NEURO-OPHTHALMOLOGY FUNDAMENTALS OPTHALMOLOGY

Dr. Noel de Jesus Atienza

March 17, 2021 8.0
Outline VISUAL PATHWAY
I. Neuro-Ophthalmology Fundamentals
II. Confrontation Test
III. Optic Nerve
IV. Optic Chiasm
V. Retrochiasmatic Visual Pathway
VI. The pupils
VII. Cranial Nerve Palsies

LEGEND
 Book  Recording  Previous Trans Must know
Important Concept

References:
1. PowerPoint Lecture
2. Upper Batch trans

I. NEURO-OPHTHALMOLOGY

Figure 2. The Visual Pathway. Light passes through the lens

and reaches the retina, where the formed image is reversed and
inverted. Axons leaving the retina forms the optic nerve. Fibers
will then pass through the optic chiasm where the nasal side of
the optic nerve would decussate to the contralateral optic tract
while the temporal side of the optic nerve would remain on the
ipsilateral optic tract. Axons in the optic tracts will synapse in
the lateral geniculate nucleus (LGN) of the thalamus. Fibers
from the LGN would then be optic radiations until it eventually
synapses with the primary visual cortex.

• Summary of conscious vision perception

o Retina → Optic Nerve → Optic Chiasm →
Optic Tract → Lateral Geniculate Body →
Figure 1. Visual Field Defects. (a) Hemianopsia, (b) Optic Radiation → Primary Visual Cortex
Quadrantanopia, and (c) Scotoma.
• Additional pathways
• Specialty dealing with the problems of the Optic nerve. o Retina → Optic Nerve → Optic Chiasm →
• Could be the first to diagnose tumors, strokes, and Optic Tract → Pretectal Area and Superior
small lesions in the brain (multiple sclerosis, Colliculus
degenerative brain disease). ▪ Pupillary Light Reflex
• Deals with CN II, III, IV, V, VI, VII, and IX. ▪ Eye movements towards visual
• Use of CT scans and MRI to corroborate and identify stimuli
suspicious brain lesions.

How to identify if a lesion is Glaucomatous vs.

Neurological?
• Neurologic problems have a vertical line (in
cases like hemianopia wherein whole left or right
visual field is lost).
• Glaucomatous lesion usually horizontal line
(defects are seen either in up or down visual field).

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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

VISUAL FIELD DEFECTS • More congruous (more similar in size, shape and
location) – more posterior lesion.

Figure 4. Difference in the visual field affected by lesions in the

optic tract and lateral geniculate nucleus. (NFT: This was
supposed to be an example showing “the more congruous, the
more posterior the lesion” analogy, but as you can see the lesion
in the LGN is more incongruent even though its more posterior.
So idk with doc. It is what it is I guess.)

• Optic Tract Lesions vs. Occipital Lobe Lesions

o Optic Tract – incongruous homonymous
defects
o Occipital lobe – identical defects in each field
(congruous)

