Papilledema and Idiopathic Intracranial Hypertension (IIH)

Key Points at a Glance

Papilledema is a term limited to bilateral optic disc swelling secondary to elevated intracranial pressure.
It is a warning sign of serious intracranial diseases such as brain tumor, cerebral venous thrombosis, and IIH.
The annual incidence of IIH in the US is 1.15 per 100,000, and the prevalence in women aged 18–55 is 3.44 per 10,000 (increasing with the obesity epidemic). ^{2, 3)}
Early stages may be asymptomatic or only transient visual obscurations. Early treatment is reversible, but delay leads to irreversible visual impairment.
Treatment to lower intracranial pressure (removal of space-occupying lesions, ventriculoperitoneal shunt) is fundamental. For IIH, acetazolamide (Diamox®, off-label), mannitol, and lumbar puncture are used.
Differentiation from pseudopapilledema (e.g., drusen) is key to diagnosis.
Fulminant IIH (FIH) occurs in 2–3% of IIH patients and is an emergency with rapid visual loss within 4 weeks. ¹⁾

1. What are Papilledema and Idiopathic Intracranial Hypertension (IIH)?

Papilledema is bilateral optic disc swelling due to elevated intracranial pressure (ICP). The term “papilledema” (choked disc) is reserved for ICP elevation, while other causes of disc swelling are termed “optic disc edema.” Increased pressure in the subarachnoid space around the optic nerve compresses the nerve, leading to axoplasmic flow stasis and disc swelling.

The annual incidence of IIH is 1.15 per 100,000 (US data 1997–2016, female 1.97 vs male 0.36) ²⁾, with the highest rate in ages 18–44 (2.47 per 100,000). Prevalence in US women aged 18–55 is 3.44 per 10,000 (95% CI 2.61–5.39) ³⁾. By race, incidence per 100,000 is Black 2.05 > White 1.04 > Hispanic 0.67 > Asian/Pacific Islander 0.16 ²⁾, generally consistent with obesity prevalence geographically (Moran I=0.20, P=0.03) ³⁾.

Normal ICP is <250 mmH2O in adults and <280 mmH2O in children. Fulminant IIH (FIH) occurs in 2–3% of all IIH patients and is an emergency characterized by rapid visual loss within 4 weeks of symptom onset. ¹⁾

Q What is the difference between papilledema and optic disc edema?

Papilledema is a term limited to elevated ICP, while optic disc swelling from other causes (e.g., optic neuritis, ischemia, infiltrative lesions) is distinguished as optic disc edema. This distinction is important because it directly links to identifying the cause and selecting appropriate treatment.

2. Main Symptoms and Clinical Findings

Peripapillary hyperreflective ovoid mass‐like structures: Multimodal imaging—A review. Clin Exp Ophthalmol. 2023 Nov 6 Jan-Feb; 51(1):67-80. Figure 4. PMCID: PMC10099767. License: CC BY.

Idiopathic intracranial hypertension in a 45-year-old obese woman (headache, bilateral vision loss, papilledema). Opening pressure 27 cmH2O. OCT shows PHOMS and internal flow signals at the superior and inferior disc margins. MRI/MRV shows optic nerve sheath distension, partial empty sella, and relative stenosis of both transverse sinuses.

Subjective Symptoms

Acute papilledema is often asymptomatic in the early stage, and central visual function (best-corrected visual acuity, color vision) is usually preserved.

Transient visual obscurations (TVO): Bilateral transient vision loss lasting seconds. Triggered by postural changes or Valsalva maneuver. Mechanism is transient ischemia of the optic nerve head.
Headache: Positional, worse in the morning. Occurs in about 90% of cases. ²⁾ May be accompanied by nausea and vomiting.
Pulsatile tinnitus: Occurs in 52% of cases. Caused by turbulent venous flow. ²⁾
Back pain: Present in 53% of cases. ²⁾
Diplopia: Horizontal diplopia due to abducens nerve (CN VI) palsy. A false localizing sign of elevated intracranial pressure.
Visual field loss and vision loss: After several months, inferonasal or concentric visual field loss appears, followed by vision loss.
Hyperopic shift: Due to axial shortening from flattening of the posterior globe.

