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THE TOP TEN THINGS YOU SHOULD KNOW ABOUT THE OCULOMOTOR SYSTEM. 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.
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THE TOP TEN THINGS YOU SHOULD KNOW ABOUT THE OCULOMOTOR SYSTEM
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. • Additionally, accommodation and pupillary responses are produced by intraocular muscles Video OF Duane’s Video of Opsoclonus
9. The stretch reflex is absent. Gently press on your eye and you’ll see the world move. • Proprioceptive feedback from the extra-ocular muscles is not used to keep track of eye position. • The 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.
8. Except for changes in viewing distance, normal eye movements are yoked. • Yoking: the eyes move the same amount in the same direction. • Vertical eye movements are normally always yoked. • Projections from the abducens nucleus to medial rectus motoneurons by way of the medial longitudinal fasciculus provides the basis for horizontal yoking. During convergence, the eyes move equal amounts in opposite directions.
MVN - Medial vestibular nucleus NPH - Nucleus prepositus hypoglossi EBN - Excitatory burst neuron IBN - Inhibitory burst neuron VIDEO SHOWING INTERNUCLEAR OPHTHALMOPLEGIA Excitatory Inhibitory
7.Eye movements are controlled by distinct neurological subsystems. • Eye movements stabilize the image of the external world on the retina • Eye movements bring images of objects of interest onto the fovea
Vestibulo-ocular reflex MVN - Medial vestibular nucleus NPH - Nucleus prepositus hypoglossi EBN - Excitatory burst neuron IBN - Inhibitory burst neuron Excitatory Increased firing rate with rightward head turns Inhibitory
VESTIBULAR NUCLEUS NEURON A. ROTATION IN DARKNESS (Vestibular but no Optokinetic) B. ROTATION IN LIGHT (Vestibular and Optokinetic) C. NO ROTATION. OPTIC FLOW. (Optokinetic but no Vestibular)
Vestibular-optokinetic interactions Schematic summary of vestibular-optokinetic interaction occurring in response to velocity-step rotations. Graphs on the left show characteristics of the stimulus (head velocity during rotation or drum velocity during optokinetic stimulation); graphs on the right show the responses (slow-phase eye velocity, quick phases having been removed). R, right; L, left; t, time. In the top panel, constant-velocity rotation to the left in the dark produces slow-phase movements to the right (per-rotatory nystagmus, RN) with initial eye velocities equal to head velocity (VOR gain = 1.0). When rotation stops, nystagmus starts in the opposite direction (postrotatory nystagmus, PRN). In the middle panel, an optokinetic stimulus (drum rotation to the right) causes a sustained optokinetic nystagmus (OKN), with slow phases to the right during the entire period of stimulation. When the lights are turned off during stimulation, eye movements do not stop immediately but persist as optokinetic after-nystagmus (OKAN). In the lower panel, the subject is rotated in the light (natural situation of self-rotation). This gives a combined vestibular and optokinetic stimulus. The response is a sustained nystagmus. When the chair stops rotating, eye movements stop nearly completely: postrotatory nystagmus is suppressed by the opposite-directed optokinetic after-nystagmus and by visual fixation of the stationary world.
B A B A B A 4. Saccadic eye movements. You can’t look at anything interesting without them. • FAST - 40-90 MS IN TOTAL DURATION • BALLISTIC
VERTICAL SACCADES ARE GENERATED HERE Horizontal saccades are generated in the paramedian pontine reticular formation (PPRF) Vertical saccades are generated in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF)
MVN - Medial vestibular nucleus NPH - Nucleus prepositus hypoglossi EBN - Excitatory burst neuron IBN - Inhibitory burst neuron Excitatory Increased firing rate with rightward head turns Inhibitory
OMNIPAUSE NEURON (OPN) Burst size proportional to saccade size NI - Neural Integrator EBN
OMNIPAUSE NEURON (OPN) Burst size proportional to saccade size NI - Neural Integrator EBN
2-D map of contralateral saccades THE SUPERIOR COLLICULUS PROJECTS TO THE PPRF
SUPERIOR COLLICULUS MOTOR MAP
A block diagram of the major structures that project to the brain stem saccade generator (premotor burst neurons in PPRF and riMLF). Also shown are projections from cortical eye fields to superior colliculus. FEF, frontal eye fields; SEF, supplementary eye fields; DLPC, dorsolateral prefrontal cortex; IML, intramedullary lamina of thalamus; PEF, parietal eye fields (LIP); PPC, posterior parietal cortex; SNpr, substantia nigra, pars reticulata. Not shown are the pulvinar, which has connections with the superior colliculus and both the frontal and parietal lobes, and certain projections, such as that from the superior colliculus to nucleus reticularis tegmenti pontis (NRTP).
Disorders of the saccadic pulse and step. Innervation patterns are shown on the left, eye movements on the right. Dashed lines indicate the normal response. (A) Normal saccade. (B) Hypometric saccade: pulse amplitude (width ´ height) is too small but pulse and step are matched appropriately. (C) Slow saccade: decreased pulse height with normal pulse amplitude and normal pulse-step match. (D) Gaze-evoked nystagmus: normal pulse, poorly sustained step. (E) Pulse-step mismatch (glissade): step is relatively smaller than pulse. (F) Pulse-step mismatch due to internuclear ophthalmoplegia (INO): the step is larger than the pulse, and so the eye drifts onward after the initial rapid movement. Experimental cerebellectomy completely abolishes the adaptive capability-for both the pulse size and the pulse-step match.296 Monkeys with lesions restricted to the dorsal cerebellar vermis cannot adapt the size of the saccadic pulse; they have pulse-size dysmetria .416,416a On the other hand, monkeys with floccular lesions cannot match the saccadic step to the pulse to eliminate pulse-step mismatch dysmetria.298 This evidence suggests that the repair of conjugate saccadic dysmetria is mediated by two different cerebellar structures: the dorsal cerebellar vermis and the fastigial nuclei control pulse size, and the flocculus and paraflocculus control the pulse-step match.
B A • Smooth pursuit: Tracking eye movements - conjugate. Velocity of visual target • Visual cue: retinal slip velocity of visual target. B A B A
3. Smooth pursuit eye movements. You can’t track anything interesting without them • Smooth pursuit: Tracking eye movements - conjugate. Velocity of visual target. Slow. • Visual cue: retinal slip velocity of visual target.