supranuclear control of eye movements dejong & paul brazis dr shameej muhamed kv

1. DR SHAMEEJ MUHAMED KV
SENIOR RESIDENT
DEPARTMENT OF NEUROSURGERY
GMC KOZHIKODE

2. + Successful use of vision is because of properly aligned gaze which
result from the sum of body, head & eye movements.
+ To achieve these ,there are different oculomotor systems or eye
movement systems each with their own characteristics.
+ The supranuclear mechanisms that control gaze are designed to
ensure that the fovea maintains fixation on the object of interest
despite movements of the object, the eyes, or the head

3. Level 1
Supranuclear
Level 2 Nuclear
Level 3 Infranuclear
Cerebral cortex , cerebellum ,
vestibular apparatus , basal
ganglia
Brainstem nuclei , oculomotor
cranial nerve nuclei
Oculomotor nerves &
extra ocular muscles

4. + The different types of eye movement can be either gaze
shifting or holding.
+ GAZE SHIFTING
+ Its moving the eye to a new position & its also an eye
movement which follows a moving target.
+ Its acquisition of an image on the fovea and maintaining foveal
fixation while the object is moving.
+ Includes --- Saccades Smooth pursuit Vergence

5. + GAZE HOLDING
+ It’s a type of eye movements that fixate on a stationary objects
& maintain that fixation despite our head movements.
+ These Include;
– Visual fixation
– Vestibuloocular reflex (VOR)
– Optokinetic reflex (OKR)

6. GAZE HOLDING GAZE STABILIZATION
Saccades : To bring images of objects of
interest onto the fovea
Optokinetic : To hold images on the retina
during sustained head rotation
Smooth pursuit : To keep the image of a
moving target on the fovea
Vestibular : To hold images on the retina
during brief head rotations
Vergence : To move the eyes in opposite
directions to bring images of a single object
on to the fovea
Fixation : To hold eyes conjugately in a
particular position

7. + The elastic structures in the orbit support the globe and impose
a mechanical restraint on gaze control.
+ To overcome the viscous drag of supporting tissues, a strong
contraction of the extraocular muscles is required.
+ For rapid movements (e.g. saccades), a phasic increase, or burst
of neural activity in the ocular motor nuclei is required—the
pulse of innervation.
+ Once at its new position,, the eye must be held against the
elastic restoring forces acting to return the globe to central
position.
+ To hold the eye in an eccentric position, a steady contraction of
the extraocular muscles is required, arising from a new tonic
level of neural activity —the step of innervation.

8. + Without the pulse (velocity command), the progress of the eye
would be slow.
+ Without the step (position command), the eyes could never be
maintained in an eccentric position in the orbit.
+ Moreover, the pulse and step must be correctly matched to
produce an accurate eye movement and steady fixation
following it.

9. + Neurophysiological evidence indicates that the position command
(e.g., for saccades, the step) is generated from the velocity
command (e.g., for saccades, the pulse) by the mathematical
process of integration with respect to time.
+ A neural network integrates, in this mathematical sense, velocity-
coded signals into position-coded signals; this network is referred
to as the Neural Integrator.
+ When this process is faulty, the eye is carried to its new position by
the pulse but cannot be held there and drifts back to the central
position. This is evident clinically as gaze-evoked nystagmus

10. + Neural integrator for :-
+ Conjugate horizontal eye movements – Nucleus propositus
hypoglossi (NPH) and the adjacent MVN.
+ Conjugate Vertical eye movements – Interstial Nucleus of Cajal.

11. + The cerebral cortex participates in the control of all classes of eye
movements.
+ In general, reflexive stimulus-bound eye movements originate in
posterior portions of the brain, while voluntary movements arise
from frontal areas.
+ The frontal cortex contains several areas responsible for the
initiation of horizontal saccades. These include-
+ 1. Frontal eye fields (FEFs),
+ 2. Supplementary eye fields (SEFs), and
+ 3. Dorsolateral prefrontal cortex (DLPC).

