examination of the peripheral ocular system

1. DR rzgar hamed
Demyer 2017
4- Examination of the Peripheral Ocular
Motor System

2. One : OCULAR ALIGNMENT AND DIPLOPIA
A. The goals of the ocular motor system
1. The ocular motor system finds, fixates, focuses/aligns
on, and follows visual targets.
* To foveate means to align each eye so as to cause the
central light ray to fall on the fovea and the entire retinal
image to fall on corresponding retinal points of both eyes.
2. The eyes must continually foveate whether the target
remains fixed or moves or whether the eyes remain fixed
or move in any direction.
* Foveation promotes visual acuity and a single (fused)
mental image and secures the advantages of binocular
stereoscopic vision for survival.

3. B. Ocular alignment, the visual axes, and diplopia
1. To examine ocular alignment,start with primary position
of the eyes.
2. A line drawn from the fovea centralis of one eye to the
center of its visual field defines the visual axis.
* This line runs through the center of the media of the eye,
striking the fovea centralis without undergoing any
refraction. It is the “line of sight” of that eye.
3. With the eyes in the primary position, fixating on
infinity, the visual axes are essentially parallel .
4. When looking at a near point, the eyes converge
(adduct). Because each eye adducts, the central
light ray from the fixation point remains on the fovea,
the region of maximum visual acuity.

5. C. Self-demonstration of the visual axis of the
dominant eye
1. With both eyes open, fixate strongly on a doorknob
across the room. Then place your index fingertip 20 cm
away from your eye, so that the knob appears to rest on
the fingertip. Be sure to maintain fixation on the doorknob,
but see the fingertip secondarily.
2. Alternately, wink the right and then the left eye as you
fixate on the doorknob. the image of the Finger shifts to
one side after closing one eye but does not shift when
closing the other eye
3. Explanation of the shifting image: The shift occurs
because you fixate primarily along the visual axis of the
dominant eye; the other eye angles secondarily onto the
target.

6. D. Self-production of physiologic diplopia
* With both eyes open, first strongly fixate on the doorknob,
and then hold up your fingertip to make the doorknob seem
to balance on it.
* Then fixate strongly on your fingertip but secondarily
attend to the doorknob.
* Alternate focusing strongly on one target while you attend
to the other target.
* The object appears double when you shift from one to the
other.)

8. * In Fig. 4-4, rays from only one distance, the fixation point,
strike the fovea. All other rays deviate from the fovea in
proportion to their distance from the fixation point.
* Only the rays coming in along the visual axes strike
correspondingly on the fovea centralis of each eye.
# Why do not we have diplopia all the time?
Recall that you had to consciously attend to the point of
nonfixation to get diplopia. Ordinarily, we have learned to
suppress physiologic diplopia. It only appears when we
make a determined effort to break through its physiologic
suppression. We attend only to the nondiplopic images.

9. E. Self-production of pathologic diplopia by canthal
compression
1. Place the tip of your right index finger on your right
lateral canthus
2. Hold up your left index finger at arm’s length and fixate
on it.
3. While fixating, press very gently on your right eyelid just
above the canthus with your right index finger. By changing
the pressure, you should experience diplopia.
*If you fail to produce diplopia when looking

10. Explanation for diplopia produced by canthal
compression.
* The visual image of the aligned eye is called the true
image, and that of the misaligned eye is called the false
image.
* Because the right eye fails to
abduct to align with the left as it
adducts, the retinal image of the
right eye falls on the nasal half of
the retina, the mind projects the
visual image to the right
(temporal) side.

11. Two : THE ACTIONS OF THE EXTRAOCULAR
MUSCLES
Types of eye movements and nomenclature
* The eyeball can rotate laterally or medially around its
vertical axis, upward or downward around its horizontal
axis, and torsionally (rotate in or out) around its A-P axis.
* Ductions are monocular rotations when the opposite eye
is covered, for example, adduction.
* Versions are binocular parallel rotations to the sides, up,
or down.
* Vergences are binocular nonparallel rotations, for
example, convergence or divergence.

14. Three :CLINICAL TESTS
A. Initial inspection of the relation of the limbus to the
eyelid
* inspect the relation of the limbus to the lid margins
* Then look for gross malalignment of the eyes
B. Technique for the corneal light reflection
(Hirschberg) test
1. Darken the room and locate one distant light source
such as a light bulb .
2. Face the light source and gaze straight ahead , Observe
that one bright diamond of light reflects off each cornea.
3- the exact location of the corneal light reflection fall
slightly medial to the true corneal centers.
4- the examiner (Ex) checks for ocular malalignment in
two ways:

16. C.Technique for evaluating the range of movement of the
eyes
* Start with the Pt sitting. Gently press on top of the Pt’s head
with one hand and fix the head in position ,permitting only the
eyes to move.
* Ask the Pt to fixate on your finger, which you hold up in the
midline, about 50 cm away.
* Request the Pt to follow your finger horizontally For testing
horizontal eye movements and vergences.
* hold the finger vertically; for testing vertical movements ask
about diplopic images that might occur.
* Hold the finger at station 2 and inspect the corneal light
reflections and the relation of the limbus to the lid margins,
canthi, and caruncles. Look for nystagmus.
* Move your finger back to station 1 and say, “Look right at my
finger,” as you move it in to touch the bridge of the Pt’s nose.
Look for convergence and the accompanying
pupilloconstriction.

19. * Select the best-phrased question regarding diplopia:
a. You are seeing two fingers instead of one, are not you?
b. Do you have diplopia?
c. Do you see one or two fingers?
* If the Pt reports double vision, darken the room and
watch the corneal light reflections as the Pt pursues a
tiny light, such as an otoscope lamp.

