Ocular motility disorders: the Approach Supra- vs infra- nuclear disorders and its related basic science Other: synkinesis/aberrant regeneration, nystagmus

1. Ocular Motility
Clinical
Yong Meng Hsien 2020

2. EOM problem- Approach
Supranuclear
• horizontal gaze
– pons
–PPRF/MLF- INO/one &
half/BINO/WEBINO
• vertical gaze
– midbrain
– Parinaud/Dosal Midbrain
Syndrome
– Limited upgaze @elderly
– Progressive supranuclear
palsy
– Niemann-pick disease
– Whipple’s disease
Infranuclear
• nuclei
– motor neuron dz
– brainstem lesion
(vascular/ifx/inflame/demyelin/
tumour)
• nerve
– pathway (aneurysm/high
ICP/compression/ifx/inflame/demyelin)
– vascular (DM)
• NMJ
– MG
• Muscle
– TED/myositis/pseudotumour
– orbital wall #
– CPEO (mitochondria dz)
– muscular dystrophy

4. DDX- complete ophthalmoplegia
Infranuclear
• Congenital fibrosis of EOM
• Mitochondrial d/o
– CPEO
– Kearns-Sayre
• MG
• GBS/MFS
• Orbital apex syndrome
(tumour/inflam)
• Cavernous sinus (CCF)
Supranuclear
• PSP
• Encephalopathy
– Wernicke

5. INO
Signs
• Ipsi adduction failure
• Contra abduction nystagmus
• convergence N –post INO
• convergence abn- ant INO
(Cogan’s) with XT/WEBINO
• Abn saccade
• Abn VOR or Doll’s eye
• Abn vertical component
(nystagmus/pursuit abn/VOR
abn, upgaze maintenance abn)
Others
• Intro: Ipsi MLF
• Causes: MS > CVA >
tumour/ifx
Variant:
•BINO
• WEBINO
• one & half

6. NeuroOphthal:
Cranial Nerve Palsy
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7. Syndrome Features
Nuclear III BL ptosis/BL mydriasis, IL MR/IR/IO, CL SR
Weber’s IL III, CL hemiparesis (pyramidal tract)
Benedict’s IL III, CL hemitremor/hemisensory loss (red nucleus & medial
lemniscus)
Nothnagel’s IL III, CL ataxia (superior cerebellum)
Claude ‘s Benedict + Nothnagel
Nuclear VI IL VI + VII, IL horizontal gaze (PPRF/MLF)
Millard Gubler IL VI + CL hemiparesis (corticospinal tract) *ventral pons
Raymond Cestan’s Millard Gubler + IL INO/ataxia/tremor *upper/dorsal pons
Foville’s Millard Gubler + IL VII/PPRF/Horner *lower/dorsal pons
Locked in BL horizontal gaze + quadriplegia *BL pons
Gradenigo’s IL VI + V1 pain +/- VII/VIII
(otitis media/mastoiditis → petrous temporal bone)
CPA IL V/VI/VII/VIII + cerebellar
Cavernous sinus IL III/IV/V1,2,3/VI/Horner
SOF IL III/IV/V1/VI
Orbital apex IL II/III/IV/V1,2/VI

8. Notes: 6th CNP
• improve CL eye mvm if affected eye closed
• a/w A pattern (NOT V)
• Faden operation (rectus muscle only)
Six causes of “pseudo VI CN palsy”
- Thyroid eye disease
- Myasthenia gravis
- Duane’s syndrome
- Medial wall fracture
- Esotropia (longstanding)
- Convergence spasm

9. SO4 CNP
• Parks-Bielschowsky 3-steps test
• causes:
–congenital: nerve/muscle/tendon hypoplasia
–acquired: trauma/DM/vascular/tumour
• SSx:
–worse on distance
–Parks-Bielschowsky 3 steps (hyperopia/WOOG/BOOT) or face turn + tilt opposite = better
–If + 3rd CNP: no intorsion on out & down
–double maddox rod
• congenital (vs acquired)
– no cyclotorsion
– + A pattern
– + vertical fusional amplitude high/>4 PD
– AHP, facial asym
– need TRO BSV impairment
• BL SO4 (vs UL)
– + chin down (no head tilt)
– + less hyperdeviation at primary gaze
– + reversal of hyperdeviation/diplopia on lat version
– + large V pattern
– + extorsion >10 degree
– + 3-step test at BL tilt (BOOT)
– + subjective incyclodiplopia
– need Harato-Ito procedure (transposition of ant ½ SO4 tendon (reduce extorsion)

