The Differential Diagnosis of an Optic Nerve Disorder
When you suspect an optic nerve disorder, your differential diagnosis should include retinal, glaucomatous and congenital conditions.
Release Date: April 2010
Expiration Date: April 30, 2013
Optic nerve disorders usually have characteristic features; however, other conditions often present similarly. Then, the challenge becomes determining if the disease is of the optic nerve, retina, both or neither. The author reviews several common diseases of the optic nerves, as well as conditions with “lookalike” signs.
Denise Goodwin, O.D.
This course is COPE approved for 2 hours of CE credit. COPE ID 27962-PS. Please check with your state licensing board to see if this approval counts towards your CE requirement for relicensure.
This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.
Dr. Goodwin has no relationships to disclose.
Eye care professionals must
frequently evaluate anomalous optic nerves. Many
optic neuropathies are treatable, so we need to understand
the features, associated findings,
pathology and ancillary testing
that will allow us to promptly and
correctly diagnose and manage the
Diseases of the optic nerve usually result in characteristic features,
including reduced visual acuity
and color vision, a relative afferent pupillary defect (RAPD), visual
field defects and changes in the
optic disc appearance (e.g., swelling, pallor or cupping).
But, it can be a challenge to
determine if it is a disease of the
optic nerve or retina—or if it is due
to another condition altogether.
Optic Atrophy Warns of Nerve Damage
One key warning sign: optic atrophy. This represents irreversible damage to the optic nerve. Atrophy is diagnosed based on the color and structure of the optic nerve, nerve fiber layer and retinal blood vessels. It may be diffuse or sectoral (figure 1A). In many cases of optic atrophy, most notably in ischemic optic neuropathy, the retinal arteries become narrowed or attenuated at the edge of the optic disc (figure 1B). In some cases, however, the retinal vessels remain of normal caliber.
1A, B. Sectoral optic atrophy (left), and diffuse optic atrophy.
Optic Nerve Pathology …
... vs. Retinal Disease
Disorders affecting the optic
nerve must be differentiated from
other ocular pathologies, which are
typically visible on biomicroscopy
and fundus examination. Some
conditions, however, such as subtle
macular edema, epiretinal membrane and cone dystrophy, may not
be obvious on routine examination (figure 2). The ability to recognize
characteristic signs and symptoms
can help differentiate retinal and
optic nerve disorders. (See “Features of Macular Dysfunction vs. Optic Neuropathy,” below.) Also, when
examining the patient with retinal
disease, ensure that the amount of
vision loss is consistent with the
retinal condition as there may be an
Features of Macular Dysfunction vs. Optic Neuropathy
Poor vision in bright light
Poor vision in dim light
|Afferent pupillary defect
||Absent with subtle retinal disease
|Sense of brightness
||May have hyperopic shift
||Signs of retinal or macular disease
fundus biomicroscopy, OCT,
fluorescein angiography, or focal
Optic disc abnormalities
... vs. Glaucomatous Optic
The most common optic neuropathy is glaucomatous optic
neuropathy. Because other chronic
optic neuropathies, including those
resulting from ischemia, inflammation and compression, may result
in cupping despite normal intraocular pressure, it is important to
differentiate glaucoma from other
optic neuropathies. Keep in mind
that patients can have both glaucoma and another optic neuropathy
Loss of visual acuity, color
vision and visual field usually occur early in non-glaucomatous
optic neuropathies. Acuity loss only
occurs late in the glaucomatous process when there is absence of at least
a portion of the neuroretinal rim.
An RAPD can occur if the glaucoma
is unilateral or asymmetric.
Visual field defects secondary to
glaucoma generally occur only with
significant cupping, and visual field
loss should correspond with the
area of focal neuroretinal rim loss.
In glaucoma, visual field defects are
usually arcuate or paracentral in
nature, respect the horizontal meridian, and occur between 5º and 30º
from fixation. Early visual field loss
often presents as a nasal step.
Cupping is more profound in
glaucoma than in other optic neuropathies and often has focal loss
of the neuroretinal rim. The neuroretinal rim may be absent in glaucoma, but if present, the color of the
remaining rim should have a normal
pink hue. The rim is rarely absent in
non-glaucomatous optic neuropathies, and the remaining neuroretinal rim is usually pale in color.
• Optic nerve hypoplasia. In this
case, the optic nerve head appears
abnormally small due to a low number of axons. The disc may appear
gray or pale and is surrounded by
a light-colored peripapillary halo (figure 3). At the normal junction
between the sclera and lamina
cribrosa, there is another change in
pigmentation, a “double ring sign,”
associated with the hypoplasia.