Figure 5. Incongruent Homonymous Hemianopsia of a lesion

in the Optic Tract vs. Congruent Homonymous Hemianopsia in
lesions in the Right Occipital Lobe. (NFT: This one is properly
Figure 3. Visual Field Defects. Transection in the different
showing the “more posterior, the more congruent” rule.)
areas of the optic nerve would have different manifestations
depending on the area of the lesion. Correlate with Figure 2.
II. CONFRONTATION TEST
Table 1. Visual Field Defects
• To screen for visual field defects
DEFECT LESION • Finger counting
A Scotoma Retina • Simultaneous finger counting
B Monocular vision loss Optic Nerve • Penlight (for patients who only have light perception)
C Bitemporal Hemianopsia Optic Chiasm • Test set-up
o Test each eye separately.
o Seat the patient 1 meter (3 feet) facing the
D Contralateral Optic Tract
examiner.
Homonymous
o By convention, test the patient’s right eye or
Hemianopsia
whichever is the better eye first.
E
Figure Contralateral
SEQ Figure \*Superior Inferiorinsert
ARABIC 1. Always optic radiation
caption!
o Completely occlude the patient’s other eye
How? Right click the image and look (Temporal
Quadrantanopia for “Insert Caption”.
lobe)
Italicized caption liftedInferior
from [insert reference]. that is not being tested.
F Contralateral Superior optic radiation
o The examiner must close the eye that is
Quadrantanopia (Parietal lobe)
directly opposite the patient’s occluded eye.
K Contralateral Occipital Lobe
▪ For example: to test the patient’s
Homonymous
right eye, the patient’s left eye and
Hemianopsia with
the examiner’s right eye must be
Macular sparing
covered.
o Ask the patient to focus on a target in a
• Hemianopsia should have intact visual acuity in the
straight gaze position (example, the
spared visual field. examiner’s nose)
• Lesions that are:
o Anterior to the optic chiasm – Unilateral
o At the chiasm – Bitemporal Hemianopsia
o Posterior to the chiasm – Contralateral
Hemianopia or Quadrantanopia

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OTORHINOLARYNGOLOGY BASIC EYE EXAM
Figure 6. The Confrontation Test.
III. THE OPTIC NERVE
• Features of optic neuropathy
o Reduced visual acuity
o Afferent pupillary defect
o Poor color vision
o Optic disc changes
o Visual field defect
• Very bad lesions presenting immediately.
• Optic nerve in the canal is most susceptible to
damage.
• Axons can be dysfunctional long before the optic nerve
becomes atrophic.
OPTIC DISC EDEMA
• Predominantly in diseases directly affecting the
anterior part of the optic nerve.
o increased intracranial pressure
o compression of the intraorbital optic nerve
• Papilledema – optic disc edema caused by an
increase in intracranial pressure.
o A common cause of neurologic emergency. If
presenting with headache, we immediately
consider doing a CT-scan
o Generally will not cause BOV, only increase
in the size of physiologic blind spot.
• Other causes include retinal disease (in CRVO),
uveitis, and ocular hypotony.
Important Concept
• It is important to differentiate optic neuritis from
papilledema – both will present with blurred disc
borders, elevated disc margins, tortuous vessels,
possible hemorrhage
• Papilledema – usually normal vision
o In very severe papilledema – florid
hemorrhage and disorganized posterior pole
• Optic neuritis – often associated with blurred
vision
[INOCENCIO] EDITOR: [JARIEL]
LECTURE 8.0
Figure 7. Optic disc edema. Left image: Elevated disc with
indistinct disc and cup borders. Right image: severe papilledema
It may be caused by hypertensive retinopathy grade 4.
OPTIC ATROPHY
• Non-specific response to optic nerve damage from
any cause including retinal diseases such as:
o retinitis pigmentosa and CRAO
• May be a sign of prior disc edema.
• May be a late sign of compressive optic
neuropathy.
Figure 8. Optic Atrophy. Pale disc but with distinct disc border.
Loss of the normal pinkish color of a normal nerve and the cup
is hardly seen. Patients with optic atrophy usually has
permanent visual loss.
OPTIC HEMORRHAGE
• If located in the nerve fiber layer (NFL) of the retina
– splinter or flame-shaped hemorrhages.
• If located deeper – disc hemorrhages (appear round
and blotchy)
• Two theories:
o Mechanical (shearing forces)
o Vascular (ischemia)
Figure 9. Optic Nerve Hemorrhage. Left image, hemorrhage
involving eyes with well-developed papilledema. Middle and
Right image showing a localized flame hemorrhage.
OTHER OPTIC NERVE PATHOLOGIES
• Optic Neuritis
• Anterior Ischemic Optic Neuropathy
• Papilledema
• Neoplastic Optic Nerve Infiltration
• Neoplastic Optic Nerve Compression
• Nutritional and Optic Neuropathies
• Optic Nerve Trauma
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 OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

• Hereditary Optic Neuropathies

o Leber’s Hereditary Optic Neuropathy

IV. THE OPTIC CHIASM

Figure 13. Bitemporal Hemianopsia. Visual field of a patient

with a lesion affecting the optic chiasm.