In children, elevated intracranial pressure is often discovered due to esotropia associated with bilateral abducens nerve palsy.

Clinical Findings

Fundus findings in acute papilledema:

Opacity of the retinal nerve fiber layer. Loss of peripapillary sheen.
Elevation and blurring of the optic disc margins. Hyperemia of the disc surface and loss of physiologic cupping.
Vascular changes: dilation and tortuosity of retinal veins, hemorrhages, cotton-wool spots, macular star.
Loss of spontaneous venous pulsation (SVP): Present in about 90% of normal individuals. Disappears with elevated ICP. Note that it is absent in 10–20% of the normal population.
Paton lines: Concentric peripapillary folds.

Additional findings in chronic papilledema: Optic disc pallor, gliosis, optociliary shunt vessels, refractive bodies. In the chronic phase, dead nerve fibers do not swell, so edema may resolve even if elevated ICP persists (atrophic end-stage).

If there is bilateral optic disc redness with good visual acuity, always consider papilledema in the differential diagnosis. In papilledema, visual acuity remains nearly normal until the end stage.

Frisén Scale for Grading Papilledema

The severity of papilledema is assessed using the Frisén scale (stages 0–5) and used as an indicator of visual prognosis.

Stages 0–1

Stage 0 (Normal): Blurring of the nasal, superior, and inferior borders. Radial NFL.

Stage 1 (Very early): Obscuration of the nasal disc border. No elevation of the border. Subtle grayish halo. Concentric or radial choroidal folds.

Stages 2–3

Stage 2 (early): Blurring of all borders. Elevation of the nasal border. Complete peripapillary halo.

Stage 3 (moderate): Increased optic disc diameter. Partial obscuration of segments of major vessels. Finger-like extensions at the outer edge of the halo.

Stages 4–5

Stage 4 (marked): Elevation of the entire optic disc. Complete obscuration of major vessel segments on the disc.

Stage 5 (severe): Dome-shaped protrusion. Halo narrow with smooth borders. Obliteration of the physiologic cup.

Q If transient visual obscurations occur, does vision always worsen?

TVO is a characteristic symptom of papilledema, but it is not a direct predictor of vision loss. However, if intracranial hypertension persists for a long time, it can progress from severe peripheral visual field loss to central vision loss. If TVO occurs frequently, it is important to promptly see a specialist and investigate the cause.

3. Causes and Risk Factors

The rate of papilledema formation depends on the rate of intracranial pressure increase. With gradual ICP elevation, it may appear over several weeks; with rapid elevation, it can appear within hours to one day.

Five mechanisms of intracranial hypertension

Skull too small for the brain: e.g., craniosynostosis.
Increased brain volume: Space-occupying lesions (brain tumor, abscess, subdural hematoma), cerebral edema.
Obstruction of CSF pathways: e.g., obstruction of the foramen of Monro (colloid cyst).
Increased CSF production: e.g., choroid plexus papilloma.
Decreased CSF absorption: Meningitis, cerebral venous sinus thrombosis (CVST), etc.

Risk Factors for Idiopathic Intracranial Hypertension

Obesity / recent weight gain: Most important risk factor. BMI > 40 increases risk of irreversible vision loss.
Associated conditions: PCOS, iron deficiency anemia, thyroid disease, obstructive sleep apnea (OSA), kidney disease.
Medications: Tetracyclines (minocycline), vitamin A derivatives, lithium, steroid withdrawal. Minocycline disrupts cAMP signaling in arachnoid granulations, reducing CSF absorption ¹³⁾. ICP elevation may persist for 2–5 weeks after discontinuation. ¹³⁾
Genetic factors: Candidate loci on chromosomes 5, 13, and 14 (GWAS) ²⁾. AQP1 gene polymorphisms may contribute to increased CSF production.
Infection / inflammation: Recent infection/inflammatory disease increases IIH risk approximately 3-fold. ¹⁷⁾ IIH cases reported after COVID-19 in non-obese, non-female patients (45-year-old male, BMI 22.8).
CVST: Annual incidence 1–2 per 100,000 person-years ¹⁷⁾. Mortality 3–15%. MRV is essential to rule out.
Severe anemia: Papilledema reported with Hb 5.7 g/dL and ferritin 0.1 ng/mL. Proposed mechanism: elevated EPO → thrombocytosis → hyperviscosity → increased venous pressure → elevated ICP.
MIS-C (Multisystem Inflammatory Syndrome in Children): Neurological symptoms in 13–21%.
VITT: CVST after AstraZeneca vaccine.

