Differential Diagnosis of Papilledema

Overview and differential diagnosis of papilledema - UpToDate 7/21/19, 12(01 PM
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Overview and differential diagnosis of papilledema

Author: Don C Bienfang, MD
Section Editor: Paul W Brazis, MD
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2019. | This topic last updated: May 10, 2019.
INTRODUCTION
While the term "papilledema" is often used broadly to denote a swollen optic nerve head, the term
"papilledema" should be reserved for optic disc swelling that is due to raised intracranial pressure.
This topic will provide an overview and differential diagnosis of papilledema. The entity of
increased intracranial pressure and specific causes of papilledema are discussed elsewhere. (See
"Evaluation and management of elevated intracranial pressure in adults".)
ETIOLOGIES AND PATHOGENESIS
Papilledema occurs when raised intracranial pressure is transmitted to the optic nerve sheath. The
raised pressure mechanically disrupts axoplasmic flow within the nerve. Obstipation of intra-axonal
fluid results in swelling of the axons and leakage of water, protein, and other cellular contents into
the extracellular space of the optic disc giving rise to optic disc edema [1,2]. Venous obstruction
and dilation, nerve fiber ischemia, and vascular telangiectasias are secondary phenomena.
Any entity that increases intracranial pressure may lead to papilledema. These include:
● Intracranial mass lesions (eg, tumor, hematoma)
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● Cerebral edema (such as in acute hypoxic-ischemic encephalopathy, large cerebral infarction,

severe traumatic brain injury)
● Increased cerebrospinal fluid (CSF) production (eg, choroid plexus papilloma)
● Decreased CSF absorption (eg, arachnoid granulation adhesions after bacterial meningitis)
● Obstructive hydrocephalus
● Obstruction of venous outflow (eg, venous sinus thrombosis, jugular vein compression, neck
surgery)
● Idiopathic intracranial hypertension (pseudotumor cerebri)
Rarer entities causing increased intracranial pressure include increased arterial inflow as from an
arteriovenous fistula [3,4], intraspinal lesions [5,6], chronic respiratory illness [7,8], and other toxic
metabolic conditions that cause diffuse cerebral edema [9]. Reported cases of papilledema in
acute or chronic inflammatory demyelinating neuropathy may represent a consequence of elevated
CSF protein, which may impair resorption or circulation of CSF [10-13].
Idiopathic intracranial hypertension (pseudotumor cerebri) is discussed in detail separately. (See

"Idiopathic intracranial hypertension (pseudotumor cerebri): Epidemiology and pathogenesis" and
"Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis" and
"Idiopathic intracranial hypertension (pseudotumor cerebri): Prognosis and treatment".)
CLINICAL MANIFESTATIONS
Papilledema is usually discovered when a patient is evaluated for other symptoms of increased
intracranial pressure, rather than for symptoms directly resulting from optic nerve pathology.
Because the causes of intracranial hypertension are generalized phenomena, papilledema is

almost universally bilateral, although it may be asymmetric. If there is underlying optic nerve injury
or disease, then the appearance of papilledema may be unilateral, since the damaged nerve does
not swell. The classic example is the Foster-Kennedy syndrome, in which a frontal lobe tumor
compresses and destroys the optic nerve on one side before causing increased intracranial
pressure. This gives rise to optic atrophy in one eye and disc edema in the other.
Symptoms of increased intracranial pressure — Headache is a cardinal symptom of increased

intracranial pressure. However, few features of the headache specifically point to intracranial
hypertension as a cause. Nausea and vomiting are frequent in this setting, but they are also a
manifestation of migraine. Worrisome features include a positional quality to the headache, usually
worsening with recumbency, as well as a diurnal pattern; headaches associated with intracranial
hypertension are classically worse in early morning. (See "Evaluation and management of
elevated intracranial pressure in adults".)
Another classic symptom of increased intracranial pressure is binocular horizontal diplopia

