The Diagnostic Dilemma of Pseudopapilledema

Tiffenie Harris, OD, FAAO

Associate Professor
Western University College of Optometry

Author’s Bio

Dr. Harris is a graduate of Indiana University School of Optometry. She practiced

primary care optometry in the Detroit Metropolitan Area for 10 years prior to starting
her academic career in 2004 at her Alma matter. She joined Western University
College of Optometry in 2008. Dr. Harris is the Course Director for Principles and
Practice of Anterior Segment and Posterior Segment courses.

Diagnostic Dilemma

Optic nerve head (ONH) elevation tends to be the most intimidating ocular finding especially when it presents
bilaterally. The purpose of this article is to provide the clinician with clinical strategies that will enhance their
assessment and management of bilateral disc elevations. In addition, this topic is important to review
because effective management will reduce over-referrals for neurological evaluations, thus decreasing health
care costs while avoiding needless and expensive neurological testing.

The optometrist’s role includes detection of disease with a timely and appropriate referral to specialists as
well as co-management and/or monitoring once under the care of a physician. A clinical case in which the
optic nerves are severely swollen is easy to diagnose. Yet, a case in which the nerves appear to be mildly or
moderately elevated or swollen makes the diagnosis more challenging, especially when the patient presents
with symptoms of headaches. This type of quandary frequently can cause alarm for the clinician, which often
eclipses the fact that the patient has no other signs or symptoms of increased intracranial pressure (ICP).1,2
Thus, the diagnostic dilemma begins with making the clinical decision and answering the question, “is it or is it
not swollen?”.

The foremost clinical goal is to differentiate congenital causes of disc elevation from acquired disc edema.
Papilledema (PE) is acquired bilateral optic disc swelling attributed to increased intracranial pressure as listed
in Table 1. Pseudopapilledma (PPE) is the appearance and false impression of bilateral disc swelling that is
associated with an underlying anomalous condition as listed in Table 2. A thorough history and a dilated
fundus examination will often facilitate the diagnosis. However, the use of current diagnostic technologies can
increase clinician confidence and augment our ability to diagnose and manage these challenging cases.
 Table 1
Differential Diagnosis of PE

Mass or Space Occupying Lesion

Malignant HTN (Hypertensive Crisis)
Idiopathic Intracranial Hypertension
Intracranial Hypertension Secondary to:
Subdural Venous Thrombosis
Saggital Sinus Thrombosis
Chiari I Malformation
Arteriovenous Malformation
Menigitis/Encephalitis

Table 2
Differential Diagnosis of PPE
Optic Nerve Head Drusen (ONHD)
Congenitally Full Disc (CFD)
Malinserted (Oblique insertion)
Tilted Disc Syndrome
Optic Nerve Hypoplasia
**DDx for bilateral presentations**

Background on Papilledema

In papilledema the acquired bilateral, occasionally asymmetrical, ONH swelling is due to increased intracranial
pressure. 1,3 The term papilledema should be strictly reserved for optic disc edema as a result of increased
cerebral spinal fluid (CSF), which bears specific etiologic implications. The most important entity to consider in
cases of increased intracranial pressure is a space occupying lesion of the brain. This is often done with
diagnostic tools such as Magnetic Resonance Imaging (MRI) and/or Computerized Tomography (CT) scans in
conjunction with a lumbar puncture (LP). Computerized Tomography has traditionally been the imaging study
of choice because of its availability and lower cost per patient than MRI.4,5 However, MRI has emerged as the
technically optimal imaging modality.

Papilledema due to increased CSF in the absence of mass lesion on brain imaging has been historically
associated with the term Pseudotumor Cerebri (PTC).1,3,4 The nomenclature of the syndrome of elevated CSF
with no mass effect, no ventriculomegaly, and with normal CSF composition remains controversial, yet, Benign
Intracranial Hypertension is no longer accepted. Current literature based on clinical experiences and advances
in neuroimaging technology supports the terminology of Idiopathic Intracranial Hypertension (IIH).1,3,4,6 The
pathogenesis underlying the increased cerebral spinal fluid in IIH is not fully understood.1,3, 6 Apparently, there
is a disruption of the CNS homeostasis resulting in increased CSF production and decreased CSF absorption.
Several mechanisms have been proposed. Sugerman et al suggested that intra-abdominal obesity causes
increased intrathoracic pressure resulting in a decrease in cranial venous flow. Conversely, most of the clinical
evidence points to an overall decrease of CSF absorption by the arachnoidal villi concurrent with intracranial
venous hypertension.1,4
The treatment and management of the underlying condition is crucial in the resolution of papilledema. In the
presence of chronic PE the swelling eventually subsides leaving the nerve atrophic. The loss of axons is
considered to begin with the peripheral axons with sparing of central axons explaining why in cases of PE the
acuities and pupils are rarely affected. The rate at which a patient develops optic atrophy from PE is not
specific. It depends upon many factors such as severity and prolonged duration of the increased ICP.1,4 It can
take anywhere from days, months, to even years. On rare occasions a patient can present with no evidence of
PE, yet still have increased ICP.1,4 Again, there is the diagnostic dilemma of optic nerve elevation as compared
to swelling. Knowing that some cases of increased CSF may not present with overt PE, making the diagnosis of
PPE is even more crucial. The conundrum can also lie in the fact that congenitally anomalous nerves can
become swollen.

