Supranuclear eye movement control (1)


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Supranuclear eye movement control (1)

  1. 1. Supra Nuclear Eye Movement Control
  2. 7. Vision – Special(ity) Sense <ul><li>Man depends on his visual sense more than on his other senses. </li></ul><ul><li>A sophisticated ocular motor system exists to collect visual input that ultimately results in visual perception. </li></ul><ul><li>Eye movements bring visual stimuli to the fovea and also maintain foveal fixation on a moving object and during head movements. </li></ul>
  3. 10. Eye Movements-Morphological Classification
  4. 11. Eye Movements-Functional Classification Gaze Shift Gaze Maintenence Saccades : To bring images of objects of interest onto the fovea Optokinetic : To hold images on the retina during sustained head rotation Smooth pursuit : To keep the image of a moving target on the fovea Vestibular : To hold images on the retina during brief head rotations Vergence : To move the eyes in opposite directions Fixation : To hold eyes conjugately in a particular position
  5. 12. Saccade Control
  6. 13. Major Structures in Saccade Control
  7. 14. Saccadic System
  8. 17. Final Common Integrator Hypothesis
  9. 18. Neural Integrators <ul><li>For eye movements, a pulse (velocity command) causes a phasic contraction of the extraocular muscles that overcomes the viscous drag of the orbit and moves the eye to its destination. Once this destination has been reached, a step (position command) holds the eye steady at its new position by resisting the elastic restoring forces of the orbit. </li></ul><ul><li>A mathematical integration is necessary to convert velocity-coded information to position-coded information and the structures responsible are called the neural integrator. </li></ul><ul><li>Conjugate,Horizontal eye movements - Nucleus propositus hypoglossi (NPH) and the adjacent MVN . </li></ul><ul><li>Conjugate Vertical eye movements – Interstial Nucleus of Cajal. </li></ul>
  10. 19. Summary <ul><li>Horizontal gaze: </li></ul><ul><li>Excitatory Burst Neurons – PPRF </li></ul><ul><li>Neural Integrator - NPH & MVN </li></ul><ul><li>Inhibitory Burst Neurons - Nucleus paragigantocellularis dorsalis in the dorsomedial portion of the rostral medula </li></ul>
  11. 20. VERTICAL GAZE <ul><li>EBN – ri MLF </li></ul><ul><li>Neural integrator – INC </li></ul><ul><li>Inhibitory Burst Neurons – Nucleus paraphles </li></ul>
  12. 22. Smooth Pursuit Control
  13. 23. Smooth Pursuit System
  14. 25. Optokinetic Reflex <ul><li>Combination of saccades and smooth pursuit that allow tracking of targets in turn (e.g. counting sheep as they jump over a fence). </li></ul><ul><li>smoothly pursue one target, then saccade in the opposite direction to pick up the next target </li></ul><ul><li>parieto-temporal junction (smooth pursuit area) projects down to ipsilateral vestibular nucleus, inhibits it allowing ipsilateral smooth pursuit </li></ul><ul><li>then, the FEF of the same hemisphere generates a saccade back (contralateral) to the next target </li></ul>
  15. 26. Vestibulo Ocular Reflex
  16. 27. Vestibulo Ocular Pathways
  17. 28. Vergence <ul><li>Four sources </li></ul><ul><ul><li>Disparity </li></ul></ul><ul><ul><li>Accomodation </li></ul></ul><ul><ul><li>Tonic </li></ul></ul><ul><ul><li>Proximal vergence </li></ul></ul><ul><li>Brainstem </li></ul><ul><ul><li>Burst and Burst-tonic neurons </li></ul></ul><ul><li>Similar to saccadic system </li></ul>
  18. 29. Coordinated vergence/version movements <ul><li>Vergence starts sooner </li></ul><ul><li>Saccade finishes faster </li></ul><ul><li>Systems interact </li></ul><ul><ul><li>Saccade omnipause inhibits vergence bursters </li></ul></ul>
  19. 30. Eye Movement Control – Overview
  20. 32. Cerebral Cortex <ul><li>Frontal eye fields : </li></ul><ul><li>Located at Brodman's area 8, the posterior end of the second frontal convolution. </li></ul><ul><li>Generation of vertical and horizontal saccades. </li></ul><ul><li>Three different pathways from the FEF to the brain stem. </li></ul><ul><li>Ventral pathway : The posterior portion of the anterior limb of the internal capsule and the medial part of cerebral peduncle to reach the pons, where there is a partial decussation and termination in the PPRF. </li></ul><ul><li>Dorsal pathway : thalamus, the pulvinar, the pretectal nuclei, and the superior colliculus to reach the brain stem. </li></ul><ul><li>Intermediate pathway : From the FEF to the rostral ocular motor nuclei and the interstitial nucleus of Cajal. </li></ul><ul><li>Although there are ipsilateral and contralateral projections, the predominant projections from the FEF to both the PPRF and the riMLF appear to be contralateral. </li></ul>