12. + FEF neurons discharge for voluntary saccades, memory-guided
saccades, and vergence movements.
+ The SEFs are involved in learned patterns of ocular motor behavior.
+ The DLPC controls planned saccades to remembered targets &
cancellation reflexive saccades
+ The posterior parietal region is involved in shifting gaze toward
novel objects of interest and modulating spatial attention.
+ The parietal eye fields (PEFs) project to the FEFs and are involved in
exploring visual scenes & initiating reflexive visually guided
saccades.
+ The FEF and PEF are heavily and reciprocally interconnected.

13. + Hemispheric control of horizontal saccades is contralateral.
+ The FEF in the lateral portion of the precentral sulcus receive afferent input from the
PEF (involved in reflexive saccades) and SEF
+ Signals arising from the FEF (predominately non–visually guided saccades) and the
PEF (predominately visually guided saccades) descend to the burst cells of the
contralateral PPRF.
+ The PPRF (horizontal gaze center, lateral gaze center, pontine gaze center) is a
premotor area that consists of cells lying ventrolateral to the MLF from the level of
the abducens nucleus extending rostrally to near the trochlear nucleus
+

14. + Excitatory burst neurons (within the PPRF &rostral to VI nucleus)
discharge in anticipation of a saccade and project to the motor
neurons of the I/L abducens nucleus. Inhibitory neurons project to
the C/L Sixth nucleus.
+ Omnipause neurons are distributed throughout the brainstem
project to burst cells, and exert a tonic inhibitory effect.
+ They primarily act to prevent unwanted and intrusive saccades.
+ Omnipause neurons cease to fire approximately 15 milliseconds
before a saccade.

15. + Silence of omnipause neurons allows the EBN (within the [PPRF] of
the pons for horizontal movements, and within the [riMLF] of the
midbrain for vertical movements to fire.
+ While inhibitory burst neurons suppress activation of the
antagonist extraocular muscles (eg inhibition of the MR with LR
firing).
+ Signals from the PPRF activate both motor neurons and
interneurons in the adjacent CN VI nucleus.
+ The motor neurons project to the I/L LR, while interneurons send
axons that cross to the C/L MLF and ascend to the C/L MR
subnucleus of the oculomotor complex.

16. + One frontal pathway projects directly to the PPRF, and another
travels through the caudate, substantia nigra, and superior
colliculus (SC) before reaching the PPRF.
+ The pathways through the basal ganglia maintain balance
between reflexive and purposeful voluntary saccades and help
prevent intrusive saccades.
+ The PEF also projects through the Superior Colliculus to the
PPRF

17. III- OCCULOMOTOR MR
SUBNUCLEUS
VI – ABDUCENS NUCLEAR
COMPLEX

18. + Signals for eccentric gaze-holding reach the abducens nucleus
from the ipsilateral Nucleus Prepositus Hypoglossi (NPH) and
Medial Vestibular Nuclei (MVN).
+ These structures and their cerebellar connections serve as the
Neural Integrator for horizontal gaze-holding.
+ They provide the eye position signal necessary to hold the eye
steady in eccentric position in the orbit.

19. + Plays an important role in the triggering of & inhibition of
reflexive visually guided saccades
+ Receive input from FEF & PEF
+ Projects into C/L PPRF

20. + Substantia nigra send inhibitory neurons to superior colliculus
+ There firing cease prior to visually or memory guided saccades
+ Substantia nigra inturn under inhibitory control from caudate
nucleus
+ Frontal pathway excite caudate nucleus that inhibit the inhibitory
effect of SN on superior colliculus & therefor activate saccade

21. + Caudate lesion cause loss phasic inhibition of superior
colliculus resulting in impaired saccade initiation
+ Lesion in substantia nigra cause loss of tonic inhibition of
superior colliculus resulting inappropriate saccades

22. + THUS
+ The I/L LR and C/L MR then contract synchronously to produce
conjugate horizontal gaze.
+ A left FEF-initiated command to look right is thus transmitted
down to the right PPRF, which simultaneously influences the
(R) 6th to contract the LR and the (L) 3rd nerve to contract the
yoked medial rectus.
+ The cerebellar vermis, fastigial nucleus, and flocculus are
involved with calibrating and modulating saccadic responses.

