SUPRANUCLEAR PATH WAYS OF EYE MOVEMENT DR AISHA JEEVAN

SUPRANUCLEAR EYE MOVT SYSTEM Vestibular system Optokinetic system Smooth pursuit system Saccadic system Vergence system Position maintanace system

Vestibular and optokinetic – head movement

SUPRANUCLEAR PATHWAY Cortical centre Subcortical centres Vestibular system Cerebellum MLF CORTICAL CENTERS Frontal eye field Supplimentry eye field

Dorsolateral prefrontal cortexPost eye field

For pursuits

Middle temporal visual areaMiddle superior temporal visual

areaMT pass on to MST---dorsolateral

pontine nuclei---post vermis –flocculus –fastigeal nucleus of cerebellum—medial vest nuclei

VESTIBULAR SYSTEM Vestibulo- ocular reflex- vestibular

system moves the eyeballs in the opposite direction to the head movt

Latency of about 10 m sec Semicircular canals record angular

acceleration Otolith organs record linear accleration

CLINICAL TESTING

Caloric test- done by keeping the head flexed at an angle of 30-

Cold water into ext auditory canal- deviation to the same side – nystagmus in opposite direction

Warm water- opposite effect Abnormalities- vertigo; oscillopsia;

abnormal caloric test

OPTOKINETIC SYSTEMTo hold the images on the retinae

during the sustained head rotation

Reflex get fatiguied after 30 seconds

Optokinetic reflex is tested by using the optokinetic drum or tape

SMOOTH PURSUIT SYSTEMHelps to keep the image of a

moving object on the fovea constantly

Images moving away from the fovea- stimuli

Cannot follow objects that move faster than 30 or 40 per second

Latency of 125 msecDepend on alertness

CLINICAL TESTING

Inadequate pursuit by the presence of catch up saccades

Parietal lobe lesion decrease the amplitude and velocity on the side of lesion

Constant drift of eyes to the normal side

Imbalance of pursuit is seen in cerebellar disease

Loss of ipsilateral pursuit accompanied by “Cogan’s sign of spasticity of gaze”

In post cortical lesions the eye balls are displaced to the side opposite to the lesion

Associated with controlateral homonymous hemianopia and abnormal OKN

SACCADIC SYSTEM To bring the image of an object quickly

on to the fovea a rapid eye movt- saccade

Visual stimulus; noise can elicit a saccade

Alertness is required Saccadic omission Are ballistic movt Delay 200msec Velocity- 100|sec to 700 \sec

ANATOMY Pulse-sudden firing of the neurons to

the ocular muscle Step-tonic contraction of the muscle Eye movt is affected by “pulse-step

innervation” Brought by groups of neurons in the

brain stem controlled by higher centers

Excitatory burst neurons ; Pause cells ;Tonic neurons

EXCITATORY BURST NEURONS

Seen in the PPRF just above the abducent nuclei

The cells for horizontal saccades in the PPRF discharge at high frequencies

Burst cells in the ri MLF in the mesencephalon project to vertical ocular motor neurons to produce vertical saccade

PAUSE CELLS OR OPNS Located between the abducent nuclei

in the nuclie raphe interpositus They inhibit burst cells Prevent unwanted saccades

TONIC NEURONS Mediated by neural integrator Found just below the abducent nucleus

in the nucleus prepositus hypoglossi and medial vestibular nuclei

S

For horizontal saccades –impulses from the abducent n reach the lateral rectus of same side ; controlateral MR through the MLF

For vertical saccades from ri MLF for upwards pass through post commissure and for downward pass directly downwards

HIGHER CONTROLTwo parallel systems control the

production of saccadesFrontal system- controls the

voluntary gaze-voluntary saccades

Collicular system-control gaze to stimuli appearing in the periphery of the visual fields-reflex saccades

FRONTAL SYSTEM Impulses from frontal eye field pass

through the ant limb of int capsule; end high PPRF

HORIZONTAL SACCADES – impulses descend along the PPRF to end in the abducent nuclear complexe

VERTICAL SACCADES—reach PPRF ; through para MLF to mesencephalic reticular formation

riMLF coordinates down gaze

Upgaze is mediated by riMLF and nucleus of Cajal project into the controlateral third n through the post commissure and pretectum

Collicular system

Input from the frontal eye field and parieto –occipital cortex amd output goes to PPRF