Help in piecing the puzzle together comes in the differential diagnosis of the underlying conditions. The basic
pathophysiology of conditions that cause bilateral optic nerve swelling and that of congenital elevation can
help in differentiating PE from PPE. The pathophysiology of papilledema is a reaction to the increased CSF as it
passes from the subarachnoid space to the prelaminar optic nerve via the optic nerve sheath.1 The end result
causes axoplasmic flow stasis and swelling of the axons in the prelaminar optic nerve. The pathophysiology of
PPE is determined by the congenital anomaly associated with the disc elevation. In fact, congenitally
anomalous disc elevation must be included in the differential etiologies of presumed PE before referring a
patient for neuroimaging and a lumbar puncture.1,2

Background on Congenital Disc Anomalies

PPE, encompasses anomalies of the optic nerve head such as congenitally full discs (CFD), malinserted discs
(MID) and optic nerve head drusen (ONHD). Crowded Disc also known as CFD is the result of a normal number
of retinal axons passing through a small posterior scleral foramen. The resulting appearance is that of a
densely packed or crowded optic nerve head as the axons exit the globe.2,8 This is a nerve that is smaller than
the average sized optic disc and is often associated with hyperopic eyes. Typically, it is slightly hyperemic in
color with little to no physiological cupping along with superonasal and inferonasal blurred margins.2,9
Knowledge and appreciation of the appearance of the normal disc and its anomalies are required to
distinguish between the healthy and the abnormal. This is true in the assessment of the optic disc appearance
associated with malinserted discs.

The typical disc elevation seen in MID is due to the oblique insertion of the nerve to the globe. Primarily the
nasal portion is elevated with the temporal portion depressed and often associated with a sclera crescent.2,9 It
gives a swollen-like appearance because the nasal margins are often blurred. They typically have mirror
images in the right and left eyes and a high association with moderately myopic corrections. Malinserted disc
are tilted along its vertical axis such that the disc appears to have the nasal rim and margin raised or “heaped-
up”.2 This type of tilt should not be confused with that of tilted disc syndrome. Tilted disc syndrome refers to
a triad of tilted discs, decreased visual acuities, and bi-temporal visual field defects that do not respect the
midline.2,9,10 In tilted disc syndrome the disc’s vertical axis itself is tilted downward nasally giving the superior
temporal aspect of the nerve an elevated appearance with the inferior portion depressed. Therefore, “tilted”
discs are better described as “malinserted” discs in order to avoid confusing the term’s etiology with that of
the syndrome.

Although it is not uncommon to encounter PPE as a result of crowded disc and/or malinserted disc, they are
not the most frequent. By far the next entity frequently encountered that gives the false impression of disc
elevation is ONHD. It is the most common cause of PPE, accounting for 75% of diagnostically challenging disc
anomalies.10

Background on ONHD

ONHD are congenitally inherited as an autosomal dominant trait occurring approximately 1% of the
population with an increasing prevalence of 10-fold in family members.1,10,11 The scleral canal and optic disc of
eyes with drusen are much smaller than average. This is seen clinically where ONHD predominately occurs in
Caucasians and rarely in African Americans, whose scleral canal size is often larger.9,10,11 There are two types
of ONHD, visible and buried.

Buried ONHD are located beneath the disc surface and are not directly visible. They can cause elevation of the
optic disc with or without blurred margins. They can often have a very dramatic appearance giving the
impression of PE. In young children, the elevated optic nerve can present an ominous finding, as seen in
Figure 1. Current research and studies suggests that an abnormally narrow opening of the scleral canal can
cause a stasis of axoplasmic flow.2,10,11 This leads to abnormal axonal metabolism and mitochondrial
calcifications creating calcium-like globular deposits within the papilla.