21. D. The cover–uncover test for ocular malalignment
1. Place your thumb between the Pt’s eyes.
2. Instruct the Pt to stare at a distant point.
3. Move your thumb first in front of one eye, then back
to the bridge of the nose, and then over the other eye.
* The thumb does not have to occlude all vision, only
central, that is, foveal vision.
*Look for deviation of one or both eyes and for the corneal
light reflections as you move the thumb from station to
station.
4. Interpretation of the cover–uncover test: Covering
one eye requires the other eye to foveate. When both eyes
are locked together in fixation, neither eye moves: the Pt
has no ocular malalignment.
* Movement of an eye after occlusion of central vision

23. E. The heterotropias: naming overt ocular deviations
1. Medical terms for overt ocular malalignments are
heterotropia and strabismus.
2. Definition of heterotropia (overt strabismus): is any
ocular deviation detected by observing noncorrespondence
of the corneal light reflections with the eyes in any
position.
* The heterotropias are named according to the direction of
deviation of the errant eye:
Exotropia: eye deviates outward (laterally).
Esotropia: eye deviates inward (medially).
Hypertropia: eye deviates upward.
Hypotropia: eye deviates downward.
* If both eyes deviate outward, the Pt would have bilateral
Exotropia

25. F. Analysis of the cover–uncover test in monocular
heterotropia
* Step 1: The Pt was instructed to look straight ahead. This Pt
appears to have the right esotropia.
* Step 2: the Ex’s thumb occludes central vision of
the right eye. The ocular alignment of neither eye
changes.
* Step 3: the Ex replaces the thumb on the bridge
of the Pt’s nose. The eyes maintain the same
angulation of the visual axes.
* Step 4: the Ex re-instructs the Pt to maintain
fixation on the original distant point and covers the
Pt’s left eye. The Pt’s right eye then shifts to bring
the central light ray onto the fovea, and the left eye
rotates inward
* Step 5: the Ex replaces the thumb on the bridge
of the Pt’s nose. The eyes shift to return fixation to
the dominant left eye.

26. G. Analysis of the cover–uncover test in
alternating heterotropia
* In steps 1 and 2, the Pt ostensibly has
the ocular malalignment called right
esotropia
* Subsequent steps show that the Pt
alternates fixation when allowed free vision.
* In step 1, the Pt fixates with the left eye,
and in step 5 the Pt fixates with the right
eye.
* In contrast, Fig A shows that the Pt always
returns to fixation with the left eye when
allowed free vision.
* Work through Fig. 4-24B, imagining that
the Pt’s eyes deviated out rather than in.
This heterotropia would be called
(alternating esotropia)

27. H. The cover–uncover test for
heterophorias, the latent rather than
the overt ocular deviations
* In some Pts, the eyes appear straight
during preliminary testing and show
normal motility, but upon blocking
central vision in one eye, the eye
deviates.
* After removal of the cover, thus re-
establishing central vision, the fusion–
fixation reflexes immediately realign the
eye.
* Ocular deviations appearing only
when central vision is blocked and
disappearing when central vision is re
established are heterophorias.

28. * An ocular deviation apparent when the Pt is permitted
free central vision is called heterotropia whereas a
deviation apparent only after occlusion of central vision is
called heterophoria
* Inward deviation, or adduction, of the eye only during
occlusion of central vision is called ( esophoria)
* Overt in-turning of an eye when the Pt has free central
vision is called (esotropia)
* Abduction of an eye only during occlusion of central
vision is called (exophoria)
* Upward deviation of an eye only during occlusion of
central vision is called (hyperphoria)

29. * Pay particular attention to step
3. Because the Pt starts and
finishes with apparently straight
eyes, the deviation of one eye is
only intermittent. Therefore, the
abnormality is called
(intermittent right exotropia)
* The abnormality in Fig. 4-24D is
a tropia rather than a phoria
because (the right eye remains
overtly deviated even after
restoration of central vision)

30. I. Clinical classification of heterotropia
A-The paralytic type: caused by a neuromuscular lesion.
B- The non-paralytic type: usually caused by lesions that impair
central vision in one eye and therefore impair fixation: refractive
errors, opacification of the cornea or lens (refracting media), or
macular lesions.
# Effect of paralytic heterotropia caused by nerve or muscle
lesions :
a. After paresis or paralysis of an ocular muscle, the intact muscles
act unopposed. Hence, the eye deviates away from the direction of
pull of the afflicted muscle.
b. The degree of heterotropia and diplopia increases when the Pt
looks in the direction of action of the afflicted muscle.
c. When turning in the direction of pull of a weak muscle, the eye
rotates too little, whereas the normal eye may rotate too far as the
brain strives to move the laggard eye.
* With a lateral rectus paralysis on the right, the Pt’s left eye would
adduct too far when the Pt looks to the right.

31. * Hering law: states that the nervous system stimulates
the yoke muscles equally.
* If a muscle is weak,the Pt automatically overstimulates in
an attempt to rotate the afflicted eye.
* The normal yoke muscle receives the same excessive
stimulus and contracts too strongly.
# Use of the cover–uncover test to analyze
neuromuscular heterotropia:
- Primary deviation is the deviation of the eye with the
paretic muscle when the sound eye is fixing.
- Secondary deviation is the deviation of the sound eye
when the eye with the paretic muscle is fixing.
* In paresis, secondary deviation is greater than primary
deviation.

32. * The primary and secondary deviations exemplify this law:
The fixating eye, the one that foveates, determines the
amount(intensity) of innervation from brain to both
eyes.
* To encourage the weak muscle to act when fixating, the
central nervous system (CNS) sends out a strong stimulus
that only the intact eye responds fully to.
# Effect of neuromuscular (paralytic) heterotropia on
head position
a. To avoid diplopia, the Pt tends to compensate for a
paretic eye muscle by turning or tilting the head.
* A face turn implies a horizontally acting muscle palsy,
chin elevation or depression implies a vertically acting
muscle palsy, and a head tilt implies a torsional acting
muscle palsy.