resulting from unilateral or bilateral lateral rectus paresis. Cranial nerve six, the abducens nerve, is
believed to be peculiarly vulnerable to the effects of increased intracranial pressure because of its
long course in the subarachnoid space and its bend to enter the cavernous sinus.
A pulsatile machinery-like sound in the ear, probably due to venous sinus obstruction, is also
common and often persistent even after the raised intracranial pressure is relieved.
Visual symptoms — While rarely the presenting symptom, visual symptoms are common in
patients with papilledema. These are typically visual obscurations that clear completely, are often
unilateral, and are typically very brief (just seconds) [14]. They may occur spontaneously or with
changes in position, and they are believed to represent transient fluctuations in nerve head
perfusion. Their presence correlates with the degree of intracranial pressure elevation. Increasing
intensity, frequency, and duration of these symptoms can be a prognostic sign for permanent visual
loss, but this symptom is not reliably predictive.
It is unusual for patients to have persistent deficits of visual acuity or field loss until quite late in the
course. Untreated, chronic papilledema can lead to progressive visual field loss in the form of
peripheral field contraction, nerve fiber bundle defects, and even blindness [15,16]. The field loss
often mimics the field loss of glaucoma.
Funduscopic findings — Because the findings in papilledema evolve over time, ophthalmologists
often characterize papilledema into stages: early, fully developed, and chronic or late.
Clinicians often photograph patients' fundi in order to follow changes in the examination and
monitor response to treatment. Another approach might be to use a grading scheme, but some of
these have not been well validated or universally accepted [17].
Early — One of the earliest findings in papilledema is loss of spontaneous venous pulsations,
occurring with pressure elevations of only 200 mm [18-28]. This is a sensitive rather than specific
sign, as 20 percent of normal individuals do not have detectable venous pulsations. These
pulsations are best seen in the section of the central retinal vein that is going into the optic nerve
cup.
The optic cup is retained when the papilledema is mild. However, splinter hemorrhages in the
nerve fiber layer, at or beyond the disc margin, may be seen early (picture 1). This is also a
nonspecific sign, especially in older patients [28].
Fully developed — As the edema progress, the optic disc becomes elevated, the cup is
obliterated, and the disc margins become obscured. Blood vessels are buried as they course the
disc. Serpentine engorgement of retinal veins is evident, and the disc appears hyperemic. The
edema extends into the retina, giving the appearance of an enlarged optic nerve head. Multiple
flame hemorrhages and cotton wool spots, resulting from nerve fiber infarction, appear. Retinal
microfolds form around the swollen disc. At this stage, the blind spot will be increased (picture 2)
[28].
Chronic — The central cup remains obliterated. Hemorrhagic and exudative components
resolve. The appearance of hard exudates in the nerve fiber layer indicate a process of some
months' duration. The nerve now appears flat with irregular margins; nerve fiber attrition leads to
disc pallor (picture 3). One usually can detect some loss of visual field at this stage.
DIFFERENTIAL DIAGNOSIS
There are many causes of an elevated optic nerve head. While the term "papilledema" is
sometimes used to describe the findings in these conditions, it should be reserved for patients who
have elevated disc heads as a consequence of increased intracranial pressure. The causes of
papilledema (ie, increased intracranial pressure) are listed above. (See 'Etiologies and
pathogenesis' above.)
While there is overlap between the two categories, it is useful to consider those conditions that
cause bilateral abnormalities versus those that are more usually unilateral (table 1).
Bilateral disc abnormalities — Funduscopic findings, the clinical setting, and the presence of
associated visual loss may help distinguish the following entities from true papilledema.
● Pseudopapilledema – Congenital anomalies of the disc, including drusen and myelinated