11. DDX
Abduction defect
• 6th CNP
• Duane
• Mobius
• TED/MG/CFEOM
Adduction defect
• 3rd CNP
• INO
• Duane > type II
• TED/MG/CFEOM
Hypotropia
• IO palsy
• Brown
• Monocular elevation def
• TED/MG/CFEOM
Hypertropia
• SO4 CNP
• TED/MG/CFEOM

12. Synkinesis
= Aberrant Regeneration
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13. Synkinesis
= Aberrant Regeneration
• miswiring of nerves after injury that results
in involuntary action/movements accompanying
voluntary movements/action
• Causes: nerve trauma/tumour, or compression/
inflammation, congenital
• 3 mechanisms for synkinesis:
– aberrant nerve regeneration
– interneuronal ephaptic transmission (artificial
synapse/cross talk)
– nuclear hyperexcitability.
• Rx: botox (chemical neurectomy), physio, surgical
neurolysis/myectomy

14. Aberrant Regeneration- Congenital
1. Marcus Gunn jaw-winking
= trigemino-oculomotor or pterygoid-levator synkinesis
– AD (incomplete)
– Trigeminal stimulation (pterygoid muscles of jaw)
• Jaw thrust/forward & mouth opened wide (external pterygoid)
• Teeth clenching (internal pterygoid)
– Oculomotor nerve (LPS)
• Jerky upward movement of eyelid
• If falling eyelid = inverse MGJW
2. Duane retraction syndrome
= oculomotor–abducens synkinesis
– Absence or diseased 6th CN nuclei/nerve
– Globe retraction & narrowing of palpebral fissure n adduction
– Type 1-3: abduction/adduction/mixed inability,
ET/XT/orthophoria

15. Duane Syndrome

16. Aberrant Regeneration- 3rd
- Oculomotor Synkinesis -
• Usually following traumatic and compressive lesions
(usually aneurysm or meningioma)
• Ischemia unlikely to cause this – since no disruption of
endoneurial integrity!
1. Lid-gaze
– upper lid retraction in down gaze (pseudo von Graefe’s),
upgaze or adduction (inverse Duanne)
2. Pupil-gaze
– miosis in down/upgaze/adduction (pseudo Argyll
Robertson)
3. Btw rectus muscles (eg, adduction with vertical gaze)

17. Aberrant Regeneration- 7th
-Facial Synkinesis-
• Autonomic synkinesis (crocodile tears)=
tearing (lacrimal fiber) with chewing (salivary
fiber)
• Motor synkinesis= btw facial - o.oculi - o.ori
– contracture of the facial muscles while smiling or
closing the eyes
– eye closure associated with lip pursing
– mouth grimacing with blinking of the eye

18. Aberrant Regeneration- 4/5/6/9th
• 6th to 3rd
• eye abduction → eye adducts and the eyelid retracts
• eye abduction → pupil constricts
• 4th to 3rd
• Eye adduction with depression → eyelid retracts
• Trigeminal-Abducens Synkinesis
• eating or chewing → involuntary eye abduction
• Trigeminal-Facial Synkinesis
• weakness in voluntary chewing
• facial movements/blinking → chewing muscles contract
• High AC/A ratio with esotropia
• focusing for near → involuntary excess convergence
• Frey’s Syndrome (CN IX salivation fiber-sympathetic fibers)
• Flushing/sweating when eat

19. Nystagmus
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20. Nystagmus in Brief
• Def (x 5)
• Description (x 5)
• Classification
– physiology/motor/sensory
– early/late onset
– central/peripheral
– pattern
• TRO sensory deprivative
– slit lamp
– electrophysio (ERG.VEP)
• TRO CNS abn
– neuroimaging
Principles:
• Alexander law
• null pt
• neutral zone (reverse)

23. Nystagmus Mx
• Conservative/Refractive/Botox/Surgery
• Fresnel prism
– To correct AHP by shift image to null pt (apex toward
null pt & opposite direction of head turn)
– To induce convergence & damp nystagmus (BL base
out prism)
– To check post op response.
• Surgery
– To correct AHP by shift null pt to primary position
– To reduce intensity of nystagmus
– Anderson procedure: conjugate recession
– Kestenbaum procedure: recess-resect BE
– Recession of all 4 horizontal muscles

