3. Six cardinal positions of gaze are those positions in which one muscle in
each eye (yoke muscle) has moved the eye into that position. These are as
follows-
1. Dextroversion (right lateral rectus and left medial rectus).
2. Laevoversion (left lateral rectus and right medial rectus).
3. Dextroelevation (right s uperior rectus and left inferior oblique).
4. Laevoelevation (left superior rectus and right inferior oblique).
5. Dextrodepression (right inferior rectus and left superior oblique).
6. Laevodepression (left inferior rectus and right superior oblique).
These paired muscle (one from each eye) are known as yoke muscle.
4. Nine diagnostic positions of gaze are those in which deviations are
measured. They consist of the six cardinal positions, the primary position,
elevation and depression
5. Normal eye movements are a prerequisite to vision.
The goal is to bring an object of interest onto the fovea and to hold it
steadily.
Allowable retinal drift varies with the spatial frequency of the object
being viewed 50/s for standard visual acuity charts).
Excess retinal motion degrades visual acuity and may causen
oscillopsia (illusory movement of the visual environment).
Since head perturbations are frequent during normal activities (such as
walking), compensatory mechanisms have evolved to prevent retinal
drift with head and body movements.
6. Class of eye
movement
Main function
Fixation Holds images of stationary objects upon the fovea
Vestibulo-ocular
reflex
Gaze-holding: keeps images steady on the fovea during brief head rotations
Optokinetic Keeps images stable on retina during prolonged sustained head rotations
Smooth pursuit Holds images of small moving targets steady upon the fovea
Saccades Brings objects of interest onto the fovea
Vergence Moves eyes in opposite directions to bring images of a single object onto the
fovea
Nystagmus
(quick phase)
Reset the eyes during prolonged rotation and direct gaze toward the oncoming
visual scene
7. Vestibulo-ocular reflexes depend on the ability of the labyrinthine
mechanoreceptors to detect head accelerations,
while visually mediated reflexes (optokinetic and smooth pursuit
systems) rely on the brain’s ability to determine retinal image drift.
These reflexes act as gaze-holding mechanisms that stabilize gaze and
hold images steadily on the retina.
The afferent visual system plays a critical role in gaze-holding by
providing appropriate feedback regarding desired and actual target
position and eye position.
8. Saccades are rapid conjugate eye movements that redirect fixation so
that a new object of interest falls onto the fovea.
Vergences are dysconjugate movements (ie, the eyes are moving in
opposite directions) that shift gaze between far and near targets
(convergence and divergence).
Both of these systems act as gaze-shifting mechanisms, which aim to
bring new objects of interest onto the fovea.
Normal eye movements can then be conceived in terms of a balance
between gaze-shifting and gaze-holding mechanisms, with
continuous feedback and reprogramming from the afferent visual
system.
9. 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).
10. Cortical and sub-cortical pathways involved in
the generation and modulation of horizontal
saccades.
11. In clinic or at the bedside, voluntary saccades are assessed by asking
the patient to refixate between two targets (such as the examiner’s
fingers), usually 300 to 400 apart.
Normal refixation movements should be accomplished with one
saccade or may undershoot the target and require one or two catch-up
saccades to reach the target.
Three or more refixation saccades are considered hypometric and
abnormal, particularly if asymmetric.
Hypermetric saccades overshoot the targets and are always abnormal,
often indicating I/L cerebellar system dysfunction.
Saccadic hypometria indicates cerebral dysfunction but is otherwise
(in isolation) non-localizing.
12. Smooth pursuit eye movements are used to track objects moving in the
environment.
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.
Smooth pursuit pathways are less well understood than saccadic pathways,
but a critical area, is the junction of the occipital and temporal lobes,
analogous to the medial temporal (MT) and medial superior temporal
(MST) region in monkeys.
The posterior parietal lobe and both the SEF and FEF contribute to smooth
pursuit.
14. Smooth pursuit is examined clinically by having the patient
track a slowly moving accommodative target, such as the
20/200 letter on a near card.
We can normally smoothly pursue a target moving at 100 to
400 per second.
It is important to move the target at this rate; rapidly moving
a target back and forth will overcome even a normal smooth
pursuit system and give a false impression of impaired
pursuit.
