gaze palsy
TRANSCRIPT
Gaze Palsy
Presenter- Dr Shubhangini J Moderator-Dr Monica Samant
Ocular Motor system-
Nuclear
Supranuclear
Infranuclear
Inter nuclear
Supranuclear control of ocular motility-
Versions-Same
direction
Vergence-Opposite direction
Supranuclear control
Eye Movements-
Eye Movement
s
Version
Saccades
Smooth Pursuit
Optokinetic
Vestibulo-ocular
Vergence
Divergence
Convergence
Saccadic System-
Cells in PPRF
Burst Cell-sends pulse step to move
the eye
Pause Cell-inhibits firing of burst cell
allowing burst cell to initiate
saccade
Tonic Cell –maintain the eye position
Smooth Pursuit System
Vestibulocerebellar system-Important input of gaze systemModulate eye movementsStabilize eye against the gravitatinal &
accelerational forceMaintaining clear vision
Cerebellum-Eye movementsFixation accuracySuppress the vestibulo-ocular reflexControls smoothness of pursuit movements Accuracy of saccades
Lesion of Supranuclear oculomotor pathways -Based on anatomical location-
Lesions of internuclear systemImmediate premotor structure in the brain
PPRF Posterior commisure Rostral mesencephalon
Cerebral hemisphereDescending pathway from cerebral hemisphereSuperior colliculusThalamus
Clinical ExaminationAsymptomatic for gaze palsyBlurring of visionDiplopia
Pre-requisite-Observe position of eye in primary gazeDuctions Versions & vergence Pursuit Saccades
Oculocephalic maneuvers-Dolls eye reflexTilt the head 30 degree forward & fixate a
distant targetRotate the head in direction opposite to gaze
palsy Direct projection from vestibular system to
ocular motor nuclei Prenuclear,nuclear infranuclear reflex does
not overcomeLesion in cerebral cortex overcome by VOR
Vestibular ocular reflex -Tilt the head by 60 degree & irrigate external
auditary meatus with cool/warm water In normal subject/supranuclear gaze palsy
eye deviate towards the irrigated side- nystagmus with fast phase to opposite side
Fast phase towards the stimulated eye when warm water is used
Supranuclear eye movement disorder-
Gaze palsy
Horizontal
Vertical
Vertical gaze palsy-Midbrain lesionB/L cerebral hemisphere
dysfunctionParkinsons diseaseProgressive supranuclear
palsylipidosis
Parinaud syndrome-Dorsal midbrain syndrome
Lesion of posterior commisure & MRFCause- compression by mass in pineal
regionDilatation of third ventricleMidbrain infarctionmultiple sclerosisAV malfomation
Poor to absent upgazeConvergence retraction nystagmus in
upgazeColliers signSetting sun sign
Parinaud syndrome-EMG shows co-contraction of occulomotor
innervated muscles- retraction of globeNeuroimaging scanSurgical treatment causes resolution of
ocular findings
Progressive supranuclear palsy-
Lesion of mesencephalic structure-Steele-Richardson-Olszewski syndromeOnset –after 40 yearsDisorder of basal gangliaMarked rigidity –trunk & neckLittle tremorDifficulty with vertical eye movements down
> upProgresses to horizontal gaze disorderEnd stage – global ophthalmoplegia
Progressive supranuclear palsy-
Vertical direction more severely affected initially Voluntary saccades affected first, convergence,
and smooth pursuit later Slowing of saccade velocitySupranuclear movements primarily affected
(vestibulo-ocular reflex spared)Square wave jerksGait abnormalitiesNuchal rigidity
Progressive supranuclear palsy-
Eyelid abnormalities: upper eyelid retraction reduced blink rate apraxia of eyelid opening blepharospasm
Postural instability with falls (often backwards)Cervical and axial dystonia
Progressive supranuclear palsy-
Wilson’s diseaseHuntington diseasKernicterous
Parkinsons disease-Lesion of descending pathway from cerebral
hemisphereUpgaze palsy affecting saccades followed by
pursuitCogwheel pursuit
Lipidosis-Lipid storage disease variant of niemann
picks diseaseVertical saccadesIntact vertical oculocephalic maneuversProgressive dementia in late childhoodChoreoathetosishepatosplenomegaly
Whipples disease-Involvement of CNS – supranuclear gaze
palsyInitially verticalProgressive dementiaHypersomniaAtaxiaUveitis
Monoocular elevation paresis-No ocular deviation in primary gaze Inability to elevate one eyePrenuclear congenital unilateral midbrain
lesion Oculocephalic maneuver is normal Lesion in pretectum Connection of riMLF to the occulomotor
nucleiForced duction & tensilon test are negative
Monoocular elevation paresis-
Skew deviation-Skew deviation is a vertical divergence“prenuclear” lesion of the vertical vestibulo-
ocular pathways in the brainstem or cerebellum.