OPTIC CHIASM PATHOLOGIES

Figure 10. Relationship of the Optic Chiasm to neighboring
structures (median sagittal section). Closely related to the base
of the brain
Figure 11. Relationship of the Optic Chiasm and the Pituitary
Gland.
• Chiasmal lesions cause Bitemporal Hemianopsia.
• Early stage – field defects are incomplete and
asymmetric.
• Later stage – temporal field defects become complete.
• Pituitary Adenoma – common in Adults
• Craniopharyngioma – common in Children
• Suprasellar Meningioma
• Chiasmatic and Optic Nerve Glioma
V. RETROCHIASMATIC VISUAL PATHWAY
THE LATERAL GENICULATE BODY
V. RETROCHIASMATIC VISUAL PATHWAY
• Starts from the Optic tract to Primary visual cortex
• Cerebrovascular disease and tumors are the most
common lesions of the retrochiasmatic visual
pathways.
• Due to their multiple vascular supply, the optic tracts
and LGN are rarely affected by vascular lesions.
• Retrochiasmatic field defects are homonymous.
• In patients above 50 years old, vascular lesions are
the most common (80%) cause of occipital lobe
conditions.
• The pattern of field defect depends on the affected area
of the occipital lobe.
• Macular sparing occurs due to the dual blood supply
of the occipital lobe:
o Posterior cerebral artery – Main blood
supply
o Branches of the middle cerebral artery –
Supplies the occipital lobe tip.
▪ responsible for the central macular
vision.
NFT: Basically pag tinamaan yung PCA cause
of vascular lesions hindi masasama yung
macula sa magkakaroon ng loss of vision kasi
iba blood supply nya which is MCA = middle
cerebral artery = MaCulA.

Figure 12. Gross and MRI image of a Pituitary Adenoma.

This lesion may cause impingement of the optic chiasm resulting
to Bitemporal Hemianopsia.

Figure 14. Left Homonymous Hemianopsia with Macular

sparing. Lesion is in the PCA, due to the dual blood supply
macula is spared.

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Figure 15. Homonymous Macular Scotoma. If the lesion is in

the MCA instead of PCA, there will be scotoma.

VI. THE PUPILS

• 20-40% of normal patients have physiologic Anisocoria
(~0.5mm).
• Anisocoria – pupils are asymmetric, one pupil is larger
than the other
o Possible cause is herniation Figure 17. Swinging Flashlight Test. Relative Afferent
Pupillary Defect (RAPD) or Marcus Gunn Pupil, caused by optic
• Pupil size varies according to the sympathetic
nerve lesion or extensive retinal disease.
innervation of the iris dilator muscle.

PUPILLARY LIGHT REFLEX

Figure 18. The difference between CN II (afferent) lesion vs.

CN III (efferent) lesion. Optic nerve lesion there will be loss of
direct pupillary reflex but consensual pupillary reflex is
preserved. Oculomotor nerve lesion there will be loss of
consensual pupillary light reflex.

