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27 Cards in this Set
- Front
- Back
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Extra-ocular muscle role, Intra-ocular
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Extra-ocular - movements of the eye
Intra-ocular - accommodation and pupillary responses |
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Sensitivity of extraocular muscle lesions
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VERY sensitive, can show CNS problems even if absent on imaging or structural scan
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Opsoclonus
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rapid saccadic eye movements with uncontrollable movement back to back that occur when CENTRAL control of eye movements damaged
uncontrollable saccades Usually VIRAL damage to omnipause neurons Good outcome |
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Duane's Syndrome
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LATERAL RECTUS of affected eye or the CNS to the eye is MISSING and show up with abnormal eye movement that is not the same amount in same direction
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6 extraocular muscles and role
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Medial rectus - adduction
Lateral rectus - abduction Superior rectus - elevation Inferior rectus - depression Superior oblique - intorsion - rotate in Inferior oblique - extorsion - rotate out |
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Intraocular muscles and role
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Ciliary muscle - positive accommodation (acts against suspenstory ligaments) - NO ANTAGONIST
Sphincter pupillae iris muscle - pupilloconstriction Dilator pupillae iris muscle - pupillodilation |
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Stretch reflex of eye, prorioceptive info
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NOT EXISTENT
Proprioceptive feedback from extra-ocular muscles IS NOT used to track eye position Brain keeps track of eye position by keeping track of the signals sent to the motoneurons that innervate the extra-ocular muscles. This is known as EFFERENCE COPY or COROLLARY DISCHARGE |
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Yoking of eye movements and exceptions
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Yoking - the eyes move the same amount in the same direction
Vertical eye movements are ALWAYS yoked Horizontal movements are normally yoked via projections from the abducens nucleus to medial rectus motoneurons by way of the MLF. Convergence has eyes move in OPPOSITE directions Also in changing viewing distance, movements aren't yoked |
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Internuclear Ophthalmoplegia, difference in vergence
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Failure of adduction (medial rectus not getting normal input from interneurons) of one eye and occurs on the same side of the ascending MLF that has been damaged
Early MS sign In convergence adduction not reduced because vergence signals go DIRECTLY to medial rectus. Lost adduction in smooth pursuit, saccade, VOR, optokinetic rsponses due to MLF damage. Loss during CONJUGATE movement but not disconjugate |
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Neurological subsystems controlling eye movements extraocular
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1) Eye movements stabilize the image of the external world on the retina. These include the:
VOR (response to head or body movement) OKN (eye movements that are elicited by large movements of visual field) both involuntary 2) Eye movements bring images of objects of interest onto the fovea (only humans and nonhuman primates). Include: Visual fixation - hold image of stationary object on fovea Smooth pursuit - hold image of a small moving target on fovea; with optokinetic responses aids gaze stabilization during head rotation Nystagmus quick phases - resets eyes during prolonged rotation and direct gase toward oncoming visual scene Saccades - bring images of objects of interest onto fovea Vergence - moves the eyes in opposite directions so that images of a single object are place simultaneously on both foveas Smooth pursuit, saccades and vergence are VOLUNTARY Nystagmus and visual fixation are INVOLUNTARY Voluntary control for some |
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Neurological subsystems controlling eye movements intraocular
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Accomodation - focus image on the fovea. Lose around 40-50 and become presbyopic and no longer accomodate well.
Pupillary light reflex - controls illumination level of retina |
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Vestibular responses, use in reading, nuclei for feedback, path
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Head turns in one direction with a certain velocity and eyes turn with EQUAL velocity (if gain is 1.0) in the OPPOSITE direction. Latency of reflex is 10ms
Eyes must remain at this new position A tonic signal proportional to the integral of the eye velocity signal is generated and sent to extraocular motorneurons to maintain new position via the NUCLEUS PREPOSITUS HYPOGLOSSI Without VOR, view would fluctute up and down This is why eyes stay at same position while reading Path: Signal from medial vestibular nucleus senses turn, Acts on CN III nucleus ipsillaterally (to medial rectus), CN VI nucleus contralaterally (to lateral rectus) Nucleus prepositus hypoglossi goes to motor neurons |
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VOR gain normal, how to measure
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At fast movements gain is near 1.0 so eyes stay in same place
At slow speeds, the gain drops precipitously and eyes will follow head Optokinetic system overrides so keep visual world on the retina Gain = eye degrees/sec divided by head degrees/sec |
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Optokinetic system role, path
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Large-field stimuli moves, eyes track the movement overall (VOR for SMALL)
Adaptive response to the slip of the image of the outside world on the retina the occurs when the VOR gain is NOT 1.0 Path: mediated by neurons in the pretectum and medial superior temporal (MST) region of the cortex that indirectly modulate vestibular neurons If VOR gain was always 1.0 there would be no "retinal slip" Path: Optokinetic input from medial superior temporal cortex input to vestibular neurons indirectly. Output is via vestibular signal. Optokinetic only comes into play if VOR gain is not 1.0 |
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Vestibular neucleus neuron conditions
a) rotation in darkness b) rotation in light c) no rotation, optic flow (i.e. spin a rotating drum) |
a) NO visual input but being spun so VOR adapts if constant speed (no acceleration), decays in 60 seconds. ALL vestibular
b) if accelerate to constant velocity then decellarate the cells maintain activity for 60 seconds. VESTIBULAR AND OPTOKINETIC c) Visual field has a rotation, 60 sec till decays. OPTOKINETIC ONLY |