Figure 1

Congenial disc anomalies often have in common a particular “look” such as anomalous disc vasculature
including early branching of the retinal vessels at the disc and secondary tortuosity.2,10 In addition, atypical
vascular loops or corkscrew vessels at the papillary border are associated with congenitally anomalous discs.
In cases of ONHD, 10% will have some type of vasculature anomaly.9,10 ONHD is associated with peripapillary
retinal pigment epithelial changes (33%) and an absent to very small cup-to-disc ratio.2,9 Drusen of the optic
nerve head have no histopathologic relationship to retinal drusen and are not considered age-related.
However, they have a tendency to become more visible as the patient ages as seen in Figure 2

Figure 2

In early life, ONHD remain deep in the nerve and always anterior to the lamina cribosa. They become more
visible at the disc surface in the second to third decades. 10 In adulthood, ONHD appear as spherical nodules
on the disc surface that are highly reflective by the ophthalmoscope light and give the disc a scalloped margin.
When illuminated with a red-free light these retractile bodies will auto fluoresce.

Most patients with ONHD are asymptomatic. However, many can present with visual field defects and rarely
with decreased visual acuities. ONHD can shear and damage the nerve fibers and vascular supply as they move
to the disc surface. The reduction of RNFL thickness results in visual field defects including enlarged blind
spots, localized depressions, arcuate nerve fiber bundle defects, or constrictions. Visual field defects are
present in 73% of visible drusen and 36% of buried disc drusen with no significant difference in the severity.
11,12
Spontaneous disc hemorrhages can occur in, around, and over the optic nerve head if progression of the
drusen interferes with the nerve’s blood supply. The incidence of retinal hemorrhage is between 2% and 10
%.10 Visible disc drusen may cause peripapillary atrophy and a break in Bruch’s membrane. As a result, the
patient is at risk of the development of peripapillary choroidal neovascular membranes, which may extend to
the macular or subfoveal area and compromise the patient’s vision.10,13,14

Conditions known to be associated with ONHD include Retinitis Pigmentosa (RP) and Angioid Streaks with or
without Pseuodxanthoma Elasticum (PXE). The ONHD in PXE are similar but in RP they do not have the same
appearance.2,10 They tend to be more visible adjacent to a normal-sized nerve. In addition, there have been
reports of non-arteritic anterior ischemic optic neuropathy (NAION) associated with ONHD. 2,10,15

Building upon the pathophysiolgy of various disorders which can result in a bilateral elevated disc appearance,
the clinician can now approach the case with a systematic framework using information established in a
checklist approach. In every case of ONH elevation there should be an “instant checklist” in order to help the
practitioner to effectively determine if the nerve is in fact “swollen” or “elevated”. A review of this checklist
provides clinical strategies to effectively manage this diagnostic dilemma. The checklist consists of the
following elements:
 • A comprehensive history to illicit symptoms associated with increased intracranial pressure
(ICP) (Table 3)
• Assessment of cranial nerve function
• Assessment of optic nerve function
• Stereoscopic examination of the optic nerve appearance and peripapillary area
• Diagnostic and anciliary testing

Table 3.
Symptoms of PE
Headaches (HA)
Transient Visual Obscurations (TVO)
Tinnitus – “Whooshing” sound
Diplopia
** HA and/or TVO are most common**

Diagnostic Testing

Differential diagnoses include any entity that can cause bilateral optic disc elevation. This includes increased
intracranial pressure and congenital disc anomalies. Special investigations for the definitive diagnosis of
bilateral disc elevation include the following: Magnetic Resonance Imaging (MRI) and/or Computerized
Tomography (CT) scans of the orbit and brain, Fluorescein Angiography (FA), B-scan ultrasonography, and
Optical Coherence Tomography (OCT). The CT scan can detect intracranial tumors as well as ONHD. However,
it is not sensitive enough to pick up subtle calcific drusen in the disc and is not reliable for ONHD diagnosis.12
The MRI is superior to CT scan for soft tissue structures and is the preferred imaging test to rule out the
etiology of increased intracranial pressure. FA can be helpful in papilledema the where the optic nerve head
will show hyperflouresence and peripapillary leakage of the dye. In congenital disc elevation, there is no
peripapillary leakage of the dye especially in the late phase. In addition, the red-free barrier used in the pre-
injection phase illuminates the autofluorescent properties of disc drusen. Buried ONHD with both of these
techniques can be missed. Less invasive diagnostic investigations are available to differentiate disc edema and
buried disc drusen.