33. b. The Pt moves the head toward the action of the weak
muscle. To avoid diplopia, a Pt with a right lateral rectus
palsy would tend to keep the head turned to the right. Then
the left eye abducts, lining up better with the in-turned right
eye.
c. With a right superior oblique palsy, the Pt has
weakness of intorsion/ extorsion of the right eye.
d. The Pt with a right superior oblique palsy tilts his or her
head to the left to prevent diplopia.
e. A persistent head tilt or turn is called torticollis.
* With a unilateral acute or acquired superior oblique
muscle palsy, the Pt will tilt the head to the side opposite
the paralytic muscle, turn the face to the same side, and
keep the chin depressed.

34. # Effect of neuromuscular heterotropia on vision in
infants: suppression amblyopia.
a. Infants with heterotropia learn to suppress the image
from the errant eye, a condition called suppression
amblyopia or amblyopia ex anopsia.
* If suppression continues for the first years of life, the
deviant eye may become completely blind, even though
the retina and visual pathways remain structurally intact.
b. Suppression amblyopia is a preventable cause of
monocular blindness, treated by the simple expedient of
placing a patch intermittently over the sound eye to require
the Pt to use the errant eye.
c. Suppression amblyopia occurs not only with
heterotropia, but also with many monocular disorders of
retinal image formation—refractive errors, opacification of
the refracting media, or retinal lesions.
d. Never neglect ocular deviations or other impediments to

35. J. Nonparalytic or concomitant heterotropia versus
paralytic heterotropia
* a concomitant heterotropia has the same amount of
deviation in both eyes in all directions of gaze, but in
nonconcomitant heterotropia, the angle of deviation
changes with the position of the eyes.
* With muscular paresis or paralysis, the eyes do not move
concomitantly; one eye moves more or less than the other.
Hence, we can classify paralytic heterotropia as
nonconcomitant.
* In concomitant heterotropia or nonparalytic heterotropia,
the eyes display the same degree of malalignment in all
positions when both eyes are open, but each eye has
vision and a normal range of movement (ductions) at
monocular testing.
* Concomitant heterotropia may be intermittent, but

36. * Concomitant heterotropia usually results from a
disturbance in image formation in one macula— cloudiness
of the cornea, a severe refractive error, a cataract, or a
macular lesion.
- It seems as if the retina establishes a new macula, off
center from the true macula, and then the visual axis aligns
on the new macula.
- the Pt alternately fixes with one eye and suppresses
vision from the other eye. When fixation alternates
between the two eyes, suppression amblyopia does not
occur.

37. The clinical characteristics of concomitant
heterotropia:
a. The deviation of the eyes is the same for the primary
position and in all directions of gaze.
b. In contrast to nonconcomitant heterotropia, the primary
and secondary deviations disclosed by the cover–uncover
test are equal in concomitant heterotropia.
* If they were not equal at all times, the Pt would have
nonconcomitant heterotropia.
c. When either eye fixates alone, it shows a full range of
motility. None of the individual muscles is paralyzed.
* The term paralytic heterotropia is essentially
synonymous with nonconcomitant heterotropia. (
nonconcomitant)
9. The term nonparalytic heterotropia is essentially

38. K. The laws of diplopia and the clinical analysis of diplopia
* The aberrant or “false” image is always hazier than the “true” image.
L. A summary of the clinical tests for diplopia
1. Observe the corneal light reflections: Locate them when the eyes look
straight ahead and when held in the various directions of gaze .
2. Identify the position of maximum diplopia:
- As you move your finger for examining light through all fields of gaze, have
the Pt report when the two images are maximally separated.
- A red glass placed over one eye (by convention placed over the right eye)
helps to keep track of the two images during motility testing.
- The point of maximum separation identifies the action of the weak muscle.
3. Identify the eye which produces the false image:
- The eye that produces the false image has the faulty muscle.
- The false image is the peripheral image. Identify it by occluding vision
alternately in the two eyes.
- After occlusion of the normal eye, the sharp, central image disappears.
- After occlusion of the abnormal eye, the hazy, peripheral image disappears.

39. M. Analyze these patients
1. If the Pt complains of double vision when looking to the
left:
a. The muscle pairs responsible for left lateral gaze are the
medial rectus muscle of the right eye and the lateral rectus
muscle of the left eye.
b. On occlusion of the right eye, the central image (true image)
disappears. On occlusion of the left eye, the peripheral image
(false image) disappears. Therefore, the afflicted eye is the left
eye and the afflicted muscle is the left lateral rectusmuscle.
2. If The Pt complains of double vision when looking up:
* The images separate greatest when the Pt looks up and to the
left.
a. Muscles responsible for this action are left superior rectus
muscle and right inferior oblique muscle.
b. On occlusion of the right eye, the central image disappears.
On occlusion of the left eye, the peripheral image disappears.

40. N. Localizing the lesion by thinking along the course of
the ocular motor nerve
1- Always start at the nucleus of origin of the nerve and
think through to its termination.
2. A central lesion will usually also affect long tracts:
a. A lesion of (CrN) III in the midbrain
- cause ataxia if the dentatothalamic tract is interrupted
- contralateral tremor : the red nucleus involvement
- Idisturbances in vertical gaze if the lesion is
dorsomedial to the red nucleus
- hemiplegia if the lesion affects the midbrain basis.
b. A lesion of CrN VI in the basis pontis
- contralateral hemiplegia because that is where CrN
VI comes into conjunction with the pyramidal tract.

41. 3. In peripheral lesion: will affect more than one structure.
a. In the region of the cavernous sinus, CrNs III, IV, V,
and VI and the carotid sympathetic nerve
b. Within the orbit, a lesion will cause a different set of
signs involving several of the same nerves.
4. Diseases that can cause diplopia and ocular palsies,
but do not directly interrupt ocular motor nerves:
1-myasthenia gravis
2- hyperthyroidism
3-botulism
4-diabetes
5-arteritides
6- aneurysms, inflammation, and primary or metastatic
neoplasms.