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Classes of Voluntary extraocular muscle movement
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Smooth pursuit
Saccades Vergence |
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Saccadic eye movement, properties, damage where disrupts
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Bring images of objects of interest onto the fovea
Voluntary rapid eye movement to look at objects of interest, Made at objects of same distance and occur in 20-90 msec in duration (five dots on a page) Duration proportional to amplitude of movement (bigger saccade takes longer) Ballistic eye movements, WILL NOT STOP MIDWAY, CAN"T START ANOTHER TILL FINISH FIRST. finishes with minimal drift forward or back VERY precise and FAST (fastest movement in body) Damage to cerebellum, precerebellar structures or cortical structures can cause specific deficits in amplitude or post-saccadic drift |
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How are saccades generated
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Transient increases in extraocular muscle forces to overcome intrinsic and extrinsic viscous drag of the eyeball
HUGE burst of force causes rapid contraction to overcome drag, Sustained tonic firing after reached target to hold in position despite elastic forces or others trying to restore to origin , i.e PREVENTS DRIFT |
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Neural Circuitry controlling saccades, Major generators/controllers
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Horizontal saccades - generated in the Paramedian pontine reticular formation (PPRF)
Vertical saccades - generated in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) [located anterior to the ocular motor nucleus] Major generators are the OMNIPAUSE neurons anterior to the abducens nucleus that fire 100 APs per second continuously but pause to allow saccades. Also get signals from superior colliculus (via the PPRF) and frontal eye fields to allow saccades Then excitatory burst neurons give a brief burst of activity for the saccade proportional to how big it is. Activates motor neurons Excitatory burst neurons project to nucleus propositus (nerual integrator) too which integrates for sustained tonic firing rate (eliminate drift) and to cerebellum (changes gain) |
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How does the superior colliculus modify saccades, direction
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via the PPRF (horizontal saccades) and riMLF (vertical saccades) and helps allow for oblique saccades
Right SC controls LEFT saccades Uses a 2D map for contralateral saccades. Rostral part for small saccades, caudal for large saccades. Anterior for 2 degree and posterior for 40-50 degree saccades. Left of map downward, right of map upward Integration of signals to PPRF and riMLF produces direction of saccade |
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Cortical override paths for saccades, cerebellar input and output
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Frontal lobe - frontal eye fields, supplementary eye fields
Parietal lobe - parietal eye fields Frontal lobe acts directly to superior colliculi and via Caudate (inhibits SNpr which inhibits colliculi so net is +) Parietal directly acts on colliculi Colliculi feeds to brainstem saccade generator Cerebellar loops (Fastigial nuclei) also receive frontal lobe input and feed to brainstem saccade generator. Normally substantia nigra pars reticularis INHIBITS superior colliculi to stop saccades, override allows them to occur |
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Smooth pursuit eye movements Cue, Pathway, Properties, Obstruction
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For tracking a slow moving target back and forth
Only works for going about 100 degrees/sec until gain stops and can't keep up and just try to track with saccades Cue: retinal slip velocity of visual target Pathway: Frontal eye fields has parts separate from saccadic part. Has visual and predictive parts. Projects through pontine nuclei (DLPN) then too cerebellar cortex then to cerebellar (fastigial nucleus) circuits, part goes to vestibular nucleus. All projections end at CN III motor neurons Obstruction: If object moves behind something can continue to track because prefrontal cortex has made an internal representation of the target (predictive) |
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Smooth pursuit vs saccades
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For slow moving objects (100 degrees/sec) use smooth pursuit, if faster give up and try using saccades
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Vergence Properties, Path, eye position for far viewing, near target, accommodation role
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Eye movements in depth, DISCONJUGATE, left and right eyes move in OPPOSITE directions
Far viewing - look straight and lens focused on faraway object Near target - blurred images fall on non-corresponding retinal locations, blur and disparity signals.Then get convergence (eye rotation to move projection to fovea) and accommodation (lens focus) to reduce blur and disparity Accommodation and vergence normally coupled Pathway: Premotor cells near ocular motor nucleus control vergence, Edinger Westphal nucleus (PNS of CN III) controls accommodation. NOT NEAR PPRF |
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Pupillary Light Reflex, Path
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Direct (light on) and Consenual contraction of the pupil that should be EVENLY MATCHED
Path: pretectum and projections to EWN. Afferent detects light via CN II and efferent via CN III. |
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Pupillary light reflex afferent defect vs efferent defect
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Afferent defect - visual system problem. Pupils EQUAL in size. but response to light in one eye is LESS than the other
Efferent defect - pupils may be DIFFERENT sizes (anisocoria). Pupil of one eye may react MORE to light in either eye than the other pupil to light in either eye. Also just may be different size regardless of which eye you shine light in |
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TOP ten list of eye problems
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1. Pupillary light reflex. If it’s absent, there’s a problem.
2. Vergence. Without it, you can’t get a closer look. 3. Smooth pursuit eye movements. You can’t track anything interesting without them 4. Saccadic eye movements. You can’t look at anything interesting without them. 5. Optokinetic responses. The world drifts without them. 6. Vestibular responses. You can’t read without them. 7. Eye movements are controlled by distinct neurological subsystems. 8. Except for changes in viewing distance, normal eye movements are yoked. 9. The stretch reflex is absent. Gently press on your eye and you’ll see the world move. 10. Movements of the eyes are produced by six extra-ocular muscles. If they, or the neural pathways controlling them, are not functioning normally, eye movements are abnormal. |
