Supranuclear pathways and lesions

Supranuclear pathways and lesions

1. SUPRANUCLEAR PATHWAYS AND LESIONS Moderator: Dr. Seema Bhosale Presenter : Shruti Chandra Jain

2. Overview of the Presentation Fundamentals of Extra-ocular movements Anatomy of cortical and brainstem centers Basic binocular e ye movements and their pathways Step-wise evaluation of EOMs Lesions of Supranuclear Pathways

3. Fundamentals of Extra-ocular movements

4. FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROL

5. FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROL Efferent ocular motor system Supranuclear pathways : Affect both eyes simultaneously Infranuclear pathways : Affect eyes differently

6. FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROL Moving objects present a special challenge GAZE SHIFT GAZE STABILIZATION

7. HIERARCHY OF OCULAR MOTOR CONTROL LEVEL 1: SUPRANUCLEAR LEVEL 2 :NUCLEAR LEVEL 3: INFRANUCLEAR

8. Anatomy of cortical and brainstem centers

9. CORTICAL CENTRES

10. BRAINSTEM CENTRES VERTICAL SACCADES HORIZONTAL SACCADES

11. BRAINSTEM CENTRES

12. BRAINSTEM CENTRES

13. ROLE OF CEREBELLUM Cerebellum plays an important role in fine tuning all eye movements, including modulation and adaptation of vestibulo -ocular responses, saccades, pursuit, and vergence .

14. ROLE OF CEREBELLUM Two distinct parts of the cerebellum contribute to ocular motor control: (1) the vestibulocerebellum ( flocculus , paraflocculus , nodulus , and ventral uvula) and (2) the dorsal vermis of the posterior lobe and fastigial nuclei. The vestibulocerebellum deals with stabilization of sight during motion, whereas the dorsal vermis and fastigial nuclei influence voluntary gaze-shifting (i.e., saccades, pursuit and vergence ).

15. Basic binocular eye movements and their pathways

16. EYE MOVEMENTS

17. EYE MOVEMENTS CLASS MAIN FUNCTION Vestibular Holds retinal image steady during brief head rotation or translation Optokinetic Holds images steady on the retina during sustained head rotation Smooth pursuit Holds target image steady during linear movement of object or self Saccades Rapidly bring object of interest to focus on fovea Vergences Moves the eye in opposite directions so a single image is simultaneously held on each fovea

18. 1. SACCADES Rapid movement to bring object of interest on fovea Clinical exam to Check saccades

19. SACCADIC SYSTEM STIMULUS Visually reflexive – Parietal lobe Contralateral Memory guided or volitional – Frontal lobe Contralateral CENTRE Horizontal Saccades -> PPRF -> Pons Vertical Saccades -> riMLF & PC -> Midbrain

20. SACCADIC PATHWAY- HORIZONTAL C / l Frontal cortex I/l PPRF & VI n Nu Via MLF to C/l IIIn Nu Created by: Dr. S hruti Chandra

21. VERTICAL SACCADE PATHWAY riMLF : upward and downward eye movements and for ipsilateral torsional saccades. P rojects to motoneurons of elevator muscles bilaterally but projects to motoneurons of depressor muscles only ipsilaterally The INC projects by way of the posterior commissure to motoneurons of the contralateral nuclei of the third and fourth cranial nerves and the contralateral INC

22. VERTICAL SACCADE PATHWAY

23. SACCADIC SYSTEM – Features of a saccade Latency : duration of stimulus to movement Accuracy : arrival of eyes on target Velocity and conjugacy : degree to which 2 eyes move together Hypometric saccades : saccade that falls short of intended target Hypermetric saccades : overshoots the target

24. SACCADIC DYSFUNCTION CLINICAL FEATURE SITE OF LESION Prolonged Latency Degenerative disorders Hypometric saccades PPRF lesion Slow saccades in horizontal plane Pons Slow saccades in vertical plane Midbrain Hypermetric saccades Cerebellar lesions

25. 2. SMOOTH PURSUIT Saccade and pursuit have common neural pathway Cortical centres Middle Temporal & Medial Superior Temporal Ipsilateral cortical control