Q Will papilledema improve with weight loss?

In cases of IIH, a 5–10% weight loss improves ICP symptoms and papilledema. Normalization of ICP (remission) requires a 24% reduction in body weight (per protocol analysis of IIHWT) ¹⁵⁾. If lifestyle modification alone is insufficient, bariatric surgery is an option. Weight management is part of conservative treatment and may need to be combined with medication or surgery depending on the degree of papilledema and visual dysfunction.

4. Diagnosis and Examination Methods

Evaluation proceeds in the following order: ophthalmoscopy to confirm bilateral papilledema → fluorescein angiography → OCT → CT/MRI plus contrast-enhanced MRV → lumbar puncture (LP). First, measure blood pressure to rule out malignant hypertension, then perform emergency imaging (CT → MRI plus contrast-enhanced MRV) to assess for mass lesions and venous sinus thrombosis. Perform LP after confirming no risk of brain herniation.

Ophthalmic Examination

Ophthalmoscopy: Basic confirmation of bilateral papilledema.
Fluorescein angiography (FA): Dye leakage from the optic disc indicates true papilledema. In pseudopapilledema, there is no leakage, only staining.
OCT (SD-OCT RNFL): Detection of subtle disc swelling and follow-up. GCL-IPL OCT is useful for distinguishing atrophy from improvement.
Visual field testing (Humphrey 30-2): Evaluates enlarged blind spot, arcuate scotoma, nasal step, and concentric constriction.
B-mode ultrasound, fundus autofluorescence, EDI-OCT: Useful for differentiating pseudopapilledema (drusen).

Neuroimaging

MRI plus contrast-enhanced MRV is optimal; evaluation of venous sinus stenosis/occlusion is essential in IIH. The following signs of high ICP are assessed:

Empty sella or partial empty sella
Optic nerve sheath distension and CSF accumulation
Optic nerve tortuosity (vertical and horizontal)
Flattening of the posterior globe (in severe cases, protrusion of the optic nerve into the globe)
Cerebellar tonsil herniation

Definite IIH Diagnosis (Modified Dandy Criteria)

Criteria	Description
1. Papilledema	Bilateral papilledema present
2. Neurologic examination	Normal except for cranial nerve abnormalities
3. Neuroimaging	Normal brain parenchyma, no ventricular enlargement, no mass, no abnormal contrast enhancement
4. CSF composition	Normal
5. CSF opening pressure	Adults ≥250 mmH2O, children ≥280 mmH2O

Suspected diagnosis: bilateral papilledema present + criteria 1-4 met but CSF pressure below threshold. 25-30 cmH2O is a gray zone and reassessment is recommended.

It has been reported that 17.8% of IIH diagnoses are inaccurate or premature, and 13.0% are misdiagnoses ¹⁸⁾. The most common cause of misdiagnosis is failure to perform MRV (42.4%) in atypical patients (men, normal BMI, children), leading to missed CVST.

Differentiation from pseudopapilledema

Pseudopapilledema can be caused by high hyperopia, drusen, tilted optic disc, myelinated nerve fibers, hamartoma, etc. The following findings suggest pseudopapilledema.

No telangiectasia or hyperemia on the optic disc surface
Absence of physiologic cup
No hemorrhages or exudates
No retinal nerve fiber layer opacity
Blood vessels on the disc surface can be clearly traced

Differential diagnosis list: Buried drusen, tilted disc, diabetic papillopathy, hypertensive papillopathy, posterior scleritis, perioptic neuritis, uveitis (sarcoidosis, VKH), optic neuritis, thyroid eye disease, CRVO, NAION, infiltrative optic neuropathy, optic nerve sheath meningioma.