25. The fixation objects should be presented at an angular separation of about 20 to 30°.

26. + Smooth pursuit are used to keep the image of a moving target
on the fovea
+ The goal of the system is to generate a smooth eye velocity
that matches the velocity of a visual target.
+ Visual motion processing in temporoparietooccipital (TPO)
junction drives pursuit& is I/L
+ The posterior parietal lobe and both the SEF and FEF
contribute to smooth pursuit.

27. + Axons descend from the I/L TPO junction and FEF to the I/L
dorsolateral pontine nucleus (DLPN) after descending through
internal sagitum striatum
+ Fibers cross and reach the C/L cerebellar flocculus and then project
to the vestibular nuclei & NPH
+ The projections cross again and reach the PPRF & then abducens
nucleus,ipsilateral to the originating cortical signal ie double
deccusates
+ Control of smooth pursuit, in distinction to saccades, is
ipsilateral: the left hemisphere is involved in leftward smooth pursuit
and vice versa.

29. We can normally smoothly pursue a target moving at 100 to 400 per second

30. + In contrast to horizontal gaze, which is generated by unilateral
aggregates of cerebral and pontine neurons, vertical eye
movements, with few exceptions, are under bilateral control of the
cerebral cortex and upper brainstem.
+ The groups of nerve cells and fibers that govern upward and
downward gaze, as well as torsional saccades, are situated in the
pretectal areas of the midbrain and involve three integrated
structures-
– 1. the riMLF (rostral interstitial nucleus of the MLF),
– 2. the INC (interstitial nucleus of Cajal)
– 3. the nucleus and fibers of the posterior commissure (PC)

32. + The riMLF lies at the junction of the midbrain and thalamus, at the
rostral end of the MLF, just dorsomedial to the rostral pole of the
red nucleus.
+ It functions as the "Premotor" nucleus with "burst cells" for the
production of fast (saccadic) vertical versional and torsional
movements.
+ The riMLF connect to the motor neurons of the elevator, (SR, IO)
nuclei bilaterally, and the depressor (SO, IR) nuclei ipsilaterally.
+ Each riMLF is connected to its counterpart by fibers that traverse
the posterior commissure

33. + The INC is a small collection of cells that lies just caudal to the
riMLF on each side.
+ Each nucleus projects to the motor neurons of the opposite
elevator muscles (SR and IO) by fibers that cross through the
posterior commissure, and it projects ipsilaterally and directly to
the depressor muscles (IR and SO).
+ The functional role of the INC appears to be in gaze holding (neural
integrator for vertical gaze)
+ Lesions of the INC produce a vertical gaze-evoked and torsional
nystagmus.

34. + The PC are white fibres crossing the midline on the dorsal
aspect of the rostral end of cerebral aqueduct & SC.
+ The nucleus of the PC contributes to upgaze generation and
coordination between eye and eyelid movements.
+ A lesion here characteristically produces a paralysis of upward
gaze (Parinaud syndrome).

35. + It’s a fiber tract which extend from the upper thoracic spinal cord
to oculomotor nuclei.
+ Majority of them are ascending fibers arising from the superior &
medial vestibular nuclei.
+ Most importantly they link contralateral abducent nucleus with
ipsilateral medial rectus sub nuclei.
+ The MLF is the main conduit of signals that control vertical gaze
from the vestibular nuclei in the medulla to the midbrain centers.
+ For this reason, with INO, along with the characteristic adductor
paresis on the affected side, vertical pursuit and the VOR are
impaired.

36. + OKN is a normal, physiologic phenomenon.
+ OKN is conjugate nystagmus induced by a succession of moving
visual stimuli with the fast phase in the direction opposite tape
movement.
+ Clinical testing by moving a striped target, a rotating drum
+ It can be viewed for clinical purposes as testing pursuit
ipsilateral to the direction of target movement, and
contralateral saccades

38. + The I/L PTOJ mediates pursuit of the acquired stripe via
connections that run in the internal sagittal stratum, deep in
the parietal lobe
+ When ready to break off, it communicates with the I/L frontal
lobe, which then generates a saccadic movement in the
opposite direction to acquire the next target.
+ A vertically moving stimulus can evaluate upgaze and
downgaze

