Peripapillary Intrachoroidal Cavitation (PICC)

Key points at a glance

Key Points at a Glance

• Peripapillary intrachoroidal cavitation (PICC) is a cavitary lesion within the choroid that occurs at the lower edge of the peripapillary conus in highly myopic eyes.
• It is identified as a hyporeflective cavity within the choroid on SD-OCT.
• The prevalence is reported to be 2.2–17%, and although many cases are asymptomatic, up to 71% of cases may have visual field defects ²⁾.
• Detection rate on fundus color photography is only 46–53%, and SD-OCT is the most reliable diagnostic tool.
• It may be accompanied by RNFL thinning, GC-IPL thinning, and RAPD, and can present with glaucoma-like visual field defects ²⁾.
• There is no established active treatment, and observation is the basic management strategy.

1. What is Peripapillary Intrachoroidal Cavitation (PICC)?

Peripapillary intrachoroidal cavitation (PICC) is a cavitary lesion that occurs at the lower edge of the peripapillary conus (a crescent-shaped area of exposed sclera around the optic disc) in highly myopic eyes. On fundus examination, it appears as a well-demarcated yellowish-orange patchy lesion.

Multiple reports have confirmed its detection using optical coherence tomography (OCT), revealing that the lesion is located within the choroid. The prevalence varies from 2.2% to 17% depending on the report ²⁾. It is a condition found in a certain proportion of patients with high myopia. The predilection for the inferotemporal region is associated with the greatest mechanical tension in the temporal area of the optic disc ²⁾.

Q In which patients is PICC more common?

A

It is a characteristic lesion in highly myopic eyes and is frequently found in eyes with posterior staphyloma or peripapillary atrophy (γPPA, PPS). Detection frequency is higher in eyes with significantly elongated axial length ³⁾, and the most common location is the inferotemporal region ²⁾.

2. Main Symptoms and Clinical Findings

Subjective Symptoms

Most PICC cases are asymptomatic and discovered incidentally during examinations. In cases where thinning of the optic nerve or inner retinal layers has progressed, subjective symptoms may occur.

• Visual field defect: Inferior arcuate scotoma is typical. Up to 71% of cases reportedly have visual field defects ²⁾.
• Visual acuity loss: Marked visual acuity loss due to the cavity itself is usually not observed. Concomitant macular atrophy or posterior staphyloma may contribute to visual acuity loss.

Clinical Findings

Fundus and Imaging Findings

Fundus color photography: Observed as a well-demarcated yellow-orange lesion at the lower margin of the peripapillary conus. Detection sensitivity is only 46–53%.

SD-OCT: Depicted as a hyporeflective cavity within the choroid. The retinal pigment epithelium is flat without detachment. It is the most reliable diagnostic method.

Multicolor imaging: Short-wavelength light cannot reach the deep choroid, and infrared light is also not reflected due to the absence of melanin in the cavity. Therefore, PICC becomes undetectable ¹⁾.

Fluorescein angiography (FA): Shows hypofluorescence in the early phase and staining in the late phase.

Functional Test Findings

Relative afferent pupillary defect (RAPD): A RAPD of 1.5 log units has been reported ²⁾.

RNFL thinning: The affected eye shows significant thinning with an average of 69 μm ²⁾.

GC-IPL thinning: The affected eye shows thinning with an average of 60 μm ²⁾.

Visual field defect: Inferior arcuate scotoma is typical. Inferotemporal defects are most common, and progression has been confirmed over 16 months ²⁾.

Differential Diagnosis from Glaucoma

PICC can cause RNFL thinning, visual field defects, and RAPD in highly myopic eyes, presenting findings that mimic glaucoma. If visual field impairment progresses despite normal intraocular pressure, OCT evaluation with PICC in mind is important. For details, see the “Diagnosis and Examination Methods” section.

Q Does PICC significantly reduce visual acuity?

A

The cavity itself rarely causes marked visual loss. However, visual field defects (inferior arcuate scotoma) have been reported in up to 71% of cases ²⁾, and progression of visual field defects has been confirmed in some cases during 16 months of follow-up ²⁾. Concomitant myopic fundus changes determine visual prognosis.

3. Causes and Risk Factors

PICC is a condition closely related to high myopia. Chronic mechanical stress on the peripapillary tissues due to posterior scleral curvature associated with axial elongation is considered the basis for PICC development.

Axial Length and Refractive Factors

High myopia and severe axial elongation: Eyes with high myopia and axial length >31 mm accompanied by posterior staphyloma have a high risk of developing PICC ³⁾.

Peripapillary atrophy (γPPA and PPS): Gamma zone peripapillary atrophy and degeneration of the peripapillary sclera are closely associated with PICC formation.

Anatomical Changes

Posterior scleral curvature: Deformation of the posterior pole due to high myopia leads to thinning of peripapillary tissues.