It is reported that 10% of patients with papilledema have treatable iron deficiency anemia, and screening is recommended.

Q Can vision be normal despite bilateral papilledema?

In choked disc (papilledema due to increased ICP), vision may be preserved in the early stages. This is because although increased ICP causes stasis of axoplasmic flow in the optic nerve head, the effect on afferent visual function is still mild. In contrast, optic neuritis often causes acute vision loss, and this difference can be a clue for differentiation.

5. Standard treatment

The three goals of treatment are: ① treatment of the underlying cause, ② preservation of visual function, and ③ relief of symptoms (such as headache).

If intracranial pressure is lowered early, papilledema is quickly absorbed and visual function is preserved. If treatment is delayed and visual impairment appears, it becomes irreversible.

Treatment by underlying cause

Malignant hypertension: Immediate emergency transport.
Space-occupying lesions: Neurosurgical procedures such as lesion removal or ventriculoperitoneal shunt are standard.
Acute cerebral venous thrombosis: Start anticoagulation with warfarin. DOACs are also an option (lower bleeding risk). Avoid acetazolamide as it may worsen the condition¹⁷⁾. Can be considered after starting anticoagulation.
Drug-induced: Discontinue the causative drug. With minocycline, ICP elevation may persist for 2–5 weeks after discontinuation. ¹³⁾
Cerebral venous sinus thrombosis: Warfarin therapy.

Conservative management of IIH

Weight loss: 5–10% weight loss improves ICP symptoms and signs. For papilledema improvement, 5–15% weight loss is expected to be effective¹⁾. Normalization of ICP requires 24% weight loss (IIHWT per protocol analysis)¹⁵⁾.
Avoidance of precipitating drugs.
Control of underlying risk factors (thyroid disease, OSA).
Low-sodium weight-loss diet: Expected synergistic effect with acetazolamide. ¹⁶⁾
Exercise therapy: Moderate aerobic exercise is recommended. Excessive exercise carries a risk of increased ICP.

Pharmacotherapy for IIH

Drug	Dose	Notes
Acetazolamide (first-line)	250–500 mg twice daily → up to 2–4 g/day	IIHTT (2014) showed efficacy for mild visual field loss in IIH¹⁶⁾. No consistent effect on headache. Not covered by insurance in Japan.
Topiramate (second-line)	Individualized dosing	Lowers ICP and promotes weight loss. Also useful for migraine-like headaches. Teratogenic → contraindicated in pregnancy.
Furosemide	Adjunctive use	Alternative when acetazolamide is not tolerated.
Methylprednisolone IV	1 g/day for 3 days	Temporary measure only for fulminant IIH. Common practice in North America.

Main side effects of acetazolamide: paresthesia (tingling in hands and feet), taste disturbance (metallic taste), gastrointestinal symptoms (nausea, vomiting, diarrhea), fatigue, kidney stones. Chronic compensated metabolic acidosis, mild hypokalemia.

Surgical Management of IIH

Procedure	Visual improvement rate	Headache improvement rate	Major complications
Optic nerve sheath fenestration (ONSF)	59%	44%	Complications 10–15% (including 1–2% vision loss from CRAO/CRVO). Recurrence rate 34% at 1 year, 45% at 3 years¹⁾
CSF shunting (LPS/VPS)	54%	80%	Shunt failure 43–50%, infection, migration¹⁾
Dural venous sinus stenting (VSS)	78%	82–83%	Antiplatelet therapy required for 6 months postoperatively. Reoperation rate 10–18%¹⁾
Bariatric surgery	—	—	IIHWT RCT showed sustained ICP reduction and weight loss over 2 years¹⁵⁾

Indications for VSS (venous sinus stenting): Confirmation of transverse sinus stenosis with pressure gradient >8 mmHg. ONSF does not lower ICP. Unilateral ONSF may have insufficient effect on the contralateral side. Lumbar-peritoneal (LP) shunt is often chosen as the primary surgical intervention for IIH.

Management of Fulminant IIH (FIH)

2–3% of IIH patients. Characterized by rapid visual loss within 4 weeks of symptom onset. Inpatient management is standard, with aggressive medical and surgical treatment.