39. + Cogan’s rule (hemianospia with normal OKN – occipital lesion –
stroke ;- hemianospia with absent OKN- deep parietal lesion –
tumour )
+ Useful for estimating visual function in patients with depressed
consciousness.
+ It may provide a clue to the presence of psychogenic visual loss

40. + The vestibulo-ocular reflex (VOR) produces conjugate eye
movements that are equal and opposite to head movements.
+ The VOR depends on direct connections between the
peripheral vestibular system (ie, labyrinth and vestibular nerve)
and the central ocular motor system (ie, the ocular motor
nuclei).
+ Components: (1) the horizontal VOR & (2) the vertical &
torsional VOR.

41. + SEMICIRCULAR CANAL-responds to angular acceleration produced
by head rotation
+ Change acceleration/deceleration signal to velocity signal send it to
ipsilateral vestibular nuclei.
+ Composed of three canals.
+ Each send signal to move the eye conjugatly to opposite side during
head rotation by supplying the yolk muscles.
– horizontal(lateral)canal - supply ipsilateral MR & contralateral LR
– anterior (superior)canal - supply ipsilateral SR & contralateral IO
– posterior (vertical )canal - supply ipsilateral SO & contralateral IR.

42. + OTOLITH ORGANS
– Include utricle & saccule
– They respond to linear acceleration of the head & head tilt.
– Keep the eye fixed in position to a change in head position.
+ Vestibular nuclei
– In lateral medulla beneath the floor of the 4th ventricle.
– Important for VOR & OKN.

43. + The horizontal VOR is produced by projections from the
horizontal semicircular canals (SC) to the I/L oculomotor
nucleus and C/L abducens nucleus, causing the yoked medial
and lateral recti muscles to fire.

44. eye movement
Head movement
(L)Horizintal
scc
Inter
neur
on
moto
r
neur
on
Right abducens nuclei
Right lateral rectus
Left MR SUB
NUCLEUS
LEFT MR
The excitatory connections
of the horizontal VOR:
Leftward head rotation
causes endolymph flow in
the horizontal semicircular
Canals to excite hair cells,
which transmit eye velocity
commands to the ipsilateral
vestibular nucleus located in the
medulla (not
shown), then project in to the
contralateral abducens
Nucleus directly & thru MLF
project MR nuclei resulting in
conjugate eye movement
opposite to head movement

45. The vertical and torsional VOR are generated by projections from the anterior
and posterior semicircular canals to the oblique and vertical rectus muscles.
+ Activation of B/L anterior(superior ) canals by downward head
acceleration induces the upward VOR, while activation of B/L posterior
(inferior)canals by upward head acceleration induces the downward VOR.
+ Contraction of the I/L SR and C/L IO, in response to activation of the I/L
anterior canal, results in elevation and C/L torsion of both eyes.
+ Contraction of the I/L SO and C/L IR, in response to activation of the
posterior canal, results in depression and C/L torsion of both eyes.

47. + HEAD THRUST
+ DYNAMIC VISUAL ACUITY
+ SPONTANEOUS NYSTAGMUS
+ CALORIC TEST

49. + The head impulse test is a more sensitive technique, able to detect
unilateral or bilateral abnormalities of vestibular function .
+ For this test, the patients are asked to fixate on a distant target wearing
their usual and appropriate correction.
+ The examiner grasps the patient’s head and rapidly rotates the head
horizontally.
+ The VOR response elicited results from excitation of the ipsilateral
horizontal semicircular canal.
+ If vestibular function is normal, the patient’s gaze remains steadily upon
the target.
+ A catch-up saccade back to the target at the end of the head rotation

50. + The dynamic visual acuity test is an easy method to detect B/L
VOR
+ The patient’s head is rotated left and right at 2 Hz to 3 Hz while
attempting to read the Snellen visual acuity chart.
+ If VOR is normal, visual acuity should be the same as their best
corrected visual acuity performed with the head stationary.
+ If Snellen visual acuity falls by two or more lines,suggests
impaired vestibular function.

