SUPRANUCLEAR PATHWAYS AND LESIONS

Moderator: Dr. Seema Bhosale Presenter : Shruti Chandra Jain

Overview of the PresentationA. Fundamentals of Extra-ocular movementsB. Anatomy of cortical and brainstem centersC. Basic binocular eye movements and their

pathwaysD. Step-wise evaluation of EOMsE. Lesions of Supranuclear Pathways

FUNDAMENTALS OF EXTRA-OCULAR MOVEMENTS

FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROL

• Detect objects • Spatial resolution

AFFERENT visual

system

• Clear and stable vision

• Binocular single vision

EFFERENT visual

system

FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROLEfferent ocular motor system

- Supranuclear pathways : Affect both eyes simultaneously

- Infranuclear pathways : Affect eyes differently

FUNDAMENTAL PRINCIPLES OF OCULAR MOTOR CONTROLMoving objects present a special challenge

GAZE SHIFT

GAZE STABILIZATI

ON

HIERARCHY OF OCULAR MOTOR CONTROLCortical Control, BG, SC, thalamus, VA, Cerebellum

Brainstem, Ocular Motor Cranial Nerve Nuclei

LEVEL 1: SUPRANUCLEAR

LEVEL 2:NUCLEAR

LEVEL 3: INFRANUCLEAR

ANATOMY OF CORTICAL AND BRAINSTEM CENTERS

CORTICAL CENTRES

BRAINSTEM CENTRES

VERTICAL SACCADES

HORIZONTAL SACCADES

BRAINSTEM CENTRES

BRAINSTEM CENTRES

ROLE OF CEREBELLUMCerebellum plays an important role in fine

tuning all eye movements, including modulation and adaptation of vestibulo-ocular responses, saccades, pursuit, and vergence.

ROLE OF CEREBELLUMTwo 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).

BASIC BINOCULAR EYE MOVEMENTS AND THEIR PATHWAYS

EYE MOVEMENTS

EYE MOVEMENTSCLASS 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

1. SACCADES

Rapid movement to bring object of interest on fovea

Clinical exam toCheck saccades

SACCADIC SYSTEM

STIMULUSVisually reflexive – Parietal lobe ContralateralMemory guided or volitional – Frontal lobe

Contralateral

CENTREHorizontal Saccades -> PPRF -> PonsVertical Saccades -> riMLF & PC -> Midbrain

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

VERTICAL SACCADE PATHWAYriMLF : 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

VERTICAL SACCADE PATHWAY

SACCADIC SYSTEM – Features of a saccadeLatency : duration of stimulus to movementAccuracy : arrival of eyes on targetVelocity and conjugacy : degree to which 2

eyes move togetherHypometric saccades : saccade that falls

short of intended targetHypermetric saccades : overshoots the target

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

2. SMOOTH PURSUIT

Saccade and pursuit have common neural pathway

Cortical centres Middle Temporal & Medial Superior Temporal

Ipsilateral cortical control

PURSUIT PATHWAY

I/l Posterior parietal cortex (PPC)

I/l PPRF

C/l MLF and VI Nu

Created by: Dr. Shruti Chandra

PURSUIT SYSTEM

Relatively slow moving target <30 degress per second

Initiation of pursuit - latencyGain of eye movements = output/input

PURSUIT DYSFUNCTION

Low gain -> saccadic pursuitPoor initiation -> Frontal / parietal lobe

lesionsDeficits found usually in both vertical and

horizontal planes

3. OPTOKINETIC NYSTAGMUS

OKN DYSFUNCTIONParietal or temporal lobe lesions -> abnormal

OKN towards the side of lesion

Locate and define extent of cerebral lesions

4. VESTIBULAR OCULAR REFLEX

Brief, high frequency rotation of the headSCC – angular movementsOtoliths of utricle & saccule – linear

accelerationCentre: Vestibular nucleiEfferent: fibres carried via MLF to cranial

nerve nucleiVelocity Storage mechanism

SCC PROJECTIONS - EXCITATORY

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

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.

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.