Mean CSF opening pressure is extremely high at 54.1 cmH2O (range 29–70) ⁶⁾. In a series of 16 patients by Thambisetty et al. ⁶⁾, 50% became legally blind despite aggressive treatment, and all had residual visual field defects and optic atrophy. Visual recovery is difficult if baseline HVF MD is less than -7 dB. ¹⁾ Higher initial pRNFL is associated with worse long-term visual prognosis. ¹⁾

There is a report of FIH recovery with acetazolamide alone at up to 4 g/day (36-year-old male, BMI 47.3, CSF OP 45 cmH2O → papilledema resolved in 4 months, 20/20 vision recovered in both eyes at 6 months) ⁸⁾. When FIH is complicated by malignant hypertension, diagnostic delay averages 3.2 months, and final visual acuity can be extremely poor (20/400 to light perception) ⁷⁾.

Management of IIH in Pregnancy

The prevalence of IIH during pregnancy is 16 per 100,000. 61% of cases occur in the first trimester ⁹⁾. Pregnancy itself is not considered an etiological factor for IIH. Visual prognosis is similar to that in non-pregnant women, and it is not usually considered a high-risk pregnancy.

First-line drug: Acetazolamide (FDA category C). No causal relationship with congenital malformations has been established (systematic review of 52 cases with use, no malformations) ⁹⁾.
Contraindicated in pregnancy: Topiramate (FDA category D, confirmed teratogenicity). NSAIDs (third trimester).
Repeated lumbar puncture: Used in 26.9% (48 of 178 pregnancies). Effect is transient (CSF is regenerated in 6 hours) ⁹⁾.
Weight gain restriction: Recommend limiting to 20 pounds (approximately 9 kg).
VSS during pregnancy: Regev et al. (2025) performed transverse sinus stenting in 2 pregnant women with FIH; one had complete recovery, the other had residual visual field defect in one eye ¹¹⁾.
Delivery management: IIH itself is not an indication for cesarean section. Vaginal delivery 56.9% vs. cesarean section 43.1% ⁹⁾. During delivery, CSF pressure can rise to 39 mmHg in the first stage and 71 mmHg in the second stage ¹⁰⁾.
Anesthesia: Epidural anesthesia is first choice. General anesthesia is avoided except in emergencies. Succinylcholine (which increases ICP due to fasciculations) should be avoided ¹⁰⁾.

Prognosis: IIH recurrence rate 9–28%²⁾. Poor prognostic factors: weight gain, severity of papilledema, and baseline headache severity²⁾.

Q Can acetazolamide be used for all types of papilledema?

Acetazolamide is established as a first-line treatment for IIH, but it is contraindicated when cerebral venous thrombosis is the cause, as it may worsen the condition. It is also contraindicated in cryptococcal meningitis. It is essential to first identify the cause and select treatment based on the underlying etiology. Note that it is not covered by insurance in Japan.

Q Is acetazolamide safe to use during pregnancy?

Although classified as FDA category C, systematic reviews have not found a causal relationship with congenital malformations⁹⁾. Even high-dose use (≥1 g/day) in the first trimester did not show an increased risk of malformations. It should always be used in consultation with an obstetrician, and in many cases, use is limited to after 20 weeks of gestation.

Q How does fulminant IIH differ from typical IIH?

Fulminant IIH (FIH) is a subtype of IIH characterized by rapid and severe visual loss within 4 weeks of symptom onset. It occurs in 2–3% of IIH patients. While typical IIH progresses relatively slowly, FIH can worsen within days and lead to irreversible blindness without prompt intervention⁶⁾.

6. Pathophysiology and detailed mechanisms

Mechanism of axoplasmic flow stasis

Increased pressure in the subarachnoid space around the optic nerve compresses the nerve, leading to stasis of axoplasmic flow and resulting in papilledema. Specifically, the following pathway occurs.

Increased ICP → increased pressure in the subarachnoid space around the optic nerve → optic nerve constriction → stagnation of anterograde axonal transport → nerve edema (papilledema). Persistent pressure → intra-neural ischemia → axonal loss → optic atrophy → visual impairment. In the atrophic stage, dead nerve fibers do not swell, so papilledema may disappear even if ICP elevation continues (end-stage atrophy).