51. + Each vestibular system exert a continuous tonic pressure to
turn eye to opposite side.
+ Lesion on the right eye moves to the right(unopposed
action from the left vestibular system)

52. + Imbalance of the VOR induces nystagmus.
+ The slow phase of peripheral vestibular nystagmus is towards
the side of lesion & fast phase towards the unaffected side
+ Can be enhanced by removal of fixation, using either Frenzel
lenses or by performing ophthalmoscopy.
+ Central vestibular nystagmus is not influenced by fixation

53. + The cerebellum plays a major role in coordinating and
calibrating all eye movements.
+ The vestibulocerebellum (flocculus, paraflocculus, nodulus,
and ventral uvula) deals with stabilization of sight during
motion.
+ The dorsal vermis and fastigial nuclei influence voluntary gaze
shifting esp saccadic eye movements

54. + INPUT
FEF & vestibular nuclei
+ OUTPUT
PPRF & riMLF
+ FUNCTION-important for saccadic eye movement
+ Stimulation of dorsal vermis evokes ipsilateral conjugate
saccades.
+ Stimualtion of fastigial nucleus elicitis contralateral saccades .
+ Fastigial nucleus is under inhibitiry control from dorsal vermis .

55. + Lesions of the fastigial nucleus (or projections) cause
hypometric C/L saccades and hypermetric I/L saccades.
+ Since the fastigial nucleus is under inhibitory control of the
vermis, ie lesions of the dorsal vermis result in hypometric I/L
and hypermetric C/L saccades.
+ Vermal lesions also impair smooth pursuit, usually toward the
side of the lesion.

56. + The floccular complex helps generate smooth pursuit and
governs the neural integrator in maintaining eccentric gaze.
+ Damage to the floccular complex results in impaired saccadic
pursuit and impaired gaze-holding, manifesting as gaze-evoked
nystagmus

57. EYE
CEREBRAL CORTEX
BRAINSTEM
(PPRF ,MLF ,MVN ,SC ,SN
RiMLF, posterior comisure
,INC
vestibular nuclei
VESTIBUALR SYSTEMCEREBELLUM
(vestibular ,dorsal
vermis , fastigial
nucleus )

59. + defect in generating voluntary saccades ( ed latency) - FEF
+ I/L Horizontal gaze deviation & I/L hemiparesis (“looking
towards lesion”)
+ Gaze palsy overcome with doll’s eye or caloric stimulation (vs
pontine gaze palsy)
+ Impaired anti saccade task – DLPC lesions
+ Impaired ability to make remembered sequence of saccades to
visible targets – SEF
+ ETIOLOGY – Tumour or stroke

60. + Increased saccade latencies
+ Hypometria for c/l saccades
+ B/L fronto-parietal lesion results in acquired oculo-motor
apraxia
+ OMA – defined as absence or defect in volitional saccade
intitiation & impaired cancellation of VOR resulting in saccadic
hypometria with a typical stair case pattern& ataxia

61. + Acute thalamic hemorrhage may be associated with a contralateral
gaze deviation (ie, right thalamic lesion causing left gaze deviation).
+ This has been called a wrong-way deviation, since it is opposite
what would be seen in a cerebral lesion.
+ The etiology is unclear but may be related to an irritative focus
causing inappropriate stimulation.
+ Thalamic esotropia (also called pseudoabducens palsy) is an eyes
turned in ,may be seen with acute thalamic lesions.
+ The mechanism may be disinhibition of medial rectus subnucleus
neurons that function in convergence.

62. + selective loss of ipsilateral horizontal saccades
+ ipsilateral gaze palsy with contralateral gaze deviation (eg, a
right gaze deviation with a left PPRF lesion).
+ Dolls maneuver or cold caloric stimulation do not affected in
PPRF lesion in contrast to abducens nucleus since vestibular
fibers directly project in abducens nucleus
+ Smooth pursuit , VOR , ability hold eccentric gaze are
preserved

63. + There is an inability to activate the I/L LR and C/L MR for all
classes of eye movements, including VOR.
+ Ipsilateral conjugate gaze palsy with contralateral gaze
deviation (eg, a right gaze deviation with a left PPRF lesion).
+ Dolls maneuver or cold caloric stimulation do not overcome
gaze palsy
+ Horizontal gaze evoked nystagmus
+ Etiology - ischemia or compression/ infiltration.