• Megalopapilla. Megalopapilla,
an abnormally large optic disc,
usually occurs bilaterally and is
associated with a large cup-to-disc
ratio (figure 4). These discs have a
surface area greater than 2.5mm2. The round or horizontally elongated cup, as well as the lack of rim
notching, helps distinguish megalopapilla from normal tension glaucoma. The neuroretinal rim may be
pale due to axons being spread over
a larger surface area.
• Morning glory disc anomaly. Morning glory disc anomaly is
evidenced by a congenital funnelshaped excavation of the posterior
pole (figure 5). The disc appears
enlarged and may be recessed or elevated centrally. A white tuft of glial
tissue covers the central portion of
the cup. Blood vessels appear to be
increased in number and emanate
from the edge of the disc. After arising from the disc, the vessels turn
sharply at the edge of the cup and
have an abnormally straight pattern
in the peripapillary region.
• Peripapillary staphyloma. In
this condition, the area around the
disc is deeply excavated, with atrophic changes in the retinal pigment
epithelium (figure 6). It is generally
unilateral, and the disc may be normal or appear pale. As opposed to those in morning glory
disc anomaly, the blood
vessels have a normal
pattern. These eyes are
or slightly myopic, but
they can also be highly
optic discs. Colobomas result from an
incomplete closure of
the embryonic fissure. They can be either
unilateral or bilateral
and are often familial. A coloboma of the
optic disc appears as a white, bowlshaped excavation of the inferior
optic nerve head. The optic disc
is typically enlarged. The inferior
neuroretinal rim is thin or absent,
and the superior neuroretinal rim
is relatively normal. The coloboma
may involve the choroid and retina (figure 7). Iris and ciliary colobomas
may also be present.
• Optic pit. An optic pit appears
as a round or oval, gray or white
depression in the optic disc (figure
8). They are most commonly found
temporally, but can be found in any
area of the disc.
• Tilted disc. Typically, the optic
nerve exits the sclera at a 90º angle.
A tilted optic nerve occurs when
the nerve exits the eye at an oblique
angle. Tilted disc is usually a bilateral condition in which the superiortemporal disc is raised, simulating
disc swelling, while the inferiornasal disc is flat or depressed (figure
9). This results in an oval-shaped
disc with the long axis at an oblique
angle. The blood vessels also enter
the globe at an oblique angle. There
is thinning of the RPE and choroid
in the inferior nasal quadrant.
6, 7, 8, 9. Peripapillary staphyloma (left). The patient’s refraction in that eye: -1.25 -1.75 x 014. Next, a coloboma that involves the
retina, choroid and optic nerve. Figure 8 shows an inferior temporal optic pit. Figure 9 (far right) shows a tilted optic disc.
• Myelinated nerve fiber layer. Myelinated nerve fibers manifest as
white, feathery patches that follow
the NFL bundles and have a striated
appearance (figure 10). The peripheral edges appear fanned out. The
myelination can simulate disc edema
due to elevation of the optic nerve
and obscuration of the disc margins
and retinal vasculature.
Normally, myelination does
not extend past the
however, in 0.6% to
1.0% of the population, myelinated NFL
is bilateral in just 8%
of cases and is continuous with the optic
nerve head in only
33% of eyes.3
Optic Nerve Head
due to disc drusen is
usually apparent in
childhood as a “full”
optic nerve that simulates papilledema (figure 11A). As the person
ages and this pseudopapilledema
changes, the optic nerve takes on a
scalloped appearance at the nasal
disc margin (figure 11B). Finally,
subtle excrescences appear on the surface of the disc (figure 11C).
The drusen enlarge, calcify and
become more visible. In later adulthood, the disc elevation decreases,
the nerve becomes pale and NFL
Buried drusen elevate the disc
and blur the disc margins. This
effect is differentiated from true
papilledema by the lack of hyperemia, dilated capillaries and vessel
obscuration. With pseudopapilledema due to disc drusen, the physiologic cup is absent, and the center
of the disc is most elevated (figure
12A). Patients often have anomalous vascular patterns, including
arterial or venous trifurcation, that
create the appearance of increased
number of vessels on the disc,
abnormal or premature branching,
tortuosity, vascular loops, and cilioretinal vessels.