Blind sight’- utilises the extrastrial pathway via sup colliculus

ROLE OF CEREBELLUM

Vestibulo cerebellum –flocculus helps to stabilize gaze holding

Lesion cause post saccadic drift; gaze evoked nystagmus; downbeat nystagmus; rebound nystagmus

Modulus- lesion produce downbeat nystagmus and positional nystagmus

Dorsal vermis and fastigial nucleus-for adjustment of saccadic pulse amplitude

CLINICAL TESTINGSaccades are tested by asking the

pt to quickly look at a particular direction

Electronystamography- ask to look quickly at the bulb that glows at the extremes of a series of bulbs arranged on a stright line

ABNORMALITIES OF SACCADE

1. impaired initiation---increased latency Seen in frontal lobe lesions; PSP;

Alzhemier’s disease

2. Abnormal saccadic velocity Fast saccades- in myasthenia slow—lesion involving burst cells

3. inaccurate saccades under shoot or overshoot seen in lesions of dorsal vermis ; fastigeal

nucleus and brain stem In Wallenberg syndrome- saccades overshoot

to the side of lesion Undershoot away from the side of lesion Post saccadic drift seen in vestibulocerebellar

lesion Hypometric saccades with post saccadic drift

seen in internuclear ophthalmoplegia; myasthenia

4. Inappropriate saccades (saccadic intrusions) - interferes with visual fixation

a) square wave jerks- it takes the eyes from the target and is followed by a corrective saccade after 200msec

Seen in cerebellar disease and Supranuclear palsy

b) Macrosquare wave jerks- larger amplitude. Seen in MS

c) Ocular flutter- to and fro horizontal saccades without inter saccadic interval

d) Opsoclonus- similar to flutter but are multidirectional

Due to disorder of pause cellsSeen in encephalitis;

neuroblastoma; tumours and head injury

VERGENCE SYSTEM To keep the image of an object on the

corresponding points of the fovea by controlling the visual axis of the eyeballs

Convergence with miosis ;accomodation– near triad “

Vergence movts are very slow dysconjugate movts

Latency is 160 msec

ANATOMY A group of neurons in the

mesencephalic reticular formation ;dorsal and caudal to the third nerve nuclear complex

ABNORMALITIES Convergence is affected by lesions in

the pretectal area It may be associated with pupillary

abnormalities ; upgaze palsy; convergence retraction nystagmus

POSITION MAINTENANCE SYSTEM To maintain a specific gaze position By rapid micromovts called flicks Slow micromovts called ‘drifts ‘ This system cordinates with other

system The same anatomical pathways for

saccadic and pursuit system

GAZE PALSIES It can be divided into two types1. Conjugate gaze palsy2. Dysconjugate gaze palsy Conjugate gaze palsya) horizontal gaze palsyb) vertical gaze palsy

HORIZONTAL GAZE PALSYFrontal lesions produce gaze palsy to the opposite

side eyes are deviated to the side of lesion away from the side of hemiparesis VOR is normal Smooth pursuit is intact

Pontine lesions gaze palsy to the same side eyes are deviated away from the side

of lesion towards the side of hemiparesis-

“Wrong way eyes” VOR is impaired smooth pursuit is affected

VERTICAL GAZE PALSYUpgaze palsy seen in lesions in the pretectal

region and post commissure accomodation is usually spared Downgaze saccades and downward

vestibular reflexes are spared Seen in tumours’

hydrocephalus;haemorrhages

Downgaze palsy it is seen in ventral midbrain lesions

involving ri MLF Ischaemic infarction in that area is the

common cause

Dysconjugate palsy1. inter nuclear ophthalmoplegia2. One and a half syndrome

Perinaud dorsal midbrain syndrome

Signs:Stright eyes in the primary positionSupranuclear up-gaze palsy defective

convergenceLarge pupilsLid retraction [collier sign ]Convergence retraction nystagmus

Causes In children – acqueduct

stenosis ;meningitis and pinealoma In young adults –demyelination;

trauma; arteriovenous malformations In elderly- midbrain vascular

accidents;mass lesions

PROGRESSIVE SUPRANUCLEAR PALSY

Steele –Richardson- Olszewski syndrome

Severe degenerative disease Present in old age Supranuclear gaze palsy affects

downgaze Later upgaze is also affected Horizontal movts get impaired Eventually gaze palsy develops

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