64. (A) Destructive lesion in the frontal lobe of the right cerebral hemisphere.
(B) Seizure arising from the frontal lobe of the right cerebral hemisphere.
(C) Destructive lesion in the right pons.

65. + Lesions of the MLF may result in impaired adduction during
conjugate gaze contralateral to the lesion: an INO.
+ The MLF lesion is on the side of the poor adduction.
+ Associated with nystagmus of the abducting eye.
+ Subtle INO may manifest as a slowing of adducting saccades
(“Adduction lag”) compared with abducting movements.
+ Normality of the lid & pupil distinguish an INO from 3RD palsy

66. (A) Primary position (0.0s);
(B) adduction lag of the right eye on a rapid left saccade (0.10s);
(C) near-complete adduction of the right eye at the end of the saccade (0.20s).

67. + Bilateral INO may cause a large exotropia (eyes turned out) known
as wall-eyed bilateral INO (WEBINO)
+ The etiology of INO varies with the age of the patient.
+ In children, the M/C cause is neoplasm => demyelination.
+ This is reversed in adults, in whom demyelination predominates.
+ In older adults, ischemia is the most frequent etiology because the
MLF is supplied by end arteries (perforating vessels from the
basilar).

68. + PPRF and MLF lesions combined on the same side give rise
to the ‘one-and-a-half syndrome
MR LR
LR MR
PPRF
&6th
M
L
F
M
L
F
PPRF
& 6tH
LESION
MR sn

69. + characterized by a combination of ipsilateral gaze palsy and
INO.
+ The only residual movement is abduction of the contralateral
eye, which exhibits abduction nystagmus.
A, Exotropia of the right eye at primary gaze.
B, Apparent left internuclear ophthalmoplegia on
rightward gaze.
C, Complete saccadic palsy on attempted leftward
gaze.

70. + Are continuum & types of saccadic intrusions
+ Ocular flutter are intermittent, rapid, back-to-back horizontal
saccades causing a quivering or shimmering movement
+ Opsoclonus are continuous, involuntary, random, chaotic saccades
in any direction (saccadomania, dancing eyes)
+ Likely lesion in cerebellum or brainstem cerebellar connections
+ In children: occult neuroblastoma (dancing eyes–dancing feet;
opsoclonus-myoclonus syndrome,
+ In adults:occult lung or breast carcinoma; encephalitis; cerebellar
disease.

71. + Disorders of saccadic accuracy imply cerebellar system disease and
typically produce hypermetria (overshoot of saccades)
+ Slow saccades are always abnormal and may be caused by several
diseases, including-
– 1. Genetic (eg, SCA, HD),
– 2. Neurodegenerative (eg, PSP, advanced AD, and, rarely, advanced ALS),
– 3. Infectious (eg, whipple disease and tetanus),
– 4. Paraneoplastic conditions,
– 5. PPRF lesions,
– 6. Ocular motor nerve,
– 7. Neuromuscular junction, or
– 8. Muscle disease.

72. + Patients with acute or subacute paresis of vertical gaze usually
have lesions located within the midbrain.
+ Since vertical gaze shifts are initiated bilaterally, unilateral
hemispheric and brainstem lesions cause only minor vertical
eye movement abnormalities.
+ Lesions at different levels of the midbrain may produce distinct
ocular motor deficits.

73. + It results from damage to the Posterior Commisure.
+ Core feature of PS is impaired upgaze
+ Additional findings –
– Tonic sustained downgaze (setting sun sign)
– Convergence-retraction nystagmus with attempted upgaze.
– Mid-dilated pupils displaying light-near dissociation (due to involvement of the pretectal nuclei).
– Eyelid retraction in primary gaze (Collier sign)
+ The nystagmus is best elicited by having the patient attempt upward saccades
+ Etiology - Mass lesion involving the region of the posterior third ventricle and
upper dorsal midbrain, such as a pinealoma, hydrocephalus (due to dilation of
the third ventricle and pressure on the dorsal midbrain)