24. Specific Nystagmus
• Ataxic/dissociated- INO, post fossa
• Convergence retraction- dorsal midbrain/Parinaud/pinealoma,
pretectal nucleus
• See-saw- bitemporal hemianopia (3rd ventricle, parasellar),
parinaud
• Up beat- medullary, post fossa, Wernicke, ant cerebella
• Down beat- lithium/phenytoin, Werniekie, paraneoplastic
cerebella, Arnold chiari/cervical medullary jx/foramen magnum
• Periodic alternating- vestibulo-cerebellar, phenytoin, ataxia
telangiectasia, congenital
• Torsional- medullary
• Jerk: congenital motor/idiopathic, extreme gaze,
brainstem/cerebellar
• Bruns (nystamus toward & away lesion)- large CPA tumour
– Toward lesion = brainstem lesion
– Away lesion = peripheral vestibular lesion

25. Specific Nystagmus
• Better on
– convergence/base out prism: congenital
– sleep/no fixation: congenital (worse on fixation)
– fixation: peripheral vestibular
• Childhood/early onset
– congenital/infantile nystagmus syndrome
• Key: birth/mth, no oscillopsia, all gaze same (uniplanar/binocular/conjugate/horizontal),
better on convergence/sleep/eye close/base out prism & null pt, worse on fixation
• head tilt/titubation, paradoxical OKN, latent nystagmus component
• pendular: sensory deprivation
• jerk: motor/idiopathic
– Spasmus nutans-
• 3-18mth  resolve in 3yo, a/w chiasma glioma/empty sella,
• UL/asym, high frequency low amplitude, horizontal, head nodding, +-amblyopia
• A/w squint
– latent/manifest latent (fusional maldevelopment) @congenital
ET/XT/amblyopia
– nystagmus blockage syndrome (convergence to reduce nystagmus)
– ciancia syndrome

26. Basic Science- EOM & Eye Mvm

27. Ocular motility- outline
• Ocular Motility
– Duction
– Version (horizontal & vertical, saccade/pursuit/VOR)
– Vergence
• Laws
– Sherrington/agonist/antogonist/synergist
– Herring/Yoke’s muslce
• Anatomy
– supranuclear & infranuclear
• Clinical features
– palsy (gaze/CN/ophthalmoplegia) & nystagmus

28. Ocular motility- Glossary
• Monocular eye movements = Ductions
– Adduction/abduction
– sursumduction (supraduction/elevation)/ deorsumduction
(infraduction/depression)
– Incycloduction (intorsion)/excycloduction (extorsion)
• Agonist= primary muscle that moves an eye in a given
direction
• Synergist= muscle in the same eye that moves the eye in
the same direction as the agonist
• Antagonist= muscle in the same eye that moves the eye in
the opposite direction of the agonist
• Sherrington law= increased innervation to any muscle
(agonist) is accompanied by a corresponding decrease in
innervation to its antagonists.

29. Ocular motility- Glossary
• Binocular eye movements = conjugate/same direction (versions) or
disconjugate/opposite direction (vergences)
– Dextroversion & levoversion
– Sursumversion (supraversion/elevation) & deorsumversion
(infraversion/depression)
– Convergence & divergence (vertical vergence/accommodative
convergence)
• Yoke muscles= primary muscles in each eye that accomplish a given
version
• Herring law= yoke muscles receive equal/simultaneous innervation
• Primary deviation= misalignment, with the normal eye fixating
• Secondary deviation= misalignment, with the paretic eye fixates
(usually larger than the primary deviation)
• Field of action= direction of rotation of the eye when that muscle
contracts. (Indicates the gaze position in which the effects of a
muscle most easily are demonstrated. Strabismus often increases in
the field of action of a weak eye muscle)

30. EOM- the Anatomy
• Embryo: mesoderm
– 5W start (primordium) → 2yr completed migration of
insertion (Tillaux)
• Functions (1/2/3)
• Macroscopic (table)
– origin/course/insertion/size
– blood supply/innervation
• Microscopic:
– characteristic (nerve-fiber ratio, fatigue resistant, fast)
– fibers (types, inner global vs outer orbital layer)
– Content of fiber cell & surrounding

31. EOM- Actions
• EOM= 2x horizontal rectus & 2x vertical rectus & 2x oblique
• Horizontal rectus (MR & LR)
– only horizontal actions (adduction or abduction)
• Vertical rectus (SR/IR)
– primary vertical actions (elevation/depression)
– forms a 23° angle relative to the visual axis in the primary
position
– greatest elevation with the eye in the abducted position
– secondary torsion & tertiary adduction.
• Oblique muscles (SO/IO)
– primary torsional actions (intorsion or extorsion)
– forms a 51° angle relative to the visual axis in the primary
position
– leads to secondary vertical actions (best when the eye is
adducted) & tertiary abduction.