B-Scan ultrasonography has been shown to be the most sensitive and diagnostically relevant test to aid in the
differential diagnosis of ONHD. 2,10, 12,16 B-scan ultrasonography uses high-frequency sound waves. The sound
waves are reflected back to the probe, converted into an image, which is used to make a dynamic evaluation
of the optic disc. When calcification of tissue is present, there is a very strong reflection of the echo back to
the probe. Therefore, B-scan ultrasonography is the single most important ancillary test to perform in the
diagnosis of ONHD. The results for ONHD will show a highly reflective nodule within the optic nerve even at a
low gain level as seen in Figure 3. In the presence of acquired disc edema, the B-scan will demonstrate a circle
within the optic nerve sheath, separating the sheath from the optic nerve at a standard gain level. This is
called a “crescent sign” produced by the increased cerebral spinal fluid transmitted along the subdural space
within the optic nerve.16
Figure 3

Optical Coherence Tomography (OCT) is analogous to the B-Scan except light, rather than sound is used to
provide images of the ocular structures. OCT is an objective, noninvasive alternative to analyze the optic
nerve head. More importantly, it is useful in quantifying the status of the retinal nerve fiber layer (RNFL).17 In
papilledema, the OCT shows an elevated nerve head along with excessive thickening of the RNFL as seen in
Figures 4 and 5. In Figure 6, the OCT shows the elevation of the disc and the underlying nodular shadows
caused by the ONHD. The key differential between ONHD and acquired disc edema is significant thinning of
the retinal nerve fiber layer with ONHD (Figure 7) and thickening in disc edema. In cases of papilledema the
RNFL curve falls above the normative, age-adjusted scale exceeding 200 microns. Many cases of early
papilledema as seen in Figure 8 can clinically mimic buried ONHD. The nasal margins are blurred and the disc
has anomalous vasculature branching. The OCT results for this example are shown in Figure 5 and clearly show
that the RNFL layer is thickened as seen in early papilledema. In cases of CFD and MID, the OCT will show a
normal to slightly thickened retinal nerve fiber layer curve that stays within the age-adjusted scale. Figures 5
and 7 demonstrate the application of testing RNFL to aid in differentiating early PE from PPE.

Figure 4
Figure 5

Figure 6

Figure 7
Figure 8

Making the Diagnosis

Making the clinical diagnosis begins with a working checklist starting with a comprehensive history. During the
history, the practitioner is listening for symptoms associated with increased intracranial pressure and any
associated neurological defects. Table 3 highlights the symptoms of PE that can often serve as the “red flag” of
increased intracranial pressure. Medical, family, and social history are also helpful in suspected cases of
increased intracranial pressure. Always include in the checklist the patient’s age, demographics, general
appearance, and ocular/medical history, medication review, and in-office blood pressure readings.

Visual acuities, pupils, color vision, extraocular muscles, and visual field screening are important to determine
if there is any optic nerve or cranial nerve dysfunction associated with elevated optic discs. Acuities are
normal in most cases of PE until optic atrophy or macular edema develops. Most patients with ONHD, CFD,
and MID are asymptomatic with normal acuities, color, and visual fields.2,9,11 Conversely, many cases of ONHD
can present with visual field defects and rarely with decreased visual acuities.10 In rare cases, ONHD can cause
an afferent pupillary defect.10,11,15 The pathophysiology of the pupil defect can be a direct result of the
drusen’s effect on the RNFL as well as a result of asymmetric RNFL loss.

Cranial nerves of the extraocular muscles (EOMs) must also be assessed. Patients with CFD, ONHD, and MID
will not exhibit any deficits of the EOMs. But, patients with PE need to be screened for a sixth nerve palsy
(SNP). Approximately 38% of patients with IIH will present with a sixth nerve palsy. The patient will report
horizontal diplopia during motility examination. In fact, the SNP is a non-localizing sign of increased ICP from
any etiology.18 The sixth cranial nerve is vulnerable to the effects of elevated ICP. As the nerve courses the
base of the posterior fossa, it runs along the petrous portion of the temporal bone. The increased ICP cause
the nerve to compress against this boney structure. A posterior fossa brain lesion can produce a bilateral SNP.
There has been a less frequent association of cranial nerves III, IV, and VII palsies with increase intracranial
pressure.4,18
A dilated fundus examination including stereoscopic views of the disc provides the most effective optic nerve
evaluation. There are key characteristics to look for in determining disc edema from elevation. Start with the
overall disc appearance looking at the size, cup, margins, neuroretinal rim tissue color, and taking note of any
spontaneous venous pulsation (SVP). SVP is present in about 20% of the normal population. Next, study the
vasculature of the disc and surrounding tissue. In the presence of papilledema, the optic nerve will appear
elevated and hyperemic with blurred margins that will obscure peripapillary vessels as they leave the disc.
The swelling includes no SVP along with venous congestion with flame-shaped hemorrhages and cotton wool
spots. Buckling or retinal folds of the temporal aspect of the disc (Paton’s lines) may be present. In contrast,
congenitally anomalous discs will not have peripapillary vessel obscuration nor will there be any cotton wool
spots. In addition, Paton’s lines are not associated with pseudopapilledema. Look for anomalous vascular
patterns including tortuosity. Clinical diagnosis and decisions are made based on the appearance of the optic
nerves and information provided by the ancillary tests.