PUPILLARY NEAR REFLEX

• Triad of
o Convergence
o Accommodation
o Miosis
Figure 16. Pathway of the Pupillary Light Reflex. CNII → • Pupillary constriction accompanying the triad. Not easy
Optic Nerve → Optic Chiasm → Optic Tract → Pretectal Area to elicit especially in children.
and Superior Colliculus → Edinger-Westphal Nucleus → CNIII o Relatively easier to see in blue-eyed
→ Ciliary Ganglion → Pupillary sphincter. Caucasian people.
• When you ask the patient to fixate from distant to near,
• Afferent arm Cranial Nerve II (Optic Nerve)
you also expect the pupils to constrict. So, pupils
• Efferent arm Cranial Nerve III (Oculomotor Nerve)
constrict not just to light stimulus, it also constricts to
near vision.
RELATIVE AFFERENT PUPILLARY DEFECT
• Also known as Marcus Gunn Pupil
ANISOCORIA
• Sensitive and specific sign to detect optic nerve
pathology or large retinal pathology.
Table 2. Anisocoria and their associated conditions
• “Relative” – in relation to the contralateral eye.
DEFECT CONDITION
• “Afferent” – refers to the afferent arm of the pupillary Anisocoria in Dark > Anisocoria in Horner’s
light pathway (optic nerve).
Bright Syndrome
Anisocoria in Bright > Anisocoria in Adie’s Tonic
Dark Pupil
Anisocoria in Dark = Anisocoria in Physiologic
Bright = Anisocoria in Near Response Anisocoria
Anisocoria in Dark = Anisocoria in Light Near
Bright < Anisocoria in Near Response Accommodation
Anisocoria ± CN 3 Palsy Aneurysm

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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

PUPILLARY LIGHT NEAR DISSOCIATION

• Miosis at near > miosis to light

• Occurs in lesions that affect the ciliary ganglion or
the midbrain, in which the light reflex pathway is
relatively dorsal compared to the near response
pathway.
• Etiology:
o Adie’s tonic pupil
o Argyll Robertson pupils
o Midbrain tumor or infarct
o CNS degenerative disease
o CNS infection
o DM
o chronic alcoholism

ARGYLL-ROBERTSON PUPIL
• Prostitute’s Pupil
• Accommodates, but does NOT react
• Small (<3mm) pupils, irregular, eccentric
• Difficult to dilate due to iris atrophy Figure 19. Pilocarpine 0.125% test for Adie's Pupil. Even with
diluted pilocarpine the right pupils constricted due to denervation
• Highly suggest tertiary (CNS) syphilis
hypersensitivity.

ADIE’S TONIC PUPILS

• Due to damage of the ciliary ganglion (in the orbit) HORNER’S SYNDROME
or short ciliary nerves
o Short ciliary nerves subserve the near
response more than they subserve the light
reaction (30:1)
• Etiology
o autonomic neuropathy
o after retinal laser photocoagulation
• Young females
• Usually isolated and benign
• In 50% of cases, the contralateral eye may be
involved in the next 10 years.
• Denervation hypersensitivity to 0.125% pilocarpine
(pupils constrict to weak pilocarpine)
• Early stage – pupil is dilated, accommodation is
impaired. Figure 20. The Oculosympathetic Pathway. 1st order
• Later stage – accommodation recovers, incomplete (central): Posterior hypothalamus to C8-T2 → 2nd order (pre-
ganglionic): C8-T2 to superior cervical ganglion → 3rd order
reinnervation of the iris (post-ganglionic): Superior cervical ganglion to the carotid
o Segmental iris constriction (more constricted plexus and CNV1 (trigeminal), which enters the orbit.
than the normal contralateral eye)
o Pupil LND • Due to damage to the oculosympathetic pathway
• ADIE-HOLMES: Adie’s tonic pupil + loss of DTRs. • Triad:
o Ptosis
o Miosis
o Anhydrosis

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 OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

• 40% Trauma – most common cause

• 30% Idiopathic
• 20% Ischemic (diabetic)
• 10% Tumor

CN VI PALSY

Figure 21. Test for Horner's syndrome. 10% cocaine

instillation to confirm it presence. Next, we do 1% Figure 24. Right CN VI palsy. Loss of function of the Lateral
hydroxyamphetamine test to localize the lesion. If the pupil rectus resulting to esotropia (unopposed action of the medial
dilates – pre-ganglionic lesion but if pupils did not change – rectus).
post-ganglionic lesion.