34. EOM- the Number
• Spiral of Tillaux= 5.5/6.5/6.9/7.7mm
(pierces tenon 10mm behind insertion)
• Angle of insertion= SR/IR 23, SO/IO 51 degree.
• CN to inner surface of rectus muscle @ junction ant 2/3-
post 1/3 (oblique muscles are outer surface)
• Nerve: fiber= 1: 3-5 (others sk muscle 1:50-125)
• Felder vs fibrillen-struktur size= 10um vs 15um
• AC:C ratio= 3-5 prism diopter
• Fusional convergence amplitude= near 25/far 15 prism
diopter
• Saccade 300-700 degree/sec, latency 100ms
• Pursuit <30 degree/sec, latency 125ms
• Globe can be moved 50° from primary position (but
normally move about 1 5°-20° before head mvm occurs)

35. AAO info

36. Supranuclear Gaze Control
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37. Binocular Movement
Aim: to establish clear, stable, and binocular vision
2x basic movement:
1. gaze shift
2. gaze stabilization/holding
6x functional systems or classes:
1. visual fixation
2. vestibular ocular reflex/VOR
3. optokinetic
4. smooth pursuit
5. saccades
6. vergence

38. Ocular Movement- Anatomy
Supranuclear
• Cerebral cortex control
– FEF, MT/MST/POT
– + subcortex: basal ganglia (BG), thalamus, and superior colliculus (SC)
• Brainstem
– Reticular formation- mesencephalic/para-pontine/medullary
– + neural integrators
– + tracts (MLF)
– + vestibular-ocular system
• Cerebellum
Infranuclear
• Ocular motor CN (III, IV, and VI)- nuclei & nerve
• NMJ
• EOMs
Supra- VS Infra-nuclear: Symmetrical BE + No diplopia + Normal VOR

39. Supranuclear control
• Cerebral cortex
– frontal lobe (FEF/Brodmann 8 & SEF)- saccade (memory-guided and volitional)
– parietal lobe (posterior parietal cortex)- saccade (visually reflexive), pie in floor VF
– temporal lobe (POT or MT/MST): smooth pursuit, prosopagnosia (unable to recognize
face- BL inf occipitotemporal lobe/fusiform gyrus), pie in sky VF, achromatopsia (BL
temporal)
– Occipital: anterior to posterior (temporal to center field), posterior tip (macular, dual
supply)
– Basal ganglia (caudate nucleus, putamen nucleus, and substantia nigra)- saccade
control, filter unnecessary reflexive saccade
– Thalamus (internal medullary lamina and pulvinar)- relay & programming of saccade
– Superior colliculus- processing unit (superficial for sensory, deep for motor) of saccade
– internal capsule- relay for pursuit
• Cerebellum
– vermis: initiation of mvm
– floculonodular lobe (paraflocculus and dorsal vermis): mediate vestibular reflex/pursuit
– brachium conjunctivum- adjust gain of all ocular movements

40. Supranuclear Control
• Midbrain (mesencephalic reticular formation, MRF)
– vertical & torsional gaze/saccade (excite/inhibit)
• Pons (paramedian pontine reticular formation, PPRF)
– horizontal gaze/saccade (excite/inhibit)
– medial longitudinal fasciculus (MLF): major pathway for relaying signals within the
brainstem
• Medulla (medullary reticular formation, MedRF)
– horizontal gaze (inhibit)
• Vestibular system/nuclei (pons/medulla)
• connect saccade generator & CN
• semicircular canal: rotator head mvm (angular) detection
• utricle & saccule: head tilt (linear)
• spontaneous nystagmus
• check: direct ophthalmoscope VS shifting of fovea , head shaking nystagmus