Now what to do about it?

Once the clinician determines that the discs are in fact swollen, the patient must be sent for neuroimaging
within 24 hours to identify the source of increased ICP. Take stereo disc photos, get a baseline threshold
visual field, and order the MRI. The visual field defects associated with papilledema start as an enlarged blind
spot. Depending on location and severity of a brain lesion, neurological visual field defects such as
quadranopsia or hemianopsia can occur.

In addition to visual field testing, the OCT provides an available option for long-term follow-up of the changes
in RNFL thickness.17,19 This is helpful in monitoring the resolution of papilledema as well as monitoring RNFL
loss in ONHD. Patients with ONHD can develop visual field defects and RNFL loss that resembles glaucoma.
Glaucoma and ONHD can coexist. 2,19,20 The OCT cannot distinguish nerve fiber layer loss that occurs from
ONHD from that which occurs as a result of glaucoma. Documentation of visual field loss and RNFL provides a
baseline measure to track progression. The lack of significant disc cupping of nerves with drusen contributes
to the difficulty in managing these patients who also develop glaucoma.

There is no existing treatment for ONHD. An annual comprehensive eye examination along with proper
diagnosis and patient education is the best available modality of care. Generally, ONHD is without visual
significance. However, patients need to be aware of potential complications that could affect vision. Patients
with ONHD should undergo regular dilated fundus examinations along with visual field testing (HVF 24-2),
stereoscopic disc photos, IOP measurement, and nerve fiber layer examinations for future monitoring

The optometrist’s role in bilateral disc elevation includes recognition, timely and appropriate referral to
specialists, and co-management when required. In addition, the clinician must rule out pathological
presentations that can be misinterpreted as anomalous while being mindful that anomalous optic nerves can
become swollen. With the aid of diagnostic tests such as Bscan and OCT, clinicians can avoid unnecessary
doubts and concerns along with expensive neurological investigations while targeting the correct diagnosis in
bilateral optic nerve elevation.
References
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CE@HomeOnline The Diagnostic Dilemma of Pseudopapilledema
CE Questions December 2012
Name____________________________ License #_______________________________
1. Every elevated optic nerve is the same as a 6. Patients with increased intracranial
swollen optic nerve. pressure will MOST often complain of the
a. True following symptom:
b. False a. Headache
b. Earache
2. Which of the following are optic nerve c. Vertigo
characteristics should be evaluated in cases d. Diplopia
of bilateral optic nerve elevation:
a. Overall disc diameter or size 7. All of the following diagnostic tests can be
b. Examination of the peripapillary vessels utilized in determining the cause of bilateral
c. Neuroretinal rim tissue color optic nerve elevation, EXCEPT:
d. All of the above a. X-ray of head
b. CT scan of brain
3. Optic nerve head drusen (ONHD) is c. OCT of optic nerve
associated with all of the following, EXCEPT: d. Humphrey visual fields
a. Thinning of the RNFL
b. Large optic disc diameters 8. Tilted disc syndrome is associated with all of
c. Glaucoma-like visual field defects the following clinical findings, EXCEPT:
d. Small optic disc diameters a. Arcuate visual field defects
b. Decreased visual acuities
4. The most common cause of c. Bitemporal visual field defect
pseudopapilledema, accounting for 75% of d. Tilted disc along the vertical axis
diagnostically challenging disc anomalies is
which of the following? 9. B-Scan ultrasonography has been shown to be
a. Crowded dics the most sensitive and diagnostically relevant
b. Malinserted discs test to aid in the differential diagnosis in which
c. Tilted disc syndrome of the following?
d. Optic nerve head drusen a. Diabetic retinopathy
b. Optic atrophy
5. The differential etiologies of bilateral disc c. Optic nerve head drusen
swelling and/or elevation include which of d. Retinitis Pigmentosa
the following?
a. Malignant hypertension 10. Congenitally Full Disc (CFD) is most
b. Optic nerve head drusen commonly associated with which of the
c. Increased intracranial pressure following?
d. All of the above a. Myopic patients
b. Hyperopic patients
c. Visual field defects
d. Large optic nerve diameters