26. PURSUIT PATHWAY I/ l Posterior parietal cortex (PPC) I/ l PPRF C /l MLF and VI Nu Created by: Dr. S hruti Chandra

27. PURSUIT SYSTEM Relatively slow moving target <30 degress per second Initiation of pursuit - latency Gain of eye movements = output/input

28. PURSUIT DYSFUNCTION Low gain -> saccadic pursuit Poor initiation -> Frontal / parietal lobe lesions Deficits found usually in both vertical and horizontal planes

29. 3. OPTOKINETIC NYSTAGMUS

30. OKN DYSFUNCTION Parietal or temporal lobe lesions -> abnormal OKN towards the side of lesion Locate and define extent of cerebral lesions

31. 4. VESTIBULAR OCULAR REFLEX Brief, high frequency rotation of the head SCC – angular movements Otoliths of utricle & saccule – linear acceleration Centre: Vestibular nuclei Efferent: fibres carried via MLF to cranial nerve nuclei Velocity Storage mechanism

32. SCC PROJECTIONS - EXCITATORY

33. VESTIBULAR OCULAR REFLEX Examination for VOR dysfunction - Spontaneous nystagmus - Horizontal head shaking VOR gain = Amplitude of eye rotation/ Amplitude of head rotation Bilateral VOR dysfunction - dynamic visual acuity

34. 5. VERGENCES Vergence eye movements drive the eyes in opposite directions to maintain the image of an object on the fovea of both eyes as the object moves toward or away from the observer. Vergence eye movements are driven primarily by a disparity in the relative location of im · ages on the retinas.

35. 5. VERGENCES Convergence centre : Pretectal area ( mesencephalic reticular formation, just dorsal to the third nerve nuclei ) Inputs from bilateral cerebral hemispheres give inputs to the centre and from there to both 3 rd nerve nuclei.

36. STEP WISE EVALUATION OF EOMs

37. EVALUATION OF EOMs Q1. Is there a manifest strabismus? How to check – Hirschberg, PBCT What to look for – Comitant or incomitant strabismus Generally a feature of infra-nuclear lesions Q2. Is there limitation of range of movement? If yes, is it horizontal, vertical or both? How to check – Ductions and versions What to look for – uniocular /binocular limitation, conjugate limitation Conjugate limitation: supra-nuclear lesion Diplopia and limitation of ductions : infra-nuclear lesions

38. EVALUATION OF EOMs Q3. Is there impairment of latency, accuracy or velocity of voluntary saccade? How to check - saccades 20 - 30° on either side of primary position What to look for – Full range of movement with slow saccades: supra-nuclear lesion Limited range of movement with slow saccades: infra-nuclear lesions Limited range of movement with normal saccades in the movement range allowed: myasthenia gravis Difference in saccadic velocity of both eyes

39. EVALUATION OF EOMs Q4 . Is their impairment of latency or velocity of smooth pursuit? How to check – Follow a small target smoothly 20° on either side of primary position What to look for – Catch up saccades C ortical lesions causing latency in pursuits: patient has catch up saccades for foveation Q5. Is their impairment of OKN ? How to check – OKN drum or scanning a newspaper in front of the patient’s eye What to look for – impaired or absent OKN Localises lesion to the cortex. OKN is also a good method for checking visual acuity in children

40. EVALUATION OF EOMs Q6. Is there impairment of VOR? How to check – doll’s head or oculocephalic maneuvers What to look for – Corrective saccades, jerk nystagmus on rapid head movement Spontaneous jerk nystagmus on head shaking: VOR dysfunction Corrective saccades after head rotation: due loss of velocity storage mechanism of VOR Q7. Is there impairment of VOR suppression? How to check - watching if the patient can keep their gaze fixed on the thumb of their outstretched hand while oscillating or being oscillated en bloc. What to look for – quick phases in direction of head movement

41. EVALUATION OF EOMs Q7 . Is there impairment of VOR suppression? How to check - watching if the patient can keep their gaze fixed on the thumb of their outstretched hand while oscillating or being oscillated en bloc. What to look for – quick phases in direction of head movement Normally the patient should be able to maintain gaze on the thumb of outstretched hand when swilled in a chair Spontaneous nystagmus indicates a VOR dysfunction

