Supranuclear pathways and lesions

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

2. Overview of the Presentation
A. Fundamentals of Extra-ocular movements
B. Anatomy of cortical and brainstem centers
C. Basic binocular eye movements and their pathways
D. Step-wise evaluation of EOMs
E. Lesions of Supranuclear Pathways

3. FUNDAMENTALS OF EXTRA-OCULAR
MOVEMENTS

4. FUNDAMENTAL PRINCIPLES OF
OCULAR MOTOR CONTROL
• Detect objects
• Spatial resolution
AFFERENT
visual
system
• Clear and stable vision
• Binocular single vision
EFFERENT
visual
system

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
Cortical
Control, BG,
SC, thalamus,
VA, Cerebellum
Brainstem, Ocular
Motor Cranial Nerve
Nuclei
Ocular motor nerves and Extra-
ocular muscles
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. Shruti Chandra

21. VERTICAL SACCADE PATHWAY
riMLF : upward and
downward eye movements
and for ipsilateral torsional
saccades.
Projects 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. Shruti 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

33. SCC PROJECTIONS - EXCITATORY

34. 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

35. 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.

36. 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 3rd nerve nuclei.

37. STEP WISE EVALUATION OF EOMS

38. 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

39. 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

40. 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
 Cortical 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

41. 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

42. 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

43. EVALUATION OF EOMs
 Q8. Is there impairment of vergence?
 How to check – Moving 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.

44. EVALUATION OF EOMs
 Q9. Is there involvement of other cranial nerves?
 How to check – Cranial nerve examination
 What to look for – 2nd 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.

45. 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?

46. 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

47. LESIONS OF SUPRANUCLEAR
PATHWAYS

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

49. HORIZONTAL GAZE PALSY
 Congenital – Mobius Syndrome
 Acquired – Pontine lesions
- Disrupt eye movements towards the side of the
lesion.
 Acquired – FEF lesions
- Disrupt eye movements towards side of lesion

50. HORIZONTAL GAZE PALSY

51. VERTICAL GAZE PALSY
 Lesions of riMLF or Posterior commissure

52. INTERNUCLEAR
OPHTHALMOPLEGIA

53. RIGHT INO
RL

54. ONE – AND – A HALF SYNDROME

55. BILATERAL INO

56. BILATERAL INO

57. ETIOLOGY OF INO
 - Multiple sclerosis (commonly bilateral): Young
patients
- Brain stem infarction (commonly unilateral): Elderly
patients

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

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

60. PARINAUD SYNDROME

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

63. References
 Neuro- Ophthalmology, American Academy of Ophthalmology,
2010-2011. 5th edition.
 Walsh & Hoyt’s. Clinical Neuro- ophthalmology. 6th edition
 Khurana AK. Anatomy and Physiology of eye. 2nd edition
 Kanski. Clinical Ophthalmology, 7th edition
 Yanoff and Duker. 6th 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

64. THANK YOU