatory from cortex
- named for fast component

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14
Q

SNS eye control

A

Hypothal -> descending -> thoracic -> cerv ganglion -> int carotid ->

  • Pupil dilation
  • Lev palpebrae + Muller’s muscles -> opening

Cilio-spinal reflex:
- noxious -> thoracic -> peripheral chain -> active dilation
- does not use central SNS pathways - can be preserved
Horner’s syndrome:
- miosis, ptosis
- anhydrosis - location by innervation (ex only forehead = int carotid, lat face = sup cerv gang, face + neck = cerv chain, arm/body = thoracic)

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15
Q

Anisocoria

A

Assymetrical pupils

Normal if <1 mm difference

16
Q

Amblyopia

A

aka “lazy eye”
Muscle weakness/scarring -> turn off input
Poor vision -> muscle weakness

doesn’t affect reflexes (not cortical)
-> permanent blindness (1mo/yr = ex 5 continuous mos in 5 yo)
Tx: force use of poor eye

17
Q

Pupil disfunction

A

Hypothal/dienceph -> lose SNS -> constrict
Pretectal (dienceph, rostral midbrain) -> sluggish
CN III (midbrain) -> dilated, non-reactive
Caudal (below midbrain) -> lose both PNS, SNS -> midposition, non-reactive

Isolated pontine lesion or narcotics -> only lose descending SNS -> pinpoint but still reactive
Metabolic/toxic - pupillary preserved until final stages

18
Q

Caloric VOR testing

A

Ice water -> decreases input (turning away) -> eyes turn toward
Warm water -> inc input (turning toward) -> eyes turn away

Cortical disfunction -> lose fast/nystagmus
-> static deviation
- proportional to disfunction
Midbrain -> disconjugate (MLF, etc)
Lower pons - loss of VOR (also corneal, etc)