Optical coherence tomography
(OCT) can also aid in differentiating optic disc drusen from optic disc
edema. Patients with disc edema
have a smooth internal disc contour
compared to the lumpy appearance
found with optic disc drusen.4 In
addition, optic disc edema demonstrates a V-shaped hyporeflective
space between the sensory retina
and the RPE that is minimal or
absent with optic disc drusen (figure
12B).4,5 OCT is also useful to follow
NFL changes over time.5
IIH and Papilledema
Patient symptoms help to
differentiate papilledema and
idiopathic intracranial hypertension (IIH) from other optic
neuropathies. Between 90%
and 98% of patients with IIH
present with headache.6-8 Other
manifestations include nausea
and vomiting (40%), pulsatile
tinnitus (16% to 60%), dizziness, and photophobia.6-8 Visual
symptoms of IIH include transient visual obscurations (32%
to 80%) and horizontal diplopia
(30% to 32%).6-8
It is rare for patients with IIH to
have loss of central vision, color
vision dysfunction, RAPD or visual
field defects (other than an enlarged
blind spot). Normal visual acuity
helps distinguish papilledema from
other causes of disc edema in which
visual acuity is often affected early.
Other features may help to differentiate papilledema from other causes
of optic disc edema (See “Differential Diagnosis of Optic Disc Edema,” below).
Differential Diagnosis of Optic Disc Edema
||VA is spared
||Pain with eye
||Small, crowded disc
in fellow eye or
signs of GCA
The appearance of the optic
nerve and retina can help determine the presence of papilledema.
Papilledema is usually bilateral and
symmetric (figure 13). The optic
nerve head appears hyperemic.
Paton’s lines (circumferential retinal folds surrounding the disc) are
often present. Linear or curvilinear folds in the choroid may also
develop. This is often accompanied
by progression of hyperopia.
cotton-wool spots, and tortuous
retinal vessels on or surrounding
the disc may be observed. Flameshaped hemorrhages indicate acute
or subacute edema. A thin, radial
hemorrhage on or around the disc
margin can indicate distended capillaries of the optic nerve—an early
sign of papilledema.
Lack of spontaneous venous pulsation (SVP) can indicate increased
intracranial pressure (ICP). SVP
is absent in cases of papilledema. It is thought that SVP is present
only if the ICP is less than 200mm
of water; however, only 80% of
normal patients will have SVP, so
the absence of the pulse does not
necessarily mean papilledema is
Typical Demyelinating Optic
Like papilledema, characteristics
associated with typical demyelinating optic neuritis help to differentiate this condition from other causes
of optic nerve disease. Symptoms of
optic neuritis include acute vision
loss, usually in one eye. Vision
often worsens over hours to days
before stabilizing and improving
after several weeks. In addition to
vision loss, 87% to 92% of patients
experience pain behind the eye that
worsens with eye movement.9,10 (This symptom helps to differentiate this from other causes of optic
neuropathy associated with painless
vision loss, such as NAION.)
Only one-third of optic neuritis
patients demonstrate visible swelling
of the optic nerve head, which may
be mild or severe and does not correlate with loss of visual acuity or
visual field.10 It is rare to find peripapillary hemorrhages, exudates or
Over four to six weeks, the optic
nerve develops pallor—even as
visual function improves. The pallor
is typically temporal, but it can be
sectoral in other areas of the disc or
Giant cell arteritis (GCA), also
known as temporal arteritis, is the
most common cause of arteritic
anterior ischemic optic neuropathy
(AAION) but accounts for only
6% of ischemic optic neuropathy
cases.11 Other causes of AAION
include polyarteritis nodosa;
Wegener’s granulomatosis; connective tissue diseases, such as systemic
lupus erythematosus; Churg-Strauss
syndrome; and rheumatoid arthritis.
The mean age at AAION diagnosis is 75 to 76 years, and it is rare
under age 50.12-14 Women and
white patients are affected more
Patients with AAION typically
have systemic symptoms, such as
headache, pain while chewing, pain
and tenderness of the temporal
artery or scalp, malaise, anorexia,
weight loss, fever, and joint and
muscle pain. However, 20% do not
have any systemic symptoms despite
Disc edema is more likely to
be pallid with AAION than with
non-arteritic anterior ischemic
optic neuropathy (NAION) (figure 14). Flame hemorrhages and
cotton-wool spots are associated
with AAION, and the optic disc of
the fellow eye is usually of normal
diameter with an average-sized cup.
The visual field is severely reduced,
but in early cases, the most common
visual field defect is an altitudinal
Within six to eight weeks, the
optic disc develops atrophy with
cupping similar to that seen with
glaucoma. Unlike glaucomatous
cupping, however, AAION patients
have pallor of the remaining neuroretinal rim.