STEP WISE EVALUATION OF EOMS

EVALUATION OF EOMsQ1. Is there a manifest strabismus?

How to check – Hirschberg, PBCTWhat 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 versionsWhat to look for – uniocular/binocular

limitation, conjugate limitation Conjugate limitation: supra-nuclear lesion Diplopia and limitation of ductions: infra-nuclear

lesions

EVALUATION OF EOMsQ3. Is there impairment of latency, accuracy

or velocity of voluntary saccade?How to check - saccades 20 - 30° on either

side of primary positionWhat 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

EVALUATION OF EOMsQ4. Is their impairment of latency or velocity

of smooth pursuit?How to check – Follow a small target smoothly

20° on either side of primary positionWhat 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 eyeWhat to look for – impaired or absent OKN

Localises lesion to the cortex. OKN is also a good method for checking visual acuity in children

EVALUATION OF EOMsQ6. 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 VORQ7. 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

EVALUATION OF EOMsQ7. 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

EVALUATION OF EOMsQ8. 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.

EVALUATION OF EOMsQ9. Is there involvement of other cranial

nerves?How to check – Cranial nerve examinationWhat 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.

EVALUATION OF EOMsQ10. Is the limitation mechanical?

How to check – FDT, FGTWhat to look for – Restriction vs Paralytic

Q11. Is there any spontaneous or inducible involuntary eye movement, ocular oscillation, or nystagmus?

SUMMARYSupranuclear lesions- BE involvementSaccade – Contralateral frontal lobe controlPursuit – Ipsilateral parietal controlHorizontal movements – PPRF, MLF – PonsVertical movements – riMLF & PC – midbrainVOR – Brief, high frequency rotationsOcular stability dysfunction – Saccadic

intrusions

LESIONS OF SUPRANUCLEAR PATHWAYS

GAZE PALSYSymmetric limitation of movement of both

eyes in the same direction.

Conjugate ophthalmoplegia

HORIZONTAL GAZE PALSYCongenital – Mobius Syndrome

Acquired – Pontine lesions - Disrupt eye movements towards the side of

the lesion.Acquired – FEF lesions

- Disrupt eye movements towards side of lesion

HORIZONTAL GAZE PALSY

VERTICAL GAZE PALSYLesions of riMLF or Posterior commissure

INTERNUCLEAR OPHTHALMOPLEGIA

RIGHT INO

RL

ONE – AND – A HALF SYNDROME

BILATERAL INO

BILATERAL INO

ETIOLOGY OF INO- Multiple sclerosis (commonly bilateral):

Young patients- Brain stem infarction (commonly unilateral): Elderly patients

PARINAUD SYNDROMEEPIDEMIOLOGYSporadicCauses: obstructive hydrocephalus,

mesencephalic hemorrhage, multiple sclerosis, A/V malformation, trauma, compression from tumor (pineal tumors)

PARINAUD SYNDROMESIGNS : MAJOR COMPONENTSVertical gaze disturbanceConvergence retraction nystagmusLight near dissociation of the pupilsLid retraction (Collier’s sign)

PARINAUD SYNDROME

PARINAUD SYNDROMEDifferential Diagnoses for Dorsal

Midbrain SyndromeLight-near dissociationVertical Gaze Palsy

ReferencesNeuro- Ophthalmology, American Academy of Ophthalmology,

2010-2011. 5th edition.Walsh & Hoyt’s. Clinical Neuro- ophthalmology. 6th editionKhurana AK. Anatomy and Physiology of eye. 2nd editionKanski. Clinical Ophthalmology, 7th editionYanoff and Duker. 6th editionPeter Their, Uwe J. The neural basis of smooth pursuit eye

movements. Current opinion in neurology 2005,15:645-652David L sparks, Ellen J Barton. Neural control of saccadic eye

movements. Current opinion in neurobiology 1993,3:966-972Chen,Chien Ming, Lin, Sung Hsuing. Wall eyed bilateral

internuclear ophthalmoplegia. Journal of Neuroophthalmology 2007,1:9-15

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