42. REFRACTION AND ACCOMMODATION
* The refracting media of the eye includes the cornea and
lens
A) The accommodation reflex
Accommodation for near vision requires three muscles to
complete three actions:
a. Convergence: medial recti (skeletal)
b. Pupilloconstriction: pupilloconstrictor muscle of the iris
(smooth muscle, parasympathetic)
c. Lens thickening: ciliary muscle (smooth muscle,
parasympathetic)

43. A) Myopia and hyperopia:

44. 1- A person with sharp vision for objects that are far away and
close is emmetropic.
2- For far vision, the emmetropic person’s muscles of
accommodation are relaxed.
3- A person with sharp vision for far objects, but blurred vision
for close objects, is called farsighted ( hyperopia)
4- The hyperopic eye focuses parallel rays behind on the
retina.
a. The hyperopic Pt requires some activity of the
accommodation reflex to thicken the lens when looking at
close and far objects
b. Normally, however, the accommodation reflex should act only
during near vision. The hyperopic Pt requires some degree of
accommodation at all times to bring the focal point forward onto
the retina.
5- A person with blurred vision for distant objects but sharp
vision for near objects is nearsighted ( myopia)
* The myopic eye focuses parallel rays from far objects in front
of the retina.
*The near object’s rays diverge more before striking the lens
and, hence, move the focal point backward, nearer to the

45. Relation of refractive errors to heterotropia and
heterophoria
1. During the first months of life, infants must develop
binocular fixation and fuse the images from the two eyes.
The infant’s eyeball is too short relative to its refracting
power. With maturation, the eyeball expands.
2. With the eyeballs too short in relation to the focal point
of the lens, the infant is basically hyperopic.
3. As the eyeball increases in diameter with maturation, the
hyperopia tends to change to emmetropia.
* If the child is more nearly emmetropic at birth, instead of
hyperopic, he/she would become myopic as the diameter
of the eye increases with growth.

46. 4. Because of the small diameter of the eyeball relative to
the focusing power of the lens, infants tend to keep their
lenses thickened. In other words, they tend to
accommodate all of the time.
* Detailed inspection of near objects places extra demands
on the accommodation mechanism of the infant’s eyes.
a. Because one of the accommodation mechanisms is
convergence of the eyes, the hyperopic child at first will
show only a latent tendency to crossing of his/her eyes,
that is, esophoria.
b. With severe hyperopia, the esophoria may convert to an
overt internal deviation of an eye, which is
called esotropia
c. Thus, refractive errors or neuromuscular lesions may
cause crossed eyes.

47. * Dystopic canthi and epicanthal folds: these are Two
eyelid anomalies in children may give a false impression of
crossed eyes because the medial margin of the limbus
appears to be too close to the medial eyelid margins.
* Tropias and phorias commonly accompany refractive
errors.
a. Esophoria or esotropia in a child would raise the
suspicion of a refractive error called ( hyperopia)
b. Exophoria or exotropia in a child would raise the
suspicion of ( myopia)

48. Presbyopia, blurred vision, myopia, and hyperopia
1. At the age of approximately 42 years, normal adults
experience blurred vision when they try to read newsprint
or look at near objects.
2. Because of aging, the lens loses its elasticity. It will no
longer thicken to increase its refractive power during
accommodation, a condition called presbyopia.
* Hyperope would suffer blurred near vision first and
foremost from presbyopia. Because Any loss of elasticity
will reduce refraction and thus blur close objects. The
myope does not need much accommodation and therefore
does not suffer much when it fails.
3- A pinhole will block off the more peripheral rays from the
near object, thus allowing only the central rays to reach the
retina. Hence, restoration of visual acuity by the pinhole
establishes a disorder of refraction, not a retinal or optic

49. 4. The parallax test for positive or negative corrective
lenses
a. The parallax test provides a quick way to test whether
the Pt’s glasses correct for hyperopia or myopia.
* Hold the glasses over any vertical line, about a foot away,
and slowly move the glasses to the right and left
alternately.
b. With a divergent (negative) lens, the line will appear to
move in the direction that you move the glasses.
- Myopia requires a divergent or negative lens to move the
focal point backward
c. With a convergent (positive) lens, the line will appear
to move in the opposite direction to the movement of the
glasses.
-Hyperopia requires a convergent or positive lens to

50. Some commoner causes of blurred vision/blindness
a. Birth through childhood: opacities of the media,
astigmatism, and refractive errors:
b. In later childhood, ages 5 to 7 years, the myopic child
has to sit closer and closer to blackboard as the eyeballs
continue to grow, and the child becomes increasingly
nearsighted.

51. c. Young adults: optic neuritis Leber hereditary optic
neuropathy and other neuropathies/neuritides.
d. At ages 40 to 45 years:
i. Presbyopia: The lens loses its elasticity to focus on near
objects
ii. Glaucoma: Signs include high intraocular pressure,
optic disc cupping, pupillodilation, and constricted
peripheral fields.
e. Older than 50 years:
i. Cataracts and macular degeneration both diagnosable
by ophthalmoscopy.
ii. Central serous retinopathy.
iii. Temporal arteritis and ischemic optic neuropathy

52. INNERVATION OF THE OCULAR MUSCLES
A. Classification of ocular muscles into intraocular and
extraocular
1. Each eye has 11 ocular muscles: four smooth muscles and
seven striated muscles.