VII. CRANIAL NERVE PALSIES RECALLS/NUGGETS

CN III PALSY
Right homonymous Left optic tract
hemianopsia
Optic disc edema

RAPD Dilate affected eye

when light is shine
through the unaffected eye
Figure 22. Right pupil with complete CN III palsy. "Down and
Out" presentation. Incomplete CN3 palsy Absence of ptosis
PLS STUDY FIGURES 1&2
• Complete or Incomplete AND TABLES 1&2
o Complete – SR, MR, IR, IO, levator
palpebrae superioris and (+) ptosis
o Incomplete – SR, MR, IR, IO with (-) ptosis
• Pupil-involving or Pupil-sparing
o (+) dilated pupil – request for a cranial MRI
to rule out cerebral aneurysm
o Normal pupil – most likely ischemic only

CN IV PALSY

Figure 23. Right CN IV palsy. “Tilted and turned AWAY” from

the lesion.

• Loss of function of the Superior Oblique – eye

torsion

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APPENDIX

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 OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

NFTH: Study these figures/tables from upper batch trans

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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

SUMMARY

I. Neuro-ophthalmology • Specialty dealing with the problems of the Optic nerve.

• Could be the first to diagnose tumors, strokes, and small lesions in the brain (multiple sclerosis,
degenerative brain disease).
• Deals with CN II, III, IV, V, VI, VII, and IX.
• Use of CT scans and MRI to corroborate and identify suspicious brain lesions.

VISUAL PATHWAY

Visual Field Defects. (a)

Hemianopsia, (b) Quadrantanopia, and
(c) Scotoma.

. The Visual Pathway. Light passes through the lens and reaches the retina, where the formed image is
reversed and inverted. Axons leaving the retina forms the optic nerve. Fibers will then pass through the
optic chiasm where the nasal side of the optic nerve would decussate to the contralateral optic tract while
the temporal side of the optic nerve would remain on the ipsilateral optic tract. Axons in the optic tracts will
synapse in the lateral geniculate nucleus (LGN) of the thalamus. Fibers from the LGN would then be
optic radiations until it eventually synapses with the primary visual cortex.

• Summary of conscious vision perception

o Retina → Optic Nerve → Optic Chiasm → Optic Tract → Lateral Geniculate Body →
Optic Radiation → Primary Visual Cortex
• Additional pathways
o Retina → Optic Nerve → Optic Chiasm → Optic Tract → Pretectal Area and
Superior Colliculus
▪ Pupillary Light Reflex
▪ Eye movements towards visual stimuli

Visual Field Defects

DEFECT LESION
A Scotoma Retina
B Monocular vision loss Optic Nerve
C Bitemporal Hemianopsia Optic Chiasm
D Contralateral Optic Tract
Homonymous
Hemianopsia
E Contralateral Superior Inferior optic radiation
Quadrantanopia (Temporal lobe)
F Contralateral Inferior Superior optic radiation
Quadrantanopia (Parietal lobe)
K Contralateral Occipital Lobe
Homonymous
Hemianopsia with Macular
sparing

II. Confrontation test III. To screen for visual field defects

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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

IV. Finger counting

V. Simultaneous finger counting
VI. Penlight (for patients who only have light perception)
VII. Test set-up
a. Test each eye separately.
b. Seat the patient 1 meter (3 feet) facing the examiner.
c. By convention, test the patient’s right eye or whichever is the better eye first.
d. Completely occlude the patient’s other eye that is not being tested.
e. The examiner must close the eye that is directly opposite the patient’s occluded eye.
i. For example: to test the patient’s right eye, the patient’s left eye and the
examiner’s right eye must be covered.
f. Ask the patient to focus on a target in a straight gaze position (example, the examiner’s
nose)
III. Optic nerve • Features of optic neuropathy
o Reduced visual acuity
o Afferent pupillary defect
o Poor color vision
o Optic disc changes
o Visual field defect
• Very bad lesions presenting immediately.
• Optic nerve in the canal is most susceptible to damage.
• Axons can be dysfunctional long before the optic nerve becomes atrophic.
Optic Disc Edema • Predominantly in diseases directly affecting the anterior part of the optic nerve.
o increased intracranial pressure
o compression of the intraorbital optic nerve
• Papilledema – optic disc edema caused by an increase in intracranial pressure.
o A common cause of neurologic emergency. If presenting with headache, we
immediately consider doing a CT-scan
o Generally will not cause BOV, only increase in the size of physiologic blind spot.
• Other causes include retinal disease (in CRVO), uveitis, and ocular hypotony.
Optic Atrophy • Non-specific response to optic nerve damage from any cause including retinal diseases such
as:
o retinitis pigmentosa and CRAO
• May be a sign of prior disc edema.
• May be a late sign of compressive optic neuropathy.
Optic Hemorrhage • If located in the nerve fiber layer (NFL) of the retina – splinter or flame-shaped
hemorrhages.
• If located deeper – disc hemorrhages (appear round and blotchy)
• Two theories:
o Mechanical (shearing forces)
o Vascular (ischemia)