74. + Degenerative diseases involving the rostral brainstem and
thalamus result in impairment first of downgaze, then of
upgaze, and eventually in global gaze paresis.
+ Other features
– Dementia
– Reflex eye movements are preserved until late in the disease.
– Parkinsonian signs
– Difficulty with the antisaccade task( sign of FL or BG dysfunction )
– Square wave jerks

75. + Skew deviation is a small, vertical misalignment of the eyes that
usually results from abnormal prenuclear vestibular input .
+ Ocular tilt reaction – triad of skew deviation , ocular torsion , &
head tilt
+ Head tilt & upper poles of both eyes tilt towards hypotropic eyes

76. + The vestibular system plays a major role in control of head-eye
posture in the roll plane – the plane in which the head or body tilt
or rotate from side to side.
+ Under normal physiologic conditions, a change in head or body
position in the roll plane initiates asymmetric sensory input from
the vertical semicircular canals and utricle to the central vestibular
system as a response.
+ For example, consider a leftward body tilt in the roll plane.
+ Physiologically, this would initiate a compensatory rightward ocular
tilt reaction.

77. + If the body is tilted to the left, it causes the left eye to be lower in space than the
right.
+ The compensatory skew deviation will cause subsequent upward rotation of the
lowermost left eye and downward rotation of the uppermost right eye to realign
them.
+ Also, when the body is tilted to the left, there is a torsional deviation of both
eyes toward the left.
+ The compensatory ocular counter-roll results in incyclotorsion of the lt eye and
excyclotorsion of the rt eye relative to the head, so that there is no torsion of the
eyes relative to space.
+ The third component of the physiologic OTR is the compensatory head tilt or
torticollis that will more closely realign the head with the gravitational vertical. In
the example of a leftward body tilt in the roll plane, this will result in a
compensatory rightward head tilt

78. + In a pathologic OTR, a unilateral lesion (or stimulation) of the
utricle or its pathways will result in asymmetric vestibular input
to the CNS that mimics a change in body position in the roll
plane as sensed by the CNS.
+ This will result in an OTR in the absence of any true body tilt in
the roll plane –
this can be tonic or paroxysmal and
can be a complete or partial with only certain components
becoming manifest

79. Left: A physiologic ocular tilt reaction (OTR) in response to a left body tilt
in the roll plane – there is a compensatory right head tilt with downward rotation
of the right eye and upward rotation of the left eye.
Right: A pathologic OTR will have the same changes in head posture, eye position
and rotation as the physiologic OTR in the absence of a change in body position in
the roll plane to stimulate it.

80. + Lesion in vestibular pathway ( ie upto caudal pons ) – results in
ipsilesional hypotropia & headtilt
+ Lesion below caudal pons ( ie after decussation – include mlf &
mibrain lesions ) results in contralesional hypotropia & headtilt
as in INO

81. + Although the pattern of misalignment may resemble a fourth
cranial nerve palsy, the direction of torsion helps differentiate
between the two disorders.
+ With a skew deviation, the higher eye is incyclotorted, while
in fourth cranial nerve palsy, the higher eye is excyclotorted.

82. + When the smooth pursuit system cannot keep up with target
movement, the more durable and evolutionarily older saccadic
system is called on to recapture the object of interest.
+ This results clinically in saccadic pursuit, in which an excessive
number of small saccades intrude on pursuit( cogwheel pursuit )
+ Symmetric loss of pursuit may be caused by a broad range of
neurologic disorders, as well as inattention, age, and medications,
and is, therefore, a nonspecific finding.
+ Asymmetric smooth pursuit suggests lateralized neurologic
dysfunction, usually cerebral (TPOJ lesion ) and ipsilateral to the
direction of abnormal pursuit.

83. + Sedative-Hypnotic Medications
+ Anticonvulsants
+ Brainstem/Cerebellar Dysfunction
+ Toxic-Metabolic Encephalopathies
+ Advanced Age
+ Inattention
+ Fatigue
+ Basal Ganglia Disorders
+ Parkinson disease
+ Huntington disease
+ Wilson disease
+ Progressive supranuclear palsy

85. + DeJong’s The neurologic examination
+ Localization in clinical neurology –paul.w. brazis
+ Online sources
+ Youman & winn

86. + Thank u