53. 2. One ocular-related muscle, the orbicularis oculi, a
sphincter that closes the eyelids, derives from a brachial
arch and belongs to the facial muscles, innervated by CrN
VII.
B. Peripheral innervation of the extraocular muscles
Six nerves innervate the eye, four motor and two sensory
1. Of the four essentially motor nerves, three convey
somatic efferent fibers: CrNs III, IV, and VI
a. Two of the three somatomotor nerves serve only one
EOM:
- CrN VI innervates the lateral rectus.
- CrN IV innervates the superior oblique.
- CrN III serves the remaining EOMs and two of the three
intraocular muscles.
b. Only CrN III of the somite group also conveys
parasympathetic (GVE) fibers. These fibers innervate two
of the three intraocular smooth muscles, the

55. 2. The fourth motor nerve of the eye, the carotid
sympathetic nerve, innervates the third intraocular
muscle, the pupillodilator muscle and one clinically
important EOM, the superior tarsal.
* The carotid sympathetic nerve travels from the carotid
artery at the level of the cavernous sinus into the superior
orbital fissure and to the eyeball by hitchhiking along other
orbital nerves.

56. EXAMINATION OF THE PUPILS
A. Technique of pupillary examination
1. Start with normal illumination of the room, with no
direct sunlight.
* Ask the Pt to gaze at a distant point to avoid
pupilloconstriction from the accommodation reflex.
a. Normal pupils : black, equal in size, round and react to
light and to accommodation, centered in the iris, or very
slightly inferomedially placed.
* A nonblack pupil, usually a whitish one, indicates an
opacification of the cornea or lens.
b. Compare the size of the two pupils and record the
pupillary size in millimeters. To measure pupillary diameter,
compare the pupil with a series of circles graded in
millimeters

57. i. Look for anisocoria: Benign congenital anisocoria in
which both pupils react normally is relatively common.
ii. Look for faint rapid oscillations of the pupillary margins,
called hippus. Although often benign, hippus may
accompany a metabolic encephalopathy.
c. Inspect the limbus for a Kayser–Fleischer ring or an
arcus senilis, also known as arcus corneae(due to
hyperlipidemia)
2. Check for pupillodilation and a dilation lag:
a. Dim the room lights and inspect the pupils immediately
and after 5 to 15 seconds.
b. Normal pupils dilate promptly, within 5 seconds of
dimming the light because of activation of the pupillodilator
fibers by the sympathetic nervous system.
c. A dilation lag of seconds to minutes indicates a lack of
sympathetic innervation (Horner syndrome) or a myotonic
pupil (Adie pupil; Table 4-5)

59. 3. Check the direct and consensual pupillary light
reflexes:
a. Instruct the Pt to look at a distant ,Beam a flashlight
slowly in from the sides to illuminate each eye separately.
i. Direct constriction of the pupil in the eye stimulated by
light is called the direct light reflex.
ii. constriction of the opposite pupil when light stimulates
only one eye is the consensual light reflex. Normally, the
direct and consensual pupillary responses are equal.
b. Do not shine the flashlight abruptly into the Pt’s eyes
from directly in front, for two reasons:
i. The Pt will automatically look at the light and
accommodate for near vision.
ii. The bright light will cause discomfort, particularly if the
Pt has photophobia, mental retardation, or dementia.

60. 4. For the swinging flashlight test:
* alternately swing the light from one eye to the other and
hold it on the new eye for 3- to 5-second intervals.
* If the Pt has an afferent defect in one optic nerve (eg, due
to optic neuritis), the pupils will dilate as the light swings
from the normal to the affected eye (Marcus-Gunn pupil or
relative afferent pupillary defect) rather than maintaining
the same degree of constriction.
5. ophthalmoscopic examination.

61. B. Pathway for the pupillary light reflexes

62. * The pupillary reflex arc has a receptor, an afferent limb,
central nuclear synapse(s), an efferent limb, and an
effector.
* Nerve impulses reach the mesencephalon, they are
distributed bilaterally to the parasympathetic (GVE)
nucleus of CrN III, called the Edinger–Westphal nucleus.
* Hence, light stimulation in one eye will constrict both
pupils equally. The consensual pupillary constriction equals
the direct constriction.
* Efferent axons travel to the eye via both III nerves.
* the ganglion of synapse of the GVE axon, the ciliary or
episcleral ganglion, is near the end organs, the ciliary
and pupilloconstrictor muscles.
* The same efferent pathway serves pupilloconstriction to
light and in accommodation.

63. Physiology and pharmacology of the pupils
* The eyeball contains three intraocular muscles, all
smooth muscles: the pupillodilator, the
pupilloconstrictor, and the ciliary muscles.
a. The pupilloconstrictor and pupillodilator muscles of the
iris adjust the diameter of the pupil.
b. The ciliary muscle is adjusting the diameter of the lens
by relaxing its suspensory ligament, to allow the lens to
thicken by its own elasticity. The ciliary muscle does not
control the pupils.
Note:
Striated muscle is specialized for quick, powerful phasic
contractions, smooth muscle for slow, tonic contractions.

64. * The pupilloconstrictor muscle is parasympathetic and
cholinergic; the pupillodilator is sympathetic and adrenergic
* Parasympathetic denervation of the eye results in
pupillodilation (corectasia, mydriasis))
* Sympathetic denervation results in pupilloconstriction
(cormiosis))
*Pupillodilation can result from mimicking the sympathetic
nervous system or by blocking the parasympathetic
nervous system.
* Parasympathetic blocking agent would also interfere
with lens thickening by paralyzing the ciliary muscle
(cycloplegia).
* pupillodilator drugs (mydriatics) cause temporary blurring
of vision,

65. Mydriatic drugs:
* cyclopentolate (Cyclogyl) 1%
* tropicamide (Mydriacyl) 1%
* phenylephrine (Neo-Synephrine) 2.5%
* To reduce burning and tearing, you can pretreat with a
topical anesthetic, proparacaine, ophthalmic solution.
* Because pupillodilation increases intraocular pressure,
check the intraocular pressure of adults older than 40
years by tonometry before instilling mydriatics.
* Two percent of all adults older than 40 years have
glaucoma. The danger of precipitating acute glaucoma with
mydriatics is greater for the hyperopic Pts

