Eye Movements & Disorders Flashcards

1
Q

Which axes do the eyes move in?

A

Vertical for LR (abduction/adduction)
Horizontal for UD (elevation/depression)
Sagittarius for torsional action

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2
Q

Explain the visual axis and plane of muscle action

A

VA: line joining fixation point and fovea

Plane: line of muscle action

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3
Q

Why do actions change with gaze position?

A

visual axis/muscle plane relationship changes with gaze

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4
Q

Which 2 laws explain why eyes move conjugately?

A

Hering’s: (equal innervation for coordination of muscle pairs for BE) so LMR/RLR work together to look right

Sherringtons: coordination of muscle pairs in one eye, agonist muscle contracts inhibiting direct antagonist muscle

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5
Q

Explain duction

A

examines any limitations

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6
Q

Explain the 2 types of gaze shifting

A

Saccades: fast eye movements bringing objects of interest onto fovea

Vergence: eyes move in equal/opposite directions (near to distant)

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7
Q

What are the 4 types of gaze holding?

A

Vestibular: holds retinal image steady on fovea during brief head rotation
Optokinetic: holds retinal image steady during sustained head rotation
Smooth Pursuit: holds image of small, moving target on fovea
Fixation: holds eye in primary position (object detail)

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8
Q

Explain neural control of eye movements involving brain stem nuclei

A

Frontal/Parietal higher cortical areas command eye movement - send input to brain stem:

oculomotor (III) nuclei
abducens (VI)
trochlear (IV)

excitatory burst neurones (vertical/horizontal movements) controlled via omnipresent neurones send signals to III nuclei for muscles

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9
Q

Explain a saccade and how they’re tracked

A

Frontal fields (frontal cortex ~ Brodmann Area 8) send commands to superior colliculus/cerebellum/parietal cortex which send signals to brain stem nuclei

can be (in)voluntary; redirects eye so image on fovea

quantitative eye trackers for clinical oculomotor disorders

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10
Q

State some saccade characteristics and the velocity-amplitude relationship

A

Latency/Amplitude/Duration/Peak Velocity

higher amplitude (bigger saccade) ~ increased peak velocity also known as the main sequence

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11
Q

What disorders involve saccades?

A

Slow saccade: FEF/Parietal lesions, muscle weakness, burst cell abnormalities, delayed latency

Inaccurate saccades: Hyper/hypometrias

Parkinson’s: saccade slows down not on main sequence

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12
Q

Explain smooth pursuit and how it’s clinically tested

A

eye movements match small target speed maintaining image on fovea

movement quality judged by gain (peak vel.) and phase (temporal sync between eyes/target)

tests with motility:
slow pursuit (interspersed with saccades)
pursuit affected by MT/FEF/cerebellum lesions

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13
Q

Explain vergence and it’s disorders

A

disconjugate eye movements in equal/opposite directions stimulated by retinal disparity/blur

Convergence insufficiency in young adults/presbyopes

Parkinson’s/progressive supranuclear palsy

brainstem lesions

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14
Q

Explain neural control of the vestibular system

A

fluid-containing semicircular canals disrupted by head movements send signals to vestibular nuclei (oculomotor in brain stem)

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15
Q

Explain the vestibulo-ocular reflex and its associated disorders

A

VOR stabilises gaze allowing clear vision during brief head movements

unsteady gaze requires corrective saccade at end to bring target onto fovea

vestibular disease (central/peripheral) due to tumours-stroke/infection/trauma

vertigo, nystagmus, dizziness

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16
Q

Explain the optokinetic system and how its tested

A

assists VO system keeping retinal image steady - mediated by vision during sustained head movements

test with moving stripes

17
Q

Explain fixation, 3 components and its disorders

A

fixation keeps eyes aligned on target under movement (high f tremors, drifts and microsaccades) - prevents image fading for optimal vision/perception processing

Involuntary saccadic fixation instability or Nystagmus

Brain tumours, MS etc.

18
Q

Explain voluntary and end point nystagmus

A

Voluntary: series of back to back saccades in V/H planes (5-8% pop.)

Endpoint: light jittery movement on gaze extremities (>40 deg.) usually brief (low amp./freq.)

19
Q

How does congenital nystagmus differ from acquired?

A

Congenital: benign in first months (children) can be idiopathic (no apparent vis. issues), sensory impaired (albinism, cataract, ON hypoplasia) which manifest latent nystagmus (strabismus)

Acquired: indicates tumour/systemic condition, associated with nausea, vertigo, movement disorders