nerve fibers, and even farsightedness or hyperopia, may cause the appearance of disc
swelling or pseudopapilledema. This term is reserved for conditions that are not due to
disease states.
Drusen are hyaline bodies thought to be remnants of calcific axonal degeneration. Drusen
tend to be buried in children (sometimes raising concern for increased intracranial pressure)
and become more exposed in adults. Most, 75 to 85 percent, are bilateral [29,30]. Present in
approximately 2 percent of the population, they may be inherited as an autosomal dominant
condition. Usually asymptomatic, some will have measurable visual field abnormalities,
including enlarged blind spot, field constriction, and inferior nasal visual field loss. An afferent
pupillary defect may be present if the condition is unilateral or asymmetric.
Disc drusen appear as a lumpy mass with refractile bodies within (picture 4). Another
anomaly, myelinated nerve fibers are white, cover the underlying retina, and have scalloped
edges. In contrast to papilledema, the appearance of the nerve fiber layer in
pseudopapilledema appears normal, not hazy. The absence of spontaneous venous
pulsations is not useful here, as they are often absent in pseudopapilledema. Other clues to
the presence of a congenital anomaly are an absent portion (often nasal) of the nerve head
and unusual patterns of the blood vessels as they emerge from the nerve head [31]. Other
signs of true papilledema, cotton wool spots, hemorrhages, hyperemia, and venous
congestion are absent [29]. Computed tomography (CT) scanning, ultrasonography, and
optical coherence tomography clarify the diagnosis of drusen by revealing calcium deposits
not visible on ophthalmoscopic examination.
● Malignant hypertension – Severe systemic hypertension can cause a change in the optic
nerve head that resembles papilledema. However, the swelling of the nerve head is usually
mild. Recognizable hypertensive changes are seen in the vessels away from the nerve head
in the posterior pole. These include hemorrhages, exudates, cotton wool spots, and even a
"star" figure pointing to the fovea (picture 5 and picture 6) [32,33]. The optic nerve functions
well, but damage to the retina can compromise vision and produce scotomata, dimming in
vision, diplopia, and photopsia [34]. (See "Moderate to severe hypertensive retinopathy and
hypertensive encephalopathy in adults" and "Ocular effects of hypertension".)
● Diabetic papillopathy – While relatively benign, this is a troublesome entity to diagnose

because it mimics both papilledema from raised intracranial pressure and anterior ischemic
optic neuropathy (AION). Optic edema may vary from minimal to extensive with
telangiectasias, hemorrhages, and macular star (picture 7) [35].
When diabetic papillopathy is bilateral or occurs in a young juvenile diabetic as traditionally

