supranuclear pathways and lesions
TRANSCRIPT
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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