41. Brainstem Control (neuron)
Midbrain
• rostral interstitial nucleus of MLF (riMLF)- vertical & torsional gaze/saccade (excitatory burst
neuron)
• interstitial nucleus of Cajal (INC): vertical & torsional gaze/saccade (inhibitory burst neuron)
• region of riMLF and INC: vertical & torsional saccades (inhibitory burst neuron)
• y-group cells: cells that project to CNs III and IV nuclei for vertical smooth pursuit and vertical
vestibular eye movements
Pons
• nucleus raphe interpositus (RIP): omnipause cells
• nucleus reticularis tegmenti pontis (NRTP): long-lead burst cells
• dorsolateral pontine nuclei (DLPN): neurons for smooth pursuit
Medulla
• nucleus prepositus hypoglossi (NPH): neural integrator for horizontal gaze/eccentric gaze
– Pathology, often metabolic, associated with alcohol consumption or anticonvulsant
medication results in failure to maintain eccentric gaze → gaze-evoked nystagmus

42. Brainstem Control (tracts)
• MLF
• CL PPRF/6th CN nuclei to ipsilateral 3rd CN nuclei
• vestibular system to gaze center/CN nuclei
• posterior commissure (PC): INC to contralateral CNs III/IV/VI/INC
• damage in dorsal midbrain syndrome (impaired vertical gaze/upgaze)
• cell groups of paramedian tracts (PMTs): neurons that project from the CN
VI nucleus to the cerebellum

43. INO
• Ipsilateral adduction palsy and horizontal jerk
nystagmus of the contralateral eye during abduction.
– with normal convergence (mostly)
• Ipsilateral MLF lesion @ pons/midbrain
• BINO, WEBINO, INO-plus (SO4)
• The MLF also carries vertical, torsional, and velocity
eye movement information
– +- skew deviation (contralateral eye hypoT)
– gaze-evoked upbeat nystagmus in upgaze @ BINO
– convergence loss in WEBINO (otolith input or ant INO
involved convergence fibers)

44. One-and-half syndrome
•INO + ipsilateral horizontal gaze palsy
•Lesions
–Nuclear: INO + 6th CN nuclei
•all eye movements are impaired
–Supranuclear: INO + PPRF
•limited voluntary rapid eye movements (saccades) can
be overcome by oculocephalic (VOR) stimulations
•+ peripheral facial nerve involvement 
eight-and-a-half syndrome.

45. Skew deviation
•acquired vertical misalignment (comitant or incomitant)
•Lesions:
–central graviceptive vestibular pathways (sense linear motion
and static tilt of the head via gravity)
–asymmetric disruption of supranuclear input from the otolithic
organs (utricle and saccule)
–Cerebellum
–Midbrain: vertically acting ocular motoneurons & interstitial
nucleus of Cajal (INC)
•If lesion below the decussation of the vestibular pathways
at the pontine level, the lower eye is on the opposite side
of the lesion
•Exception of supranuclear lesion causing diplopia
•Parks-Bielschowsky 3-step test

46. Bilateral hypertropia
•Periodic alternating skew
–Alternating hypertropia, typically with a 30–60
second periodicity, indicative of a midbrain lesion.
•alternating skew deviation on lateral gaze
–>hyperT @ same direction gaze
–Lesion: cerebellum, cervicomedullary junction, or
dorsal midbrain
•BL SO4 CNP
–>hyperT @ opposite direction gaze + excyclotropia

47. Saccade
• Def: fovea shifting to eccentric target/bring object in peripheral to fovea
• Character:
– Ballistic (cannot altered once initiated)
– V= >100/400 degree per sec (depends on amplitude of mvm)
– L= 100-200msec
– Duration < 1msec
– Supplement pursuit >50degree/sec (cogwheel pursuit)
– Fast phase of nystagmus/OKN
– Saccadic suppression/omission to avoid blurring
• Anatomy:
– FEF/SEF (volitional pathway/voluntary)
– Parietal lobe (visual reflexive pathway/involuntary)
– Subcortex: SC/BG/thalamus (signal processing)
– Decussate at midbrain
– Contralateral gaze center/PPRF
– Neural integrator (riMLF/INC for vertical gaze, NRTP/RIP/NPH for horizontal)
• Clinical:
– Latency/accuracy/velocity/conjugacy
– Hypo/hypermetric