42. EVALUATION OF EOMs Q8. Is there impairment of vergence ? How to check – M oving object towards bridge of the nose What to look for – pupillary constriction present or not, adduction present or not Light near dissociation is a feature of dorsal midbrain syndrome: Here the pretectal area is affected leading to damage of pupillary light reflex centres . But since the convergence centre lies ventral to it, accomodation reflex is spared leading to miosis on convergence. In cases of horizontal gaze palsy, there is limitation of adduction due to MLF lesion. But the convergence centre remains intact in midbrain, hence the patient can have adduction on convergence.

43. EVALUATION OF EOMs Q9 . Is there involvement of other cranial nerves ? How to check – Cranial nerve examination What to look for – 2 nd nerve important, other CN involvement helps in localisation Other cranial nerve involvement can help localise the site of lesion Eg : PPRF lesion and VI n Nu. Lesion present with similar gaze palsy. If there is associated VII n palsy, that helps localising the lesion to VI n as the VII nerve fibres loop around the VI n nucleas forming the facial colliculus .

44. EVALUATION OF EOMs Q10 . Is the limitation mechanical ? How to check – FDT, FGT What to look for – Restriction vs Paralytic Q11. Is there any spontaneous or inducible involuntary eye movement, ocular oscillation, or nystagmus ?

45. SUMMARY Supranuclear lesions- BE involvement Saccade – Contralateral frontal lobe control Pursuit – Ipsilateral parietal control Horizontal movements – PPRF, MLF – Pons Vertical movements – riMLF & PC – midbrain VOR – Brief, high frequency rotations Ocular stability dysfunction – Saccadic intrusions

46. Lesions of SUPRANUCLEAR PATHWAYS

47. GAZE PALSY Symmetric limitation of movement of both eyes in the same direction. Conjugate ophthalmoplegia

48. HORIZONTAL GAZE PALSY Congenital – Mobius Syndrome Acquired – P ontine lesions - Disrupt eye movements towards the side of the lesion. Acquired – FEF lesions - Disrupt eye movements towards side of lesion

49. HORIZONTAL GAZE PALSY

50. VERTICAL GAZE PALSY Lesions of riMLF or Posterior commissure

51. INTERNUCLEAR OPHTHALMOPLEGIA

52. RIGHT INO R L

53. ONE – AND – A HALF SYNDROME

54. BILATERAL INO

55. BILATERAL INO

56. ETIOLOGY OF INO - Multiple sclerosis (commonly bilateral): Y o ung patients - Brain stem infarction (commonly unilateral): Elderly patients

57. PARINAUD SYNDROME EPIDEMIOLOGY Sporadic Causes: obstructive hydrocephalus, mesencephalic hemorrhage , multiple sclerosis, A/V malformation, trauma, compression from tumor (pineal tumors )

58. PARINAUD SYNDROME SIGNS : MAJOR COMPONENTS Vertical gaze disturbance Convergence retraction nystagmus Light near dissociation of the pupils Lid retraction (Collier’s sign)

59. PARINAUD SYNDROME

60. PARINAUD SYNDROME Differential Diagnoses for Dorsal Midbrain Syndrome Light-near dissociation Vertical Gaze Palsy

61. References Neuro - Ophthalmology, American Academy of Ophthalmology, 2010-2011. 5 th edition. Walsh & Hoyt’s. Clinical Neuro - ophthalmology. 6 th edition Khurana AK. Anatomy and Physiology of eye. 2 nd edition Kanski . Clinical Ophthalmology, 7 th edition Yanoff and Duker . 6 th edition Peter Their, Uwe J. The neural basis of smooth pursuit eye movements. Current opinion in neurology 2005,15:645-652 David L sparks, Ellen J Barton. Neural control of saccadic eye movements. Current opinion in neurobiology 1993,3:966-972 Chen,Chien Ming, Lin, Sung Hsuing . Wall eyed bilateral internuclear ophthalmoplegia . Journal of Neuroophthalmology 2007,1:9-15

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