Optic nerve pathologies • Optic Neuritis

• Anterior Ischemic Optic Neuropathy
• Papilledema
• Neoplastic Optic Nerve Infiltration
• Neoplastic Optic Nerve Compression
• Nutritional and Optic Neuropathies
• Optic Nerve Trauma
• Hereditary Optic Neuropathies
o Leber’s Hereditary Optic Neuropathy
IV. Optic Chiasm • Chiasmal lesions cause Bitemporal Hemianopsia.
• Early stage – field defects are incomplete and asymmetric.
• Later stage – temporal field defects become complete.
• Pituitary adenoma – common in adults
• Craniopharyngioma – common in children

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OTORHINOLARYNGOLOGY
V. Retrochiasmatic Visual Pathway
VI. The pupils
Pupillary Light Reflex
Relative Afferent Pupillary Defect
Pupillary Near reflex
[INOCENCIO]
BASIC EYE EXAM LECTURE 8.0
• Suprasellar Meningioma
• Chiasmatic and Optic Nerve Glioma
• Starts from the Optic tract to Primary visual cortex
• Cerebrovascular disease and tumors are the most common lesions of the retrochiasmatic
visual pathways.
• Due to their multiple vascular supply, the optic tracts and LGN are rarely affected by vascular
lesions.
• Retrochiasmatic field defects are homonymous.
• In patients above 50 years old, vascular lesions are the most common (80%) cause of
occipital lobe conditions.
• The pattern of field defect depends on the affected area of the occipital lobe.
• Macular sparing occurs due to the dual blood supply of the occipital lobe:
o Posterior cerebral artery – Main blood supply
o Branches of the middle cerebral artery – Supplies the occipital lobe tip.
▪ responsible for the central macular vision.
• 20-40% of normal patients have physiologic Anisocoria (~0.5mm).
• Anisocoria – pupils are asymmetric, one pupil is larger than the other
o Possible cause is herniation
• Pupil size varies according to the sympathetic innervation of the iris dilator muscle.
Pathway of the Pupillary Light Reflex. CNII → Optic
Nerve → Optic Chiasm → Optic Tract → Pretectal
Area and Superior Colliculus → Edinger-Westphal
Nucleus → CNIII → Ciliary Ganglion → Pupillary
sphincter.
• Afferent arm Cranial Nerve II (Optic
Nerve)
• Efferent arm Cranial Nerve III
(Oculomotor Nerve)
• Also known as Marcus Gunn Pupil
• Sensitive and specific sign to detect optic
nerve pathology or large retinal
pathology.
• “Relative” – in relation to the contralateral
eye.
• “Afferent” – refers to the afferent arm of the
pupillary light pathway (optic nerve).
Swinging Flashlight Test. Relative Afferent
Pupillary Defect (RAPD) or Marcus Gunn Pupil,
caused by optic nerve lesion or extensive retinal The difference between CN II (afferent) lesion vs.
disease. CN III (efferent) lesion. Optic nerve lesion there will
be loss of direct pupillary reflex but consensual
pupillary reflex is preserved. Oculomotor nerve lesion
there will be loss of consensual pupillary light reflex.
• Triad of Convergence, Accommodation, and Miosis.
• Pupillary constriction accompanying the triad. Not easy to elicit especially in children.
o Relatively easier to see in blue-eyed Caucasian people.
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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