Comitant, associated with cyclotorsion of one or both eyes.
Noncomitant it can mimic a partial third or fourth cranial nerve palsy
Skew deviation-Occur most commonly with vascular lesions
of the pons or lateral medulla (Wallenberg's syndrome)
lesions of the midbrain or upper ponsAlternating skew deviation, the hypertropia
changes with the direction of gaze. The adducting eye usually is hypotropic,mimick superior oblique overaction.
Skew deviation-
Ocular tilt reaction-cyclotorsion of both eyes, and paradoxical
head tilt, all to the same side – that of the lower eye
A tonic (sustained) ocular tilt reaction occurs with lesions of the ipsilateral utricle, vestibular nerve or nuclei, or a lesion in the region of the contralateral interstitial nucleus of Cajal and medial thalamus
A phasic (paroxysmal) ocular tilt reaction occurs with lesions of the ipsilateral interstitial nucleus of Cajal and may respond to baclofen.
Horizontal gaze palsy-More commonVary from
Gaze evoked nystagmusDysmetria of movementsTotal inability to move the eyeCommonly occur in CVA patients
Internuclear ophthalmoplegia-Lesion in MLFBetween the abducens nucleus and C/L
medial rectus subnucleus of the oculomotor nerve
Impairs adducting saccades of the ipsilateral eye, which become either slow or absent
DysmetriaDisconjugate nystagmus.
Internuclear ophthalmoplegia-If INO is bilateral abduction saccades also may be slow Upward beating and torsional nystagmus Other clinical features
skew deviationdefective vertical smooth pursuitimpairment of the vertical VORimpaired ability to suppress or cancel the
vertical VOR.
Internuclear ophthalmoplegia-Occur with a variety of disorders of
brainstemVascularDemyelinatingMetastatic
Must be differentiated from the pseudo-INO of myasthenia or a long-standing exotropia.
One & half syndrome-Damage to the caudal pons Ipsilateral MLF and either the ipsilateral
PPRF or the abducens nucleusIt results in an ipsilateral gaze palsy with an
ipsilateral INOIntact horizontal movement is abduction of
the contralateral eye
One & half syndrome-If the facial nerve nucleus or fasciculus is
involved, oculopalatal myoclonus may develop Most common causes
multiple sclerosis and brainstem strokefollowed by metastatic primary brainstem tumors
Ocular myasthenia may cause a pseudo-one-and-a-half syndrome
Ocular motor apraxia-Loss of or severely diminished volitional
saccades Retention of the fast phases of vestibular
nystagmus • Difficult horizontal saccades• Head thrust towards desired
directionCongenit
al• Balint syndrome• Both Horizontal & Vertical• Simutagnosia/optic ataxiaAcquired
Convergence paralysis-Midbrain lesions ,dorsal midbrain syndrome. Cerebellar degeneration, Parkinson's
disease, and progressive supranuclear palsy, are associated with poor convergence.
Lack of pupillary constriction on attempted convergence may differentiate psychogenic convergence paralysis from organic disease.
Divergence paralysis-Uncrossed horizontal diplopia Intermittent or constant esotropia Abduction is full. Break in fusion later in life Treated easily with base-out prisms for the
distance correction Divergence paralysis is a controversial entity,
difficult to differentiate from divergence insufficiency and bilateral sixth cranial nerve palsies.
Functional gaze palsies-Horizontal gaze palsy – miosis during
attempted gazeSaccades-VOR should be stimulated
(oculocephalic maneuvers,calorics,chair rotation ), OKN test
Pursuit
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