described, it is not likely to be mistaken for AION [35,36]. However, many cases are described
in the literature in which the pathology is unilateral and the patient older. The prognosis is
good, but during the acute phase there may be loss of central vision, enlarged blind spots, or
field defects. These usually resolve. Impaired visual acuity is rare. Ischemia of the optic nerve
is considered to be the probable mechanism; this process is independent of the diabetic
retinopathy [37]. The prognosis might be worse in older patients with type II diabetes [38].
(See "Diabetic papillopathy".)
● Others – Hyperviscosity, hypotension, and blood loss have been reported to cause bilateral
disc edema [39]. Toxic optic neuropathies producing papilledema early in their course have
been described with methanol, ethambutol, ethylene glycol, and other toxins [9]. Optic atrophy
emerges more rapidly in these conditions, while it tends to appear later in chronic
papilledema. Bilateral disc edema may result from optic nerve compression by infiltrated
extraocular muscles in severe thyroid ophthalmopathy.
Unilateral disc abnormalities — Most of the entities that cause unilateral disc elevation can be
broadly classified into ischemic, inflammatory, and infiltrative lesions. Because they are usually
unilateral, they are not confused with true papilledema. However, in some situations, as noted
below, these can be bilateral and raise concern for papilledema. Similarly, in some patients
papilledema may be sufficiently asymmetric as to seem unilateral.
● Anterior ischemic optic neuropathy – AION may be arteritic (eg, giant cell arteritis) or
nonarteritic [28]. The latter occurs in older individuals and has been associated with
atherosclerotic risk factors, particularly hypertension and diabetes. Nonarteritic AION has also
been described in patients treated with phosphodiesterase-5 inhibitors such as sildenafil. (See
"Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis" and
"Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies"
and "Clinical manifestations of giant cell arteritis" and "Treatment of male sexual dysfunction",
section on 'Visual effects'.)
AION is almost always unilateral except in giant cell arteritis. There is always immediate loss
of some or all of the vision; altitudinal defects are classic. An afferent pupillary defect is
common. Prognosis for vision recovery is poor.
The swelling is not congested as it is with raised intracranial pressure but is usually pallid; if
there are hemorrhages, they are small, splinter shaped on the edge of the disk [40].
● Papillitis, neuroretinitis – Papillitis is optic neuritis of the anterior portion of the optic nerve. It
does not have the same implications as retrobulbar neuritis to the underlying etiology. For
papillitis, the underlying causes are much broader, while retrobulbar neuritis is usually due to
demyelinating disease or multiple sclerosis [41] (see "Manifestations of multiple sclerosis in
adults", section on 'Visual loss'). When there is associated inflammation in the retina, as
manifest by macular exudates, it is called neuroretinitis, and it is virtually never demyelinating
in origin. Causes include viral syndromes, toxoplasmosis, cat scratch disease, sarcoidosis,
syphilis, Lyme disease, and other vasculitides including systemic lupus erythematosus and
Wegener granulomatosis [42-46].
Papillitis is almost always unilateral. There is loss of vision, and the pupillary light reflex is
abnormal in the affected eye. Pain, especially with eye movement, is common.
On funduscopic examination, the nerve is diffusely swollen and congested. There are few
hemorrhages, but there may be some cells in the vitreous just in front of the nerve and, in
some cases, a group of yellow-white linear deposits pointing like the spokes of a wheel around
the fovea of the retina (picture 8).
● Sarcoidosis – Optic nerve involvement is rarely the initial presentation of sarcoidosis [47].
Sarcoidosis can affect the meninges and cause true papilledema. Some patients may present
with a solitary sarcoid nodule of the nerve head. A yellowish mass is seen often with other
typical lesions of sarcoid in the retina, conjunctiva, or anterior chamber. This is almost always
unilateral. There may be loss of vision associated with this mass; occasionally, patients will be
asymptomatic [48]. Other patients with sarcoid can develop disc swelling from vasculitis,
uveitis, or more subtle infiltration of the optic nerve head. (See "Neurologic sarcoidosis".)
● Central retinal vein occlusion – Occlusion or thrombosis of the central retinal vein is
associated with chronic glaucoma, atherosclerotic risk factors (age, diabetes, hypertension),
hyperviscosity, and coagulopathy [49]. The cause is often unknown. (See "Retinal vein
occlusion: Epidemiology, clinical manifestations, and diagnosis".)
The disc is typically mildly congested. Hemorrhages are prominent and extend far beyond the
posterior pole of the eye into the retinal periphery; these are much more extensive than in
papilledema. Vision loss corresponds to the hemorrhages and any superimposed retinal
ischemia (picture 9) [50].
● Papillophlebitis – This presumed inflammatory condition occurs in young people and has a
good prognosis [51]. The nerve is swollen. Funduscopic examination suggests a mild central
retinal vein occlusion. Enlargement of the blind spot correlates with the amount of retinal
hemorrhage in the macula [52]. Spontaneous improvement is common.
● Malignancy – Metastatic tumors rarely invade the nerve head. Breast and lung cancers are the
most common culprits; others include meningioma, glioma, hamartoma, dermoid tumors,
lymphoma, and leukemia [53,54]. The nerve head appears to be destroyed by the invading
tissue (picture 10). Little of the normal architecture remains. When invasion or compression of
the optic nerve occurs more posteriorly, it can appear similar to raised intracranial pressure.
There is progressive loss of vision in all cases [55]. (See "Optic pathway glioma".)
● Leber hereditary optic neuropathy – At the onset of the expression of this hereditary condition,
the optic nerve head appears to be modestly elevated [56]. It usually starts out in only one eye
but eventually affects both. The blood vessels around the nerve have a telangiectatic
appearance; however, this finding needs to be looked for carefully to be seen. There are no
hemorrhages. Vision loss is always present. Profound optic atrophy then develops. In most
cases, there is a history of this condition in the family. Genetic testing can confirm the
diagnosis. (See "Neuropathies associated with hereditary disorders", section on 'Leber