66. Determinants of pupillary size in addition to light
a. Local disease of the eye and iris.
b. Local ocular or systemic drugs affecting the autonomic
nervous system.
c. Emotionality: sympathetic nervous system predominance
causing pupillodilation and tachycardia.
d. Sleep and drowsiness: parasympathetic nervous system
predominance during sleep causes pupilloconstriction and
bradycardia.
e. Age:
* Fetus pupil fail to react to light until the 30 to 32 weeks of
gestational
age .
* at term birth the pupils are small
* The pupils enlarge through adolescence (the so-called “wide-
eyed” innocent look).
* In elderly the pupils again become small and poorly reactive.
* Small pupils give the person a “flinty-eyed” miserly look,
whereas large pupils are considered sexy and receptive, hence,
the use of atropine by women who wanted to be la belladonna

67. Pupillary abnormalities
1- Miosis
* is a sign of lesion in the sympathetic pathway which
supplies the pupillary dilator muscle.
* Classically oculosympathetic paralysis results in a Horner
syndrome which comprises the triad of miosis, ptosis, and
anhidrosis of the forehead.
* Diameter is usually reduced by 0.5-1.0 mm compared
with the normal side.
* This inequality is most marked in dim illumination.
* Other features of Horner syndrome include the presence
of dilatation lag;
* no response to cocaine test and Hydroxyamphetamine
usually cause dilatation if the lesion is preganglionic.

68. * If sweating is decreased on the entire half of the body
and the face, the lesion is central.
* Cervical lesions produce anhidrosis of the face neck and
arm. Sweating is unimpaired in post-ganglionic lesions.
Causes of Horner’s syndrome:
1- Lesions of the brainstem.
2- C8-T1 lesions e.g. syringomyelia.
3- Lesions in the neck e.g. Trauma, lymphadenopathy,
cervical ribs.
4- Lesions in the superior mediastinum e.g. aneurysm,
glandular enlargement, bronchial carcinoma.

69. 2- Mydriasis (dilated pupil)
* A variety of lesions, some of them purely ocular, such as
uveitis, may give rise to a fixed dilated pupil.
Neurologically, there are three main diagnostic
considerations:
I- Surgical Third nerve palsy: This is due to interruption in
the parasympathetic fibers. It is a safe clinical rule that the
interruption of these fibers is particularly always associated
with ptosis, impairment of the extra ocular movements, or
signs of other brain stem or cerebral disease. Sphincter is
not supersensitive to 0.1% pilocarpine but constrict when
we apply 1% pilocarpine.
* Commonest causes are: aneurysms, tumors, or temporal
lobe herniations.

70. II- Adie's tonic pupil: This is a unilateral (rarely bilateral)
dilated pupil of no sinister significance.
* The pupil reacts slowly and only to persistent bright light
or 0.25% pilocarpine eye drops.
* Accommodation is less affected.
* Absent deep reflexes in the limbs is a common
accompanying feature, especially the knee, and ankle
jerks. Site of pathology is uncertain.
III- Drug induced mydriasis: A mydriatric fixed pupil is the
result of accidental or deliberate application of an atropinic
or sympathomimetic drug.
* Failure of 1% pilocarpine drops to contract the pupil
provides proof that the iris sphincter has been blocked by
atropine or some other anticholinergic agents.

71. 3-Non-reactive pupils: This is due to a break in the
pathways for the light reflex.
* The lesion may lies in the afferent loop i.e. the retina,
optic nerve, and optic chiasm; or in the efferent loop i.e.
the parasympathetic supply from the midbrain running with
oculomotor nerve.
* If the afferent loop is involved, both the direct and
consensual reaction will be lost, if the diseased side is
stimulated.
* If the normal side is stimulated, both pupils will react.
* If the efferent loop is involved, the affected pupil can not
react, no matter which side is stimulated.

72. * Bilateral failure to react plus intact vision usually means a
midbrain lesion.
* Bilateral blindness with non-reacting pupils must be due
to a lesion between the retina and the first part of the optic
tract, for after that the pupillary constrictor fibers have left
the visual fibers
4-Light-near dissociation: Impaired pupillary reaction to
light with preserved constriction during accommodation is
usually bilateral and may result form neurosyphilis,
diabetes, optic nerve disorders, and tumors compressing
the midbrain tectum, menigo-radiculitis and Lyme disease.

73. 5-Argyll-Robertson pupils.
* These pupils are small, irregular in shape, unequal
in size and show light near dissociation.
* Neurosyphilis is the usual cause.
* The site of the lesion is not certain.
* Some favor the tectum of the midbrain, others,
the ciliary ganglion, but bearing in mind the nature of the
neurosyphilitic lesions, multiple sites can not be excluded.
*Other causes of AR pupil include diabetes mellitus, orbital
injury, hereditary neuropathies and sarcoidosis.

74. 6-Marcus Gunn pupil (relative afferent pupillary defect).
* In this condition, one pupil constricts less markedly in
response to direct illumination than to illumination of the
contralateral normal pupil, whereas normally the direct
response is greater than the consensual response.
* If a light is shifted quickly from the normal to the impaired
eye, the direct light stimulus is no longer sufficient to
maintain the previously evoked consensual pupillary
constriction and both pupils dilate.
* These abnormal pupillary responses form the basis of
the swinging flash-light test in which each pupil is
alternatively exposed to light at 3-5 seconds interval.
Relative afferent papillary defect is commonly associated
with disorders of the ipsilateral optic nerve which interrupt
the afferent limb and affect the pupillary light reflex.