GCA is an ophthalmic emergency. Patients with GCA are at
high risk for developing vision loss
in the other eye, as well as systemic
complications such as stroke or
myocardial infarction. For those
suspected of GCA, treatment with
high dose steroids should be started
immediately without waiting for confirmation of the diagnosis with a
temporal artery biopsy.
The most common cause of disc
edema in people over age 50 years
is non-arteritic anterior ischemic
optic neuropathy.17,18 The mean age
of onset is approximately 61 to 66
Visual acuity loss with NAION
is usually not as severe compared
with that in AAION. Diffuse or segmental disc edema is present with
NAION and may be more severe
either superiorly or inferiorly. Swelling can be hyperemic or pale, but
pallor is less likely to be seen than in
cases of AAION. Altitudinal visual
field loss, usually inferior or inferior
nasal, is the most common visual
field defect, but any other pattern
Peripapillary hemorrhages and
focal retinal arterial attenuation
around the disc are common. The
contralateral optic nerve head is
often undersized with a small or
absent cup. Additionally, the contralateral optic nerve has mild disc
elevation and blurred margins.
The most common cause of
inflammatory infiltrative optic neuropathy is sarcoidosis. Sarcoidosis is
more common in women and blacks.
Visual loss is usually severe when
sarcoidosis affects the optic nerve.
If sarcoidosis affects the anterior
optic nerve, the disc will be either
diffusely or sectorally elevated (figure 15). In many cases, the findings may appear identical to those
related to demyelinating optic neuritis. Or, sometimes, a white, lumpy,
nodular appearance of the optic
nerve will suggest a granulomatous
process. Other evidence of intraocular inflammation is usually present,
including inflammation of the vitreous or anterior chamber.
Infectious Optic Neuropathy
Optic nerve disease can occur
with a large number of infectious
conditions. Common viral and bacterial causes associated with optic
neuritis all result in similar clinical
signs and symptoms. Toxoplasmosis
can also result in optic neuritis due
to direct involvement or when a
lesion is contiguous with the optic
Cat-scratch disease is the most
common infection associated with
neuroretinitis. Up to 5% of cases
result in neuroretinitis.24 In this situation, vision loss is painless. Unilaterial disc edema is common, and
a stellate pattern of infiltrates surround the macula to form a macular
star two to four weeks after the disc
edema begins (figure 16).
Parainfectious optic neuritis usually occurs one to three weeks after
a viral (though sometimes bacterial)
infection. The neuritis is most common in children and often occurs
bilaterally. Bilateral optic neuritis
can also occur one to three weeks
after viral or bacterial vaccination.
Spontaneous visual recovery usually
occurs over several months.
Compressive neuropathy, due to
optic nerve sheath meningiomas,
causes proptosis, congestion and
extraocular muscle motility limitations. Disc swelling typically occurs
even if the patient is asymptomatic.
Optic disc swelling is generally mild
or moderate. Peripapillary hemorrhages are not usually present.
Horizontal or vertical chorioretinal
striae adjacent to the optic disc
may be present when the lesion is
pressing on the globe. Optociliary
shunt veins and optic atrophy often
become apparent (figure 17).
Optic nerve compression due to
thyroid eye disease (TED) can present with swelling, hyperemia, pallor
or increased cupping of the optic
nerve. Normal-appearing optic
discs are present in up to half of all
eyes.25 Restriction of the extraocular muscles, most commonly the
inferior and medial recti, is likely.26
Conjunctival hyperemia over the
horizontal rectus muscle insertions,
punctate epithelial erosions, superior limbic keratoconjunctivitis, swelling of the eyelids, eyelid retraction,
and lid lag are commonly—but not
always—seen with TED.25,27
A glioma within the orbit causes
proptosis (94%) and a swollen
(35%) or atrophic (59%) optic
disc.28 These patients can develop
optociliary shunt vessels. Increased
volume of the optic nerve can
cause retinal striae and increasing
Because the average age for adult
gliomas is 52 years, the condition
can be misdiagnosed as NAION.29 If vision loss is progressive, the disc
swelling lasts longer than six weeks,
or a central retinal vein or artery
occlusion occurs several months
after the onset, patients should
Infiltrative Optic Neuropathy
Astrocytic hamartomas can
infiltrate the optic disc. The lesion
becomes glistening and yellow, with
a mulberry appearance composed of
calcific concretions (figure 18). The
appearance must be differentiated
from optic nerve head drusen; drusen are within the substance of the
nerve, whereas astrocytic hamartomas overlie the disc.