15. The vestibulo-ocular reflex (VOR) produces conjugate eye movements
that are equal and opposite to head movements.
Components: (1) the horizontal VOR & (2) the vertical & torsional
VOR.
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).
The cerebral modulation of the VOR remains poorly understood,
Recent evidence suggests that cortical processing of vestibular input is
distributed among multiple areas, including the posterior insular cortex
and the parietal and frontal cortex
16. 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 (not
shown), then to the
contralateral abducens
nucleus
MLF
Via left vestibular
nucleus
17. VOR gain (the ratio of eye velocity to head velocity as the eyes and
head move in opposite directions) must be close to 1.0 to maintain
normal vision and can be assessed in clinic.
Abnormal VOR gain (too low or too high) causes images to move
across the retina and results in visual blur or apparent motion of the
environment (oscillopsia).
The dynamic visual acuity test is an easy method to detect B/L VOR
gain abnormalities; 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 gain 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, VOR gain is too low
or too high.
18. It is a jerky nystagmus, caused by altered input from the vestibular
nuclei to the horizontal gaze centers. Clinically, caloric test is done to
induced vestibular nystagmus in suspected gaze paralysis.
If hot water irrigated into right ear- the patient will develop right
jerky nystagmus; and if cold water into right ear- the patient will
develop left jerky nystagmus (mnemonic “C-O-W-S”; cold-opposite
and warm-saline)
If both ear are stimulated –for cold water the patient develops up-beat
jerky nystagmus and for warm water, down-beat jerky nystagmus
(mnemonic- “C-U-W-D”; cold-up and warm-down).
19. 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.
20. It is a symmetric limitation of the movement of
both eyes in the same direction(conjugate
ophthalmoplegia)
21.
22.
23. There is an inability to activate the I/L LR and C/L MR for all classes
of eye movements, including VOR.
Nuclear abducens palsies are often accompanied by an ipsilateral
peripheral facial nerve palsy (due to the proximity of the facial
colliculus).
The gaze palsy may be asymmetric with the abducting eye more
prominently affected.
The etiology is usually either ischemia or compression/ infiltration.
24. Lesions of the PPRF cause selective loss of ipsilateral horizontal
saccades.
Acutely, there may be a contralateral gaze deviation (eg, a right gaze
deviation with a left PPRF lesion).
In contrast to lesions involving the abducens nucleus, the horizontal
oculocephalic reflex (doll’s eye) in a PPRF lesion is preserved, since
vestibular fibers project directly to the abducens nucleus.
Etiologies are either ischemia or compression or infiltration.
25. Acute, unilateral hemispheric injury may cause transient gaze palsy or
gaze deviation.
This most often occurs with fronto-parietal and right-sided lesions.
The eyes are deviated ipsilateral to the lesion.
This should be distinguished from gaze apraxia, which implies
difficulty initiating visually guided saccades.
The most common causes are stroke and tumor.
26. (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.
27. A lesion in the MLF is responsible for the clinical syndrome of
internuclear ophthalmoplegia (INO);
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),
and the INO is typically unilateral.
28.
29. Unilateral INO (Fig. 19.75). Double
vision is not typically a complaint.
○ Straight eyes in the primary
position.
○ Defective adduction of the eye on
the side of the lesion and nystagmus
of the contralateral eye on abduction.
○ Gaze to the side of the lesion is
normal.
○ Convergence is intact if the lesion
is anterior and discrete but impaired
if the lesion is posterior or extensive.
Internuclear
Ophthalmoplegia (INO)
30. Bilateral INO (Fig. 19.76)
○ Limitation of left adduction and ataxic
nystagmus of the right eye on right gaze.
○ Limitation of right adduction and ataxic
nystagmus of the left eye on left gaze.
o Convergence may be intact or impaired.
○ A rostral midbrain lesion may give an
associated convergence deficit with
resultant bilateral exotropia and abducting
nystagmus: ‘wall-eyed bilateral INO’
WEBINO.
Internuclear
Ophthalmoplegia (INO)
31. An INO can be differentiated from a partial third nerve palsy by the
lack of other signs of third nerve dysfunction and the preservation, in
some cases, of medial rectus function during convergence.