hereditary optic neuropathy'.)
● Other causes – Disc swelling from low intraocular pressure or chronic intraocular inflammation
may be seen after eye surgery (cataract surgery or glaucoma) or after injuries (often
iatrogenic) to the globe [57]. They are always unilateral and easily confirmed by measuring the
eye pressure and the slit lamp examination.
An optic neuropathy occurring 6 to 24 months after radiation therapy is often associated with
disc edema at onset [58,59]. (See "Delayed complications of cranial irradiation", section on
'Optic neuropathy'.)
DIAGNOSTIC TESTING
Diagnostic testing can help differentiate papilledema from other causes of disc edema, follow the
course of papilledema, and determine the underlying etiology.
Neuroimaging — When a patient presents with findings suggestive of papilledema, diagnostic

evaluation should proceed expeditiously. The first step is neuroimaging of the brain. Magnetic
resonance imaging (MRI) with gadolinium contrast is generally preferred, but computed
tomography (CT) scan can be ordered initially if access to MRI is delayed. MRI will detect
intracranial mass lesions and hydrocephalus. Additional sequences, magnetic resonance
venography (MRV), can be used to detect venous obstruction in the dural sinuses and in the neck.
Rarely, increased intracranial pressure may arise from spinal lesions; therefore, if this diagnosis is
suggested by clinical signs or symptoms (back or neck pain, myelopathic signs, abnormal spinal
fluid) an MRI of the spine should be ordered as well.
Lumbar puncture — If neuroimaging is normal, lumbar puncture should be done for opening
pressure and analysis. The technique of measuring the opening pressure is described elsewhere.
(See "Lumbar puncture: Technique, indications, contraindications, and complications in adults".)
Using correct technique, elevated pressure is defined as greater than 250 mmH20; measurements
between 200 and 250 mmH2O are considered equivocal. Normal pressure levels in children are
still a matter of debate. Intracranial hypertension in the absence of other cause defines the entity of
idiopathic intracranial hypertension or pseudotumor cerebri. (See "Idiopathic intracranial

hypertension (pseudotumor cerebri): Clinical features and diagnosis", section on 'Lumbar
puncture'.)
Visual field testing — Formal visual field testing with perimetry is very useful in the detection of
subclinical visual field abnormalities and quantifying changes over time. Visual field testing is
mandatory in following the progress of the visual sequelae of papilledema and monitoring
response to treatment. The size of the blind spot is an indirect measure of the degree of disc
edema. Measurement in an individual patient must be done under exactly the same refractive
conditions each time, as blind spot size is sensitive to refractive error. Constrictions in field
perimetry and development of sector field defects are signs of impending serious visual loss. This
finding is more valuable for prognosis than either symptoms or fundus appearance. The clinician
should choose a perimetric technique that reliably measures the patient's visual field. Automated
perimetry may not be ideal for all patients.
Fluorescein angiography — Fluorescein angiography may be helpful in the detection of early

papilledema, showing dye leakage, disc vascularity, and excess early and late disc fluorescence.
Ophthalmologists, however, find it incompletely reliable, especially in equivocal situations, and
usually unnecessary in this clinical setting.
Optical coherence tomography — Where available, optical coherence tomography may be

useful to monitor the swelling of the nerve and also to clarify the effect upon and changes within
the surrounding retina. This technique is very dependent upon the skills of the person performing
the test and thus is prone to error. Modern technology (spectral rather than time based) has
improved reliability.
TREATMENT
The treatment of increased intracranial pressure is specific to the underlying etiology and is
discussed separately. (See "Evaluation and management of elevated intracranial pressure in
adults" and "Idiopathic intracranial hypertension (pseudotumor cerebri): Prognosis and treatment".)
VISUAL PROGNOSIS
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Permanent loss of vision is a common consequence of papilledema that is untreated or