Pathophysiology of IIH (three hypotheses)

CSF outflow obstruction hypothesis

Delayed CSF drainage via arachnoid granulations and lymphatic pathways leads to increased ICP. Minocycline disrupts cAMP signaling in arachnoid granulations and reduces CSF absorption ¹³⁾.

Venous sinus pressure elevation hypothesis

Bilateral transverse sinus stenosis is observed in over 90% of IIH patients ²⁾. The chain: obesity → increased intra-abdominal pressure → increased intrathoracic pressure → impaired cerebral venous return → increased ICP. The effectiveness of VSS supports this hypothesis.

Metabolic and hormonal abnormality hypothesis

Androgen dysregulation is suggested to be involved ²⁾. Excess leptin → choroid plexus hyperactivation → excessive CSF production. GLP-1 receptors are present in the choroid plexus, and GLP-1 RAs have been shown to reduce CSF production in rat models.

Genetic background: GWAS chr5/13/14. Increased CSF production due to AQP1 gene polymorphism. ²⁾
Functional abnormality of the glia-neuro-vascular interface is suggested to be involved. ²⁾
IIH is increasingly recognized as a systemic metabolic disease independent of obesity. ²⁾
CVST: Venous sinus thrombosis → impaired venous return → increased ICP.
Severe anemia: Elevated EPO → thrombocytosis → hyperviscosity → increased venous pressure → increased ICP. Iron deficiency → decreased red blood cell deformability → increased blood viscosity.

Laura Bonelli, Vaishnavi Menon, Anthony C Arnold et al. Managing idiopathic intracranial hypertension in the eye clinic. Eye. 2024 May 24; 38(12):2472. Figure 2. PMCID: PMC11306398. License: CC BY.

Papilledema and RNFL changes in fulminant IIH. Severe bilateral optic disc swelling and marked RNFL thickening on OCT.

7. Latest Research and Future Perspectives

IIH Weight Trial (IIHWT) and Bariatric Surgery

In an RCT comparing bariatric surgery versus community weight management intervention, the bariatric surgery group sustained ICP reduction and weight loss over 2 years ¹⁵⁾. Cost-effectiveness after 5 years was also superior to dietary therapy. The amount of ICP reduction correlated with the degree of weight loss.

GLP-1 Receptor Agonists

GLP-1RAs such as exenatide are attracting attention as new candidates for IIH treatment. They reduce CSF secretion in the choroid plexus via decreased Na⁺/K⁺-ATPase activity. In humans, a report showed ICP reduction of 5.7 ± 2.9 cmH₂O (P = 0.048) 2.5 hours after administration. A dual mechanism of weight loss promotion and direct ICP reduction is expected. However, attention should be paid to the risk of weight rebound after discontinuation leading to IIH onset.

Venous Sinus Stenting (VSS)

Reports on the safety and efficacy of transverse sinus stenting are accumulating ^{4, 5)}. An RCT comparing VSS vs VPS is ongoing in the UK. Visual improvement rate of VSS is 78%, headache improvement rate 82–83% (meta-analysis). Reoperation rate ranges from 10% to 18%.

11β-HSD1 Inhibitors

11β-HSD1 (11β-hydroxysteroid dehydrogenase type 1) inhibitors are under investigation as novel therapeutic targets for IIH ¹⁾.

Reconsideration of FIH Definition

There is discussion proposing a definition based on “vision-threatening” rather than the time criterion of “within 4 weeks” ¹⁾. The time criterion may miss cases with rapid progression.

Papilledema has been reported in patients who do not fit the traditional risk profile ¹⁾. Examples include IIH in non-obese, non-female individuals; MIS-C (multisystem inflammatory syndrome in children)-related cases; and VITT after the AstraZeneca vaccine.

Geographic Variation in IIH Prevalence

Significant interstate differences have been identified within the United States (Moran I = 0.20, P = 0.03) ³⁾. In states such as Texas and Oklahoma, a discrepancy has been observed with high obesity rates but low IIH prevalence, the cause of which remains unknown.

8. References

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