75. Squint
Squint is deviation of the eye from the optical axis. It is of
two types:
1- Concomitant (non-paralytic) squint: In this condition,
there is muscle imbalance, but the ocular movements are
full and the squint may be divergent or convergent. There
is no diplopia as faulty image has been neglected by the
patient. The commonest cause of this condition is
uncorrected error of refraction in childhood.
2- Non concomitant (paralytic) squint: It results from
paralysis of the one or more of the ocular muscles
commonly due to lesions of the third, fourth, or the sixth
cranial nerves and is characterized by limitation of eye
movements and increasing diplopia in the field of action of
the paralyzed muscle.

84. The syndrome of parasympathetic paralysis of the eye
(internal ophthalmoplegia)
* The muscles innervated by the GVE, parasympathetic
axons of CrN III, are extraocular and smooth.
* The GVE axons of CrN III constitute the only efferent
pathway for active pupilloconstriction.
* Because the GVE and general somatic efferent (GSE)
axons of CrN III originate from the same nuclear region
and travel in the same peripheral nerve, lesions affecting
CrN III generally involve both sets of axons, but important
exceptions occur.

85. * Signs of a pure parasympathetic paralysis of the eye:
1- Blurring of near vision (ciliary muscle paralysis)
2- dilated pupil, not reactive to light or in accommodation
(pupilloconstrictor muscle paralysis).)
* Apart from head injuries, causes of III nerve palsies
include ischemia, as in diabetic III nerve palsy, an aneurysm
of the circle of Willis, neoplasm, or inflammation.
* Often ischemic III nerve palsy spares the pupil, whereas
aneurysmal III nerve palsy virtually always affects the pupil

86. The syndrome of sympathetic paralysis of the eye and
face: Bernard–Horner or Horner syndrome
1. The sympathetic pathway to the eye: This pathway
displays the typical features of all sympathetic innervation.

87. a. The upper motoneuron pathway begins in hypothalamic
neurons and descends through the brainstem tegmentum
to synapses on the GVE lower motoneurons of the
intermediolateral cell column of the spinal cord gray matter.
i. The sympathetic visceral efferent column extends in the
spinal cord from T1 to L2 and L3.
ii. Axons to the eye derive from T1 and T2 (also called the
ciliospinal center of Budge).
c. As is also typical, the sympathetic GVE axons, the
second-order neurons in the sympathetic pathway, exit with
a spinal nerve to synapse in a paravertebral ganglion.
d. From the paravertebral ganglion, the superior cervical
for the carotid sympathetics, the third-order axons, then
hitchhike as a plexus along blood vessels or nerves to their
effectors.

88. e. The carotid sympathetic nerve innervates the smooth
muscles of the vessels of the entire internal and external
carotid systems.
i. The external carotid artery carries sympathetic axons to
the sweat glands of the face.
ii. The internal carotid artery carries the sympathetic axons
to the ocular smooth muscles and the sweat glands of the
forehead.
f. The sympathetic axons innervate two ocular muscles,
superior tarsal (extraocular) and pupillodilator
(intraocular).
g. Note: The sympathetic and parasympathetic systems
differ in the location of the ganglion containing the
secondary axon.
i. The ganglia of the sympathetic nervous system are
located in the paravertebral chain.

89. Signs of horner syndrome:
1- Ipsilateral ptosis
2- Pupilloconstriction (cormiosis)
3- Anhidrosis
4- Flushing (vasodilation)
* miosis occurs after sympathetic denervation of the eye.
because The pupillodilator and pupilloconstrictor muscles
tonically oppose each other. After pupillodilator muscle
paralysis, the pupilloconstrictor muscle acts unopposed.)
* After sympathetic paralysis, the miotic pupil will constrict
further in response to light or accommodation, because the
muscle receives an additive constrictor stimulus rather than
simply a “tonic” stimulus.

90. * A diagnostic feature of unilateral Horner syndrome is an
increase in the degree of the anisocoria just after dimming
the room light.
* After sympathetic activation, The normal pupil will dilate
within 5 seconds, whereas the abnormal pupil has a
dilation lag and briefly remains the same size.
* The anisocoria lessens in 15 to 20 seconds because of a
decrease in parasympathetic innervation to the abnormal
eye.
* In bright light the miosis of the normal pupil will cause it to
approximate the Horner pupil. Thus, the miosis may be
missed without examining the Pt in a darkened room.

91. Separation of the components of Horner syndrome:
a. If the lesion interrupts the sympathetic pathway distal to
the origin of the external carotid artery, the
only sympathetic denervation signs the Pt will show are
(ptosis; cormiosis)
b. If the lesion interrupts the sympathetic pathway proximal
to the external carotid artery (between hypothalamus and
external carotid artery), the Pt will show, in addition to
ptosis and cormiosis, the other two features of Horner
syndrome: (hemifacial (ipsilateral) anhidrosis;
vasodilation)
c. The vasodilation is best seen in the conjunctival vessels.
d. With a congenital unilateral Horner syndrome, such as
with an Erb brachial plexus injury, the ipsilateral iris often
becomes heterochromic.

92. Clinical testing of the ocular sympathetic pathway to
the eye: the faciociliary or spinociliary (ciliospinal) reflex.
* To test the sympathetic pathway to the eye, pinch the
skin over the face (CrN V afferent) or neck (C2 or C3
afferent) firmly for 5 seconds. Both pupils should dilate
briskly—the faciociliary reflex or the spinociliary
(ciliospinal) reflex.
* Do the test in dim light and with the Pt looking in the
distance, to avoid the strong pupilloconstriction due to light
and accommodation that could mask the
pupillodilation of the sympathetic reflex.)