48. Pursuit
• Def: fovea/fixation holding on moving object
• Characters:
– Smooth slow
– V= < 100 degree per sec (30-40)
– L =125-150 msec
– Cogwheel if V>50 degree/sec (pursuit fall behind → saccade to re-fixate
→ pursuit again)
• Anatomy:
– MT/MST/POT junction
– Subcortex: int capsule/BG/SC (signal processing)
– Vestibulocerebellum (signal processing)
– Ipsilateral gaze centre/PPRF (double decussate at pons & cerebellum)
• Clinical:
– slow component of OKN nystagmus (unilateral lesion = asymmetrical =
Cogan’s law)
– Latency/accuracy/gain (1-0, lag behind stimulus & catch up with
saccade)

49. Vestibulo-ocular reflex (VOR)
• Def: hold image/fwd fixation at brief head mvm
• Supplement pursuit with brief/high frequency head movement
• Characters:
– Involuntary/non optical reflex
– Slow 20-50 degree/sec
– Extreme short latency 10 msec (fast reflex)
• Anatomy
– Semicircular canal (endolymph mvm/velocity changes) & utricle/saccule
(otoliths/linear acceleration/gravity)
– Vestibular nerve (CN VIII) → nuclei @ rostral pons-medulla
– Modified by cerebellum
– Cross over to contralateral gaze center/PPRF
• Clinical
– Brainstem test
• doll eye reflex/oculocephalic reflex
• caloric test with COWS nystagmus)
– By pass supranuclear input above PPRF

50. Ocular Tilt Reaction (OTR)
•Abnormal eye-head postural reaction
•3 components:-
– Head tilt
– Skew deviation
•vertical misalignment of the eyes
– Ocular torsion
•incyclotorsion and excyclotorsion
•Imbalance in vestibular input to the oculomotor system (abnormal VOR)
 altered sense of true vertical
 compensatory response
•Causes
–Peripheral: vestibular apparatus (inner ear), vestibular nerve
–Central: brainstem/cerebellum
•Aetiology:
– Ischaemic stroke, demyelination, trauma, iatrogenic/post-surgical, haemorrhage, or tumour

51. Localisation of lesion for OTR
•Most common: ipsilateral lesion in VOR pathway
•Altered sense of true vertical in OTR
due to hypo-function of ipsilateral VOR pathway, or
due to hyper-function of contralateral VOR pathway
•VOR pathway decussates in the level of upper pons/midbrain
–Before decussate (otolith  upper pons)
•Hypofunction lesion: ipsilateral OTR
•Hyperfunction lesion: contralateral OTR
–After decussate (upper pons  midbrain)
•Hypofunction lesion: contralateral OTR
•Hyperfunction lesion: ipsilateral OTR

52. Optokinetic
• Def: hold image on retina on sustain eye movement
• Supplement pursuit/vestibular reflex
• Characters:
– physiology nystagmus
– Biphasic (slow pursuit/quick saccade)
– Velocity 30-100 degree per sec
– Latency 70 msec
• Anatomy
– Slow pursuit (direction of OKN)- by ipsilateral MT/MST/POT
– Fast saccade (opposite)- by ipsilateral FEF
• Clinical
– VA test
– Functional blindness
– Congenital nystagmus with paradoxical OKN reflex
– Assess homonymous hemianopia (impaired OKN when turn to opposite
hemianopic field/ipsilateral to lesion- of parietal/temporal)
– Detect INO (toward eye with adduction failure)
– Detect Parinaud convergence retraction nystagmua (rotate OKN downward)
– Detect vascular occipital lesion (symmetrical OKN)

53. Vergence
• Def: eyes move in opposite direction for BSV
(disconjugate binocular mvm)
• by relative movement toward or away from the eyes
• Character:
– Slow 20-50 degree per sec
– Latency 160 msec
• Anatomy
– Pretectal nucleus → CN III nuclei (EW & MR nucleus) & VI
nuclei
• Clinical
– Spared in solely MLF/posterior midbrain lesions
– Light-near dissociation (parinaud/Adie/Argyll Robertson)

54. Fixation mvm/Troxler’s
phenomenon/microsaccadic refixation
• Def: small eye mvm to move retinal image at
regular interval, or correction of ocular drift
(prevent image fade/bleaching of
PRC/attenuated neural response)
• 0.1-0.2 degree of visual angle, square waves,
slight pause 200ms (intersaccadic interval)

55. Pictures
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