32. Lesions of the ipsilateral abducens nucleus and ipsilateral MLF
cause loss of all horizontal eye movements except for abduction of the
contralateral eye, which exhibits abduction nystagmus.
Vertical and vestibular movements are spared, and a skew deviation is
common.
Most common causes
multiple sclerosis and
brainstem stroke
followed by metastatic
primary brainstem tumors
Ocular myasthenia may cause a pseudo-one-and-a-half syndrome
33. Left one-and-a-half syndrome due to pontine
tegmental lesion involving the left abducens
nucleus (or left PPRF projecting to the
abducens nucleus) and MLF originating from
the right abducens nucleus, sparing the latter.
Because the left abducens nucleus gives rise to the left MLF projecting
contralaterally, the lesion essentially involves MLF bilaterally and
abducens nucleus ipsilaterally.
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.
34. Patients with acute or subacute pareses 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.
35. It results from damage to the Posterior Commisure.
Signs
Straight eyes in the primary position.
Supranuclear upgaze palsy
Defective convergence
Large pupils with light–near dissociation
Lid retraction (Collier sign).
Convergence–retraction nystagmus.
Setting sun eye (tonic sustain down gaze)
36. Causes
Children: aqueduct stenosis, meningitis and pinealoma
Young adults: demyelination, trauma and arteriovenous malformations.
The elderly: midbrain vascular accidents, mass lesions involving the
periaqueductal grey matter and posterior fossa aneurysms
Limitation of upward gaze with no other features of Parinaud syndrome
is often encountered in older adults; this is believed to represent a
consequence of aging, with no lesion detectable.
39. Lesion of mesencephalic structure-
Steele-Richardson-Olszewski syndrome
Onset –after 40 years
Disorder of basal ganglia
Marked rigidity –trunk & neck
Little tremor
Difficulty with vertical eye movements down > up
Progresses to horizontal gaze disorder
End stage – global ophthalmoplegia
40. Vertical direction more severely affected initially
Voluntary saccades affected first, convergence, and smooth pursuit later
Slowing of saccade velocity
Supranuclear movements primarily affected (vestibuloocular reflex
spared)
Square wave jerks
Gait abnormalities
Nuchal rigidity
42. Wilson’s disease
Huntington diseas
Kernicterous
(A) Patient looking straight at the camera. Note the characteristic wideeyed stare
(asymmetrical here) with furrowing of the forehead.
(B) Attempted downgaze (note descent of the eyebrows).
(C) Full downward gaze, elicited with the vestibulo-ocular reflex.
43. (D) Attempted upgaze. (E) Much greater upgaze is achieved with the vestibulo-
ocular reflex.
(F, G) Voluntary horizontal eye movements are relatively less affected, but still
slightly limited.
44. It is an uncommon supranuclear motility disorder
the eyes are deviated vertically and often exhibit cyclotorsional
disturbance
Three categories have been described, corresponding to
differing motility patterns and lesion sites; both eyes can be
deviated upwards, or one can be hypertropic and one
hypotropic.
The most frequent cause is a brainstem or cerebellar stroke,
which it is thought leads to dysfunction of a primordial field
stabilization mechanism.
45. As mentioned earlier, it is possible for skew deviation to accompany
INO because the MLF contains vestibular pathways maintaining
vertical eye position in addition to interneurons from the abducens
nucleus to the MR subnucleus.
In cases where there is selective damage of the vestibular pathways,
however, skew deviation will occur in the absence of INO.
Imbalance of vestibular inputs leads to a cyclovertical misalignment
of the eyes, typically with a comitant vertical deviation that does not
follow a pattern characteristic of third or fourth nerve palsy.
46. A 30-year-old woman with MS developed horizontal, vertical, and
torsional diplopia. Examination revealed right INO (with incomitant
exotropia greatest in left gaze) and skew deviation (with comitant right
hypertropia in all directions of gaze). A demyelinating lesion of the right
MLF accounts for this pattern of misalignment.
47. 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.
This may be determined either by using a Maddox rod or observing
the fundus with a direct ophthalmoscope and noting the direction of
torsion.
The hypertropia and excyclotorsion in skew deviation are often
minimized or absent when the patient is in the supine position
compared to an upright position.
48.
49. 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.