94. CLINICAL EVALUATION OF PTOSIS
A. Elevation of the eyelid
1. Two muscles elevate the eyelid and, hence, adjust the
vertical diameter of the palpebral fissure:
a. The superior tarsal muscle: a smooth muscle, acts
tonically to elevate the eyelid. It is innervated by the
(carotid sympathetic nerve)
b. The levator palpebrae muscle, a skeletal muscle, acts
tonically and phasically to elevate the eyelid. It is
innervated by (CrN III)
Levator palpebrae paralysis causes:
a. Severe ptosis, greater than with superior tarsal ptosis.
b. Paralysis of lid elevation during upward gaze.

95. B. The causes of ptosis (blepharoptosis)
a. Central: at the hypothalamus, brainstem, or spinal cord.
b. Peripheral: along the course of the III or sympathetic
nerves.
c. Neuromyal: at the nerve-muscle junction.like MG
d. Local in the muscle itself: myopathic, congenital,
inflammatory, or traumatic
e. Other causes include edema of the eyelid and
dehiscence of the levator muscle aponeurosis
F- congenital
G- Tabes dorsalis
H- Hysterical ptosis: Very rare and is always unilateral

98. * In Bell palsy, the drooping of the eyelid occurs because of
paralysis of the frontalis muscle, , Proof of the nature of
this form of ptosis comes from the eyebrow-lifting test.
Lifting of the eyebrow by the Ex corrects the ptosis in a VII
nerve palsy, but it remains in a III nerve palsy .
* Cerebral ptosis: Pts with acute strokes may have
unilateral or bilateral ptosis in association with hemiparesis.
The development of complete bilateral ptosis may predict
brain herniation
* The ptosis with myasthenia gravis will often fluctuate or
fatigue throughout the examination and may become more
evident on one side when the fellow lid is manually
elevated (enhanced ptosis).

99. * Also an ice-bag test may improve the ptosis in patients
with myasthenia gravis. In this test, an ice pack is held
over one eye (both lids closed) for 2 minutes and afterward
the position of the lid is observed.
* Lessening of the degree of ptosis often may occur in
myasthenic patients probably due to improved
neuromuscular transmission.
* Two important points of distinction for neuropathic ptosis
are:
a. Other signs of interruption of CrN III usually accompany
ptosis from levator palpebrae paralysis.
b. Other signs of interruption of the carotid sympathetic
nerve usually accompany ptosis from superior tarsal
muscle paralysis.

100. CONJUNCTION SYNDROMES OF THE CRANIAL
NERVES
1- Conjunctions of cranial nerves with pathways of the
central nervous system
a. A midbrain lesion : causes a III nerve palsy lesion may
interrupt the dentatothalamic tract and cause contralateral
ataxia and tremor; or, if it affects the region dorsomedial to
the red nucleus, it will paralyze down gaze; or, it will cause
hemiplegia, if the lesion affects the midbrain basis
b. A contralateral hemiplegia usually will accompany a VI
nerve lesion in the basis pontis because of the conjunction
of CrN VI with the pyramidal tract at that site .

102. 2- conjunction syndromes of the peripheral parts of
ocular motor cranial nerves
* Components of cavernous sinus:

103. * The symptoms and signs consist of pain or numbness in
the ophthalmic division of CrN V, palsies of the ocular
motor nerves, with ptosis, either sympathetic or III nerve in
origin, and visual defects from
involvement of CrN II or the chiasm.
* A carotid-cavernous fistula adds proptosis.
* A painful ophthalmoplegia plus or minus sympathetic
paralysis is the core feature.
* Depending on the particular combinations of nerves
affected, the syndrome is called Gradenigo, Tolosa–Hunt
or Raeder paratrigeminal
* Typically the cause is inflammation, neoplasm, trauma, or
an internal carotid artery fistula or aneurysm.

105. * many diseases can cause diplopia and ocular palsies that
do not directly interrupt optomotor nerves:
1- myasthenia gravis
2- hyperthyroidism
3- botulism
4- myopathies
3- Other cranial nerve conjunction syndromes
1. A single lesion in the cerebellopontine angle frequently
affects CrNs VII and VIII at the internal auditory meatus
and sometimes adjacent CrNs VI, and IX and others.
2. CrNs IX, X, and XI come into conjunction at their exit
site at the jugular foramen.

107. Proptosis
* It is forward displacement of the eye balls.
* The following points must be checked in every patient
with exophthalmoses:
1-Note the lid retraction, with wide palpebral fissure.
2-Test for the presence of lid lag.
3- Check the movement of the eye balls to rule out
(exophthalmic
ophthalmoplegia).
4-Listen to any bruit over the eye balls.
5-Examine the neck for any thyroid enlargement
6-Check for tremor, tackycardia, atrial fibrillation and
pretibial myxoedema

108. Causes of unilateral proptosis
1-Thyrotoxicosis.
1- Orbital or retro-orbital neoplasm or infections.
2- Pseudo-tumor (orbital pseudo-tumor): This is an
inflammatory or
granulomatous reaction which involves the cavernous
sinus, orbital and retro-orbital parts. They cause painful
ophthalmmoplegia due to involvement of the third, fourth,
sixth, first and second divisions of the fifth cranial nerves.
They are benign, recurrent, and usually show dramatic
response to steroids.
* They are best diagnosed by ultrasound or CT scan of the
orbit and must be differentiated from the same reactions
which occur in the superior orbital fissure and anterior part
of the cavernous sinus (Tolosa-hunt syndrome). In the
later condition there is no proptosis, or injection of the

109. 3- Carotid artery-cavernous sinus fistula: The globe is
pulsatile and there is audible bruit (audible for both the
patient and the examiner).
4- Cavernous sinus thrombosis:
Causes of bilateral proptosis
1- Grave's disease (thyrotoxicosis).
2- Craniostenosis
3- Hydrocephalus.
4- Cushing's disease (steroid myopathy).
5- Chronic increase in the intracranial pressure.
6- Cavernous sinus thrombosis and all causes of the
unilateral proptosis may involve the other side.