  21. 33. Cerebral Cortex… <ul><li>Parieto-occipital-temporal (POT) junction: </li></ul><ul><li>Control of smooth pursuit eye movements and object tracking in space. </li></ul><ul><li>known as the middle temporal (MT) area in nonhuman primates </li></ul><ul><li>The area of the human brain that is the equivalent of the MT cortex of the nonhuman primate is Flechsig's area 10. </li></ul><ul><li>Receives visual information from the striate and prestriate cortex. It projects to the brain stem, cerebellum, superior colliculi, and the FEF. The latter projections modulate visually directed saccadic eye movements. </li></ul><ul><li>The POT junction cortex plays the key supranuclear role in the visual ocular reflex by way of projections to the PPRF and riMLF. This reflex keeps a moving image projecting on the fovea. There are specific efferent fibers for horizontal, vertical, and torsional movements. </li></ul><ul><li>Damage to only one side of the MT cortex slows ipsilateral slow pursuit, requiring catch-up saccades. Such lesions also temporarily impair pursuit responses to fast targets in moving in either direction. </li></ul>
  22. 35. Cerebellum <ul><li>Immediate modulation of ongoing eye movements, as well as in the long-term adaptive processes that compensate for ocular motor dysmetria. </li></ul><ul><li>Controls and adjusts the size of saccades which is essential for maintaining accurate ocular motor performance during growth and aging, during and after ocular motor disease, or even while using spectacles. For instance, the use of anisometropic spectacles produces a varying anisophoria in different directions of gaze, which must be compensated in each direction of gaze. </li></ul><ul><li>Hemicerebellectomy - ipsilateral saccadic and contralateral pursuit defects </li></ul><ul><li>Total cerebellectomy - persistent saccadic dysmetria and abolishes smooth pursuit.. </li></ul>
  23. 36. Vestibular System <ul><li>The semicircular canals, otolith organs, and vestibular nuclei </li></ul><ul><li>Semicircular canals - Angular acceleration </li></ul><ul><li>Otoliths (the saccule and the utricle) - Linear acceleration of the head (important in maintaining eccentric eye position in response to a sustained head tilt) </li></ul><ul><li>Vestibular Nuclear Complex : </li></ul><ul><li>Widely connected with nuclei in the brain stem, cerebral cortex, cerebellum, and reticular formation. </li></ul><ul><li>Labyrinthine-stimulated eye movements are modulated by connections with the reticular formation and the cerebellum. </li></ul>
  24. 37. Vestibular System… <ul><li>In addition to the labyrinthine inputs to the vestibular nuclei, visual and proprioceptive information reaches these nuclei. </li></ul><ul><li>opto-kinetic inputs from the striate cortex reach the vestibular nuclei by an accessory optic pathway. </li></ul><ul><li>Proprioceptor input comes from the neck, providing the basis for cervico-ocular reflex . </li></ul><ul><li>Each reflex acts to stabilize the orientation of the eyes in response to movements of the body and therefore opposes shifts of the line of sight caused by changes in position of the head or body. </li></ul><ul><li>Dynamic eye response : </li></ul><ul><li>This system repositions the eyes during acceleration and deceleration of the head. The endolymph within the semicircular canals is displaced when the head is moved. This results in a change in pressure on the ciliated cells of the crista ampullaris, resulting in a stimulus to the brain. Once the head movement reaches a stable unchanging velocity, the pressure gradient disappears, and the peripheral vestibular signal disappears 30 to 45 seconds later. Thus, the semicircular canals make no contribution to the maintenance of static ocular position. </li></ul>
  25. 38. Vestibular System… <ul><li>The semicircular canals function in a reciprocal fashion so that when an anterior canal is stimulated, the posterior canal is inhibited. </li></ul><ul><li>Each canal primarily drives two extraocular muscles, one in each eye, that rotate the globe in the same plane as that in which semicircular canal is oriented. </li></ul><ul><li>The horizontal canal excites the ipsilateral medial rectus muscle and the contralateral lateral rectus muscle. </li></ul><ul><li>The anterior canal excites the ipsilateral superior rectus muscle and the contralateral inferior oblique muscle. </li></ul><ul><li>The posterior canal excites the ipsilateral superior oblique muscle and the contralateral inferior rectus muscle. </li></ul>
  26. 39. Brainstem Control Centers <ul><li>Paramedian pontine reticular formation (PPRF): </li></ul><ul><li>Extends from the level of the trochlear nerve nucleus to the abducens nerve nucleus </li></ul><ul><li>Major efferent projections- Ipsilateral abducens nucleus </li></ul><ul><li>Secondary efferent projections - The rostral interstitial nucleus of the MLF (riMLF), which controls vertical gaze. </li></ul><ul><li>Most afferent connections - from the vestibular nuclei, but there also is input from the cerebellum, superior colliculus, and frontal eye fields (FEF). </li></ul>