Melanocytomas are elevated, gray
or black intraocular tumors that
occur within the substance of the
optic nerve (figure 19). The majority are less than two disc diameters.
These tumors are benign. Slight
growth may occur, but malignant
transformation is rare.
Secondary tumors may also infiltrate the optic nerve. These include
metastasis, carcinomas, lymphoma
and leukemia. In patients with a
history of cancer, the cause of an
acquired optic neuropathy should
be considered cancer until proven
otherwise. Neuroimaging should be
Toxic and Metabolic Optic
The characteristics of optic neuropathy resulting from toxicity or
metabolic problems are similar to
other optic neuropathies, especially
those that are bilateral and simultaneous. Toxic or metabolic optic
neuropathy causes mild, bilateral
disc swelling. Early stages may have
a normal disc appearance. Disc
hemorrhages may be present. Optic
atrophy, most commonly of the
temporal disc, occurs in later stages (figure 20).
Other ocular signs may aid in
the diagnosis. For example, nystagmus and ophthalmoplegia can
occur with ethylene glycol ingestion.
Pigmented, whorl-shaped corneal
epithelial deposits occur with amiodarone use, and keratopathy may
be present in cases of nutritional
Leber’s Hereditary Optic
Vision loss from Leber’s hereditary optic neuropathy (LHON)
typically occurs between the ages of
15 and 35, but it can occur in both
younger and older individuals.30-32 Males are much more likely to
acquire the disease and to be symptomatic.32-35
During the acute phase,
the optic nerve head
becomes hyperemic with
obscuration of the disc
margins. Retinal blood
vessels become tortuous and dilated. In many
cases, a classic triad of
circumpapillary telangiectasia, swelling of the
NFL around the disc and
absence of leakage from
the disc on fluorescein angiography
is visible. The absence of fluorescein
dye leakage distinguishes LHON
from true optic nerve edema.
Despite continued vision loss,
the telangiectasia and NFL swelling
resolve. The optic nerve head does
not become pale for some time, but
eventually, optic atrophy ensues.
The pallor is most pronounced in
the temporal area with coexistent
damage of the papillomacular NFL.
Attenuation of retinal arteries and
non-glaucomatous cupping may
also be evident.
Autosomal-dominant optic atrophy is the most common hereditary
optic neuropathy.36 It occurs in the
first decade of life, with an average onset of four to six years of
age. Optic atrophy may be subtle.
The pattern of pallor can be either
temporal or diffuse.37 A wedgeshaped excavation of the temporal
disc is characteristic for autosomal
dominant optic atrophy (figure 21).
Peripapillary atrophy, absent foveal
light reflex, arterial attenuation and
non-glaucomatous cupping may
also be present.
Traumatic Optic Neuropathy
Traumatic optic neuropathy
occurs in 4% of patients after
head trauma.38 Motor vehicle and
bicycle accidents—the most common causes of injury to the optic
nerve—account for up to 60% of
optic nerve injuries.39-42 Nearly all
patients develop pallor after injury
to the optic nerve.40
Examination of ocular structures
may reveal other evidence of trauma
including orbital rim fractures,
hyphema, angle recession or dislocated lens. Resistance to retropulsion of the globe is indicative of
retrobulbar hemorrhage. Blood in
the vitreous may obscure the retinal
view. Commotio retinae or a choroidal rupture may also be responsible for vision loss.
In differentiating the cause of
optic neuropathy, first look at the
age of the patient. If the patient is
younger than 40, look for signs of
typical demyelinating optic neuritis.
Suspect anterior ischemic optic neuropathy in patients who are older
than 40. If signs are not consistent
with typical optic neuritis or anterior ischemic optic neuropathy, perform neuroimaging, serologic testing
or lumbar puncture to rule out
compressive, infiltrative, infectious
or inflammatory optic neuritis. Also
look for evidence of current or past
uveitis that may indicate an inflammatory or infectious cause. Toxic,
nutritional and hereditary optic neuropathy should also be considered
in the differential diagnosis. Occasionally, only time will tell the cause
of the optic neuropathy.
Dr. Goodwin is an
Associate Professor at
Pacific University College of Optometry. She
teaches Functional Neuroanatomy and Neurobiology, Ophthalmic
Imaging and Optometric Clinical Procedures.
She also advises thirdyear students in primary
care clinic. She is Coordinator of the Neuroophthalmic Disease Referral Service
at Pacific University.
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- Danesh-Meyer H, Savino PJ, Gamble GG. Poor prognosis of visual
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- Liozon E, Herrmann F, Ly K, et al. Risk factors for visual loss in
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