• When you ask the patient to fixate from distant to near, you also expect the pupils to constrict.
So, pupils constrict not just to light stimulus, it also constricts•to near vision.
Anisocoria DEFECT CONDITION
Anisocoria in Dark > Anisocoria in Bright Horner’s
Syndrome
Anisocoria in Bright > Anisocoria in Dark Adie’s Tonic Pupil
Anisocoria in Dark = Anisocoria in Bright = Physiologic
Anisocoria in Near Response Anisocoria
Anisocoria in Dark = Anisocoria in Bright < Light Near
Anisocoria in Near Response Accommodation
Anisocoria ± CN 3 Palsy Aneurysm
Pupillary light near dissociation • Miosis at near > miosis to light
• Occurs in lesions that affect the ciliary ganglion or the midbrain, in which the light reflex
pathway is relatively dorsal compared to the near response pathway.
• Etiology:
o Adie’s tonic pupil
o Argyll Robertson pupils
o Midbrain tumor or infarct
o CNS degenerative disease
o CNS infection
o DM
o chronic alcoholism

ARGYLL-ROBERTSON PUPIL • Prostitute’s Pupil

• Accommodates, but does NOT react
• Small (<3mm) pupils, irregular, eccentric
• Difficult to dilate due to iris atrophy
• Highly suggest tertiary (CNS) syphilis
ADIE’S TONIC PUPILS • Due to damage of the ciliary ganglion (in the orbit) or short ciliary nerves
o Short ciliary nerves subserve the near response more than they subserve the light
reaction (30:1)
• Etiology
o autonomic neuropathy
o after retinal laser photocoagulation
• Young females
• Usually isolated and benign
• In 50% of cases, the contralateral eye may be involved in the next 10 years.
• Denervation hypersensitivity to 0.125% pilocarpine (pupils constrict to weak pilocarpine)
• Early stage – pupil is dilated, accommodation is impaired.
• Later stage – accommodation recovers, incomplete reinnervation of the iris
o Segmental iris constriction (more constricted than the normal contralateral eye)
o Pupil LND
• ADIE-HOLMES: Adie’s tonic pupil + loss of DTRs
Horner’s Syndrome • Due to damage to the oculosympathetic pathway
• Triad:
o Ptosis
o Miosis
o Anhydrosis

The Oculosympathetic Pathway. 1st

order (central): Posterior hypothalamus to
C8-T2 → 2nd order (pre-ganglionic): C8-T2
to superior cervical ganglion → 3rd order
(post-ganglionic): Superior cervical ganglion Figure 25. Test for Horner's syndrome. 10% cocaine
to the carotid plexus and CNV1 (trigeminal), instillation to confirm it presence. Next, we do 1%
which enters the orbit. hydroxyamphetamine test to localize the lesion. If the pupil

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OTORHINOLARYNGOLOGY BASIC EYE EXAM LECTURE 8.0

dilates – pre-ganglionic lesion but if pupils did not

change – post-ganglionic lesion.

VIII. Cranial Nerve Palsies • Complete or Incomplete

o Complete – SR, MR, IR, IO, levator
CN III Palsy
palpebrae superioris and (+) ptosis
o Incomplete – SR, MR, IR, IO with (-)
ptosis
• Pupil-involving or Pupil-sparing
o (+) dilated pupil – request for a cranial
MRI to rule out cerebral aneurysm
o Normal pupil – most likely ischemic
only
Right pupil with complete CN III palsy.
"Down and Out" presentation.
CN IV Palsy • Loss of function of the Superior Oblique – eye
torsion
• 40% Trauma – most common cause
• 30% Idiopathic
• 20% Ischemic (diabetic)
• 10% Tumor

. Right CN IV palsy. “Tilted and turned

AWAY” from the lesion.
CN VI Palsy Right CN VI palsy. Loss of function of the Lateral rectus
resulting to esotropia (unopposed action of the medial
rectus).

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