  27. 40. Brainstem Control Centers… <ul><li>Medial longitudinal fasciculus (MLF) : </li></ul><ul><li>Fiber tract that extends from the spinal cord to the oculomotor nerve nucleus. </li></ul><ul><li>Contains primarily ascending fibers, the majority of which arise in the superior and medial vestibular nuclei. </li></ul><ul><li>The MLF is in close proximity to the ocular motor nuclei and influences both ipsilateral and contralateral nuclei. </li></ul><ul><li>An abnormality of the MLF causes problems with horizontal and vertical gaze coordination of the two eyes. </li></ul><ul><li>The clinically most important connection passing through the MLF links the contralateral abducens nucleus with the ipsilateral medial rectus subnucleus. Abnormalities of this tract produce an internuclear ophthalmoplegia. Such a lesion produces slowed or complete loss of adduction of the ipsilateral eye and abducting nystagmus of the fellow eye. </li></ul>
  28. 41. BRAIN-STEM PATHWAY FOR HORIZONTAL GAZE <ul><li>Supranuclear inputs converge on the PPRF, the premotor center for horizontal eye movements. </li></ul><ul><li>The innervation for a horizontal eye movement flows from the ipsilateral PPRF to both an abducens motor neuron and an internuclear neuron in the abducens nucleus. </li></ul><ul><li>The latter internuclear neuron decussates to the contralateral medial longitudinal fasciculus, where it ascends to reach the contralateral medial rectus subnucleus . </li></ul>
  29. 42. <ul><li>Rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF): </li></ul><ul><li>Located in the mesencephalon at the rostral termination of the MLF. </li></ul><ul><li>Includes cells from the interstitial nucleus of Cajal. </li></ul><ul><li>The riMLF has connections to motor neurons in the oculomotor and trochlear nuclei, as well as to the PPRF. </li></ul><ul><li>On the basis of experimental and pathologic studies, this group of cells appears to be the immediate premotor area for vertical eye movements, both upward and downward. Its function is thus analogous to the PPRF for vertical eye movements. </li></ul><ul><li>Damage to this area generally causes more difficulty with downward movement than with upward movement. </li></ul>
  30. 43. <ul><li>Posterior commissure : </li></ul><ul><li>Dorsal and rostral to the riMLF . </li></ul><ul><li>Contains some scattered neuronal cell bodies. </li></ul><ul><li>Lesions in this region produce abnormalities of upward gaze. It is likely that the fibers for upward gaze leave the riMLF and pass through this region before reaching the oculomotor and trochlear nuclei. </li></ul><ul><li>Involvement of the posterior commissure may be part of the dorsal midbrain syndrome (Parinaud Syndrome). </li></ul><ul><li>In this syndrome, there is impairment of upwardly directed saccades or, in extreme cases, loss of all vertical movement. Other signs include pupillary mydriasis and light-near pupillary dissociation, corectopia, and convergence-retraction nystagmus. </li></ul>
  31. 44. <ul><li>Superior colliculus : </li></ul><ul><li>Receives visual input directly from branches of retinal ganglion cell axons. Visual input also comes indirectly from the visual cortex, the parietal and frontal lobes, and the substantia nigra. </li></ul><ul><li>There are efferent projections to the brain-stem premotor areas. </li></ul><ul><li>The superior colliculus can generate visually directed saccades independently and may play a role in the control of pursuit eye movements. </li></ul><ul><li>In primates, ablation of both FEFs and both superior colliculi is necessary to produce permanent saccadic defects . </li></ul>
  32. 45. Supra Nuclear Eye Movement Disorders
  33. 47. Horizontal Gaze Palsy Localization
  34. 48. Vertical Gaze Palsy Localization
  35. 49. Tonic Gaze Deviation
  36. 50. Saccadic Disorders <ul><li>Saccadic palsy : </li></ul><ul><li>Inability to generate saccades </li></ul><ul><li>Horizontal saccadic palsy may occur transiently in acute lesions of the contralateral frontal eye field or the ipsilateral PPRF. </li></ul><ul><li>Complete loss of all saccades can also be seen after cardiac surgery. </li></ul>
  37. 51. Saccadic dysmetria <ul><li>Saccades of inappropriate amplitude, which also may </li></ul><ul><li>be slow. </li></ul><ul><li>cerebellar disease : </li></ul><ul><li>centripetal saccades : hypermetric </li></ul><ul><li>centrifugal saccades : hypometric </li></ul><ul><li>PD : hypometric a/w increased latency </li></ul><ul><li>Multiple system atrophy : Mild to moderate </li></ul><ul><li>hypometria </li></ul>
  38. 52. Slow Saccades <ul><li>Spinocerebellar and olivopontocerebellar degeneration </li></ul><ul><li>PD </li></ul><ul><li>PSP </li></ul><ul><li>Huntington chorea </li></ul><ul><li>Wilson disease </li></ul><ul><li>Large unilateral lesions of the cerebral hemispheres </li></ul><ul><li>Lesions of the PPRF </li></ul><ul><li>Paraneoplastic syndromes </li></ul><ul><li>Drug intoxications with drugs such as anticonvulsants or benzodiazepines. </li></ul>
  39. 53. Ocular motor apraxia <ul><li>Loss of or severely diminished volitional saccades </li></ul><ul><li>with retention of the fast phases of vestibular nystagmus </li></ul>
  40. 54. Smooth Pursuit Disorders
  41. 55. Vergence abnormalities
  42. 57. Thank You