unresponsive to treatment. Clinical findings predictive of visual loss are high-grade disc edema,
peripapillary subretinal hemorrhages, opticociliary shunt vessels, abnormal vision at presentation,
and the development of visual field loss. Anemia, old age, myopia, glaucoma, and systemic
hypertension have been found to be risk factors for a poor prognosis in some studies [60].
Progressive changes in the visual field or acuity are useful to predict patients at risk; however,
vision loss sometimes occurs abruptly. Visual field loss attributed to hemorrhage can be expected
to resolve.
SUMMARY AND RECOMMENDATIONS
The term "papilledema" is most properly applied to optic disc edema occurring as a consequence
of intracranial hypertension.
● The causes of papilledema often have serious consequences for impending morbidity and
mortality; hence, diagnostic evaluation is urgent. (See 'Etiologies and pathogenesis' above.)
● Unilateral disc edema and abnormal visual acuity at presentation suggest alternative
diagnoses. (See 'Clinical manifestations' above.)
● The first step in the evaluation for the cause of papilledema should be a neuroimaging study;
brain magnetic resonance imaging (MRI) is preferred, but a computed tomography (CT) scan
should be done if an MRI is not immediately available. (See 'Neuroimaging' above.)
● Lumbar puncture with measurement of opening pressure and analysis of cerebrospinal fluid
(CSF) should follow a normal neuroimaging study. (See 'Lumbar puncture' above.)
● Serial clinical evaluations including measurements of visual acuity, funduscopic examination,

and visual field testing with perimetry are invaluable in following the course of papilledema and
response to treatment. (See 'Visual field testing' above.)
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tolerance. J Neurosurg 2004; 101 Suppl 3:390.
59. Jiang GL, Tucker SL, Guttenberger R, et al. Radiation-induced injury to the visual pathway.
Radiother Oncol 1994; 30:17.
60. Orcutt JC, Page NG, Sanders MD. Factors affecting visual loss in benign intracranial
hypertension. Ophthalmology 1984; 91:1303.
Topic 5241 Version 13.0
GRAPHICS
Early papilledema
Courtesy of Don C Bienfang, MD.
Graphic 72814 Version 1.0
Fully developed papilledema
Late chronic papilledema
Differential diagnosis of papilledema
Bilateral disc abnormalities*

Increased intracranial pressure
Pseudopapilledema
Malignant hypertension
Diabetic papillopathy
Others (hyperviscosity, toxins)
Unilateral disc abnormalities*

Anterior ischemic optic neuropathy
Papillitis, neuroretinitis
Sarcoidosis
Central retinal vein occlusion
Papillophlebitis
Malignancy
Leber hereditary optic neuropathy
Other causes (low intraocular pressure, ocular injury, radiation)
* There is some overlap between the two categories. Entities are classified here as to whether they are more usually
bilateral versus unilateral.
Disc drusen
Retinal examination showing severe hypertensive

retinopathy I
Retinal examination in a patient with papilledema due to severe

hypertension. There is blurring of the margins of the optic disc, distension of
the retinal veins, two cotton wool spots inferior to the disc, and a flame-
shaped hemorrhage at a venous bifurcation (arrow).
Reproduced by permission from: Gallasch G, Ritz E. The fundus in malignant

hypertension. Nephrol Dial Trans 1997; 12:1518.
Retinal examination showing severe hypertensive

retinopathy II
Retinal examination in a patient with severe hypertension and grade IV

hypertensive retinopathy. The optic disc is swollen with indistinct borders.
There is venous tortuosity with multiple cotton wool spots and numerous
flame-shaped (arrows) and punctate hemorrhages (arrowhead).
Reproduced by permission from: Gallasch G, Ritz E. The fundus in malignant

hypertension. Nephrol Dial Trans 1997; 12:1518.
Diabetic papillopathy
Papillitis
Retinal vein occlusion
Thrombosis of the central retinal vein results in venous stasis, leading to disc
swelling, diffuse nerve fiber layer and preretinal hemorrhage, and cotton
wool spots that create a dramatic appearance, often called "the blood and
thunder" fundus.
Optic nerve lung metastasis
Contributor Disclosures
Don C Bienfang, MD Nothing to disclose Paul W Brazis, MD Nothing to disclose Janet L Wilterdink,
MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
Conflict of interest policy

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Overview and differential diagnosis of papilledema - UpToDate 7/21/19, 12(01 PM

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Overview and differential diagnosis of papilledema

ETIOLOGIES AND PATHOGENESIS

● Intracranial mass lesions (eg, tumor, hematoma)

● Cerebral edema (such as in acute hypoxic-ischemic encephalopathy, large cerebral infarction,

● Increased cerebrospinal fluid (CSF) production (eg, choroid plexus papilloma)

● Idiopathic intracranial hypertension (pseudotumor cerebri)

Idiopathic intracranial hypertension (pseudotumor cerebri) is discussed in detail separately. (See

Because the causes of intracranial hypertension are generalized phenomena, papilledema is

Symptoms of increased intracranial pressure — Headache is a cardinal symptom of increased

Another classic symptom of increased intracranial pressure is binocular horizontal diplopia

● Pseudopapilledema – Congenital anomalies of the disc, including drusen and myelinated

● Diabetic papillopathy – While relatively benign, this is a troublesome entity to diagnose

When diabetic papillopathy is bilateral or occurs in a young juvenile diabetic as traditionally

diagnosis. (See "Neuropathies associated with hereditary disorders", section on 'Leber

Neuroimaging — When a patient presents with findings suggestive of papilledema, diagnostic

idiopathic intracranial hypertension or pseudotumor cerebri. (See "Idiopathic intracranial

Fluorescein angiography — Fluorescein angiography may be helpful in the detection of early

Optical coherence tomography — Where available, optical coherence tomography may be

Permanent loss of vision is a common consequence of papilledema that is untreated or

SUMMARY AND RECOMMENDATIONS

● Serial clinical evaluations including measurements of visual acuity, funduscopic examination,

Use of UpToDate is subject to the Subscription and License Agreement.

4. Adelman JU. Headaches and papilledema secondary to dural arteriovenous malformation.

7. Brockmeier B, Burbach H, Runge M, Altenkirch H. Raised intracranial pressure in chronic

13. Erşahin Y, Mutluer S, Yurtseven T. Hydrocephalus in Guillain-Barré syndrome. Clin Neurol

18. Elliot RH. THE RETINAL PULSE. Br J Ophthalmol 1921; 5:481.

19. ENGEL S. Venous pulsation as a symptom of early glaucoma. Am J Ophthalmol 1946;

27. Williamson-Noble FA. Venous pulsation. Trans Ophthalmol UK 1952; 72:317.

45. Labalette P, Bermond D, Dedes V, Savage C. Cat-scratch disease neuroretinitis diagnosed

56. Nikoskelainen EK, Huoponen K, Juvonen V, et al. Ophthalmologic findings in Leber

Topic 5241 Version 13.0

Courtesy of Don C Bienfang, MD.

Graphic 72814 Version 1.0

Fully developed papilledema

Courtesy of Don C Bienfang, MD.

Graphic 64616 Version 1.0

Late chronic papilledema

Courtesy of Don C Bienfang, MD.

Graphic 68815 Version 1.0

Bilateral disc abnormalities*

Others (hyperviscosity, toxins)

Unilateral disc abnormalities*

Central retinal vein occlusion

Leber hereditary optic neuropathy

Other causes (low intraocular pressure, ocular injury, radiation)

Graphic 54401 Version 4.0

Courtesy of Don C Bienfang, MD.

Graphic 72232 Version 1.0

Retinal examination showing severe hypertensive

Retinal examination in a patient with papilledema due to severe

Reproduced by permission from: Gallasch G, Ritz E. The fundus in malignant

Graphic 78225 Version 7.0

Retinal examination showing severe hypertensive

Retinal examination in a patient with severe hypertension and grade IV

Reproduced by permission from: Gallasch G, Ritz E. The fundus in malignant

Graphic 57183 Version 7.0

Courtesy of Don C Bienfang, MD.

Graphic 63843 Version 1.0

Courtesy of Don C Bienfang, MD.

Graphic 67875 Version 1.0