Peripapillary conus formation: PICC most commonly occurs at the lower edge of the scleral exposure area (conus) around the optic disc, with the inferotemporal quadrant being the most frequent location ²⁾.

Main Hypotheses of Pathogenesis

Elschnig body disruption theory: The theory that Elschnig bodies around the optic disc break down due to progression of myopic staphyloma, forming a cavity (Toranzo).

Fluid inflow theory: The theory that fluid flows into the choroid due to intraocular pressure fluctuations and eye movements (Wei).

Posterior scleral curvature theory: The theory that PICC occurs due to posterior scleral curvature without displacement of the retinal pigment epithelium or retina.

For those with high myopia

People with high myopia (-6D or more) are at risk for various fundus complications including PICC. Regular fundus examinations and OCT scans are recommended. If you notice changes in your visual field or abnormalities in your vision, see an ophthalmologist promptly.

4. Diagnosis and Examination Methods

SD-OCT is the standard for diagnosing PICC. The detection capabilities of each examination method are shown below.

Examination Method	Detection Capability / Remarks
SD-OCT	Highest sensitivity. Visualized as a hyporeflective cavity within the choroid.
Color Fundus Photography	Detection rate 46–53%. Many cases are missed.
Multicolor Imaging	Cannot detect (due to wavelength penetration and reflection issues) 1)
FA	Early hypofluorescence → late staining
OCTA	Decreased peripapillary vessel density (VD) on the temporal side

Key Points for Diagnosis

• SD-OCT: It is visualized as a low-reflective cavity beneath the normal retinal pigment epithelium at the lower edge of the peripapillary conus. Using EDI-OCT (enhanced depth imaging OCT) allows clearer confirmation of the relationship with posterior scleral curvature.
• Limitations of fundus color photography: The lesion cannot be detected in about half of cases. Exclusion without OCT is difficult.
• Limitations of multicolor imaging: Short-wavelength (blue/green) light cannot reach the deep choroidal layers of the conus, and since there is no melanin pigment in the cavity, infrared reflectance is also not obtained, making PICC undetectable ¹⁾.

Differential Diagnosis

PICC presents with visual field defects, RNFL thinning, and RAPD similar to glaucoma and optic neuropathy. The following differential diagnoses are particularly important ²⁾.

• Normal-tension glaucoma: Shares features of normal intraocular pressure with visual field defects and RNFL thinning. OCT confirmation in highly myopic eyes is key for differentiation.
• Anterior ischemic optic neuropathy: Differentiated by acute onset and presence or absence of optic disc edema.
• Acquired optic atrophy: Requires systemic evaluation including brain MRI.

In the case reported by Belamkar et al. (2022), blood tests (ACE, CRP, ESR, ANCA, QuantiFERON, syphilis, Lyme disease, etc.) and brain MRI were all normal ²⁾. Fluorescein angiography also showed no hyperfluorescence indicating neovascularization, confirming the diagnosis of PICC.

Q Can PICC be diagnosed with fundus photography alone?

A

The detection rate of fundus color photography is only 46–53%, and nearly half of cases are missed. Multicolor imaging also fails to detect it ¹⁾. SD-OCT is essential for a definitive diagnosis.

5. Standard Treatment

Currently, there is no established active treatment for PICC, and regular follow-up is the basic policy.

Follow-up

In asymptomatic cases without visual field defects, follow-up is performed with regular OCT and visual field testing. Even when visual field defects are present, if the progression is slow, observation may be continued.

Pharmacotherapy

In cases with glaucoma-like visual field defects, the use of eye drops aimed at lowering intraocular pressure and providing neuroprotection may be suggested. However, evidence for PICC is currently limited, and efficacy has not been established ²⁾.

Treatment of Complications

If complications related to high myopia such as posterior staphyloma, macular atrophy, or myopic choroidal neovascularization occur, treatment is given according to each condition. Anti-VEGF therapy is indicated for myopic choroidal neovascularization.

Precautions in Treatment

Brimonidine tartrate eye drops may be suggested for neuroprotection, but evidence supporting efficacy for PICC is currently limited ²⁾. Do not use eye drops without consulting your doctor. Misdiagnosing PICC as other diseases such as glaucoma or choroidal tumor can lead to unnecessary tests and treatments. Accurate differential diagnosis is important ²⁾.

6. Pathophysiology and Detailed Mechanisms

The most plausible mechanism for PICC is the mechanical hypothesis centered on posterior scleral curvature.

With axial elongation due to high myopia, the posterior sclera becomes markedly curved, and peripapillary tissues become thin. Repeated mechanical stress from intraocular pressure fluctuations and eye movements is thought to cause fluid accumulation in the choroid, forming cavities.

The main pathologies associated with cavity formation are as follows ²⁾:

• Effect on inner retinal layers: The presence of cavities leads to thinning of the peripapillary inner retinal layers (RNFL and GC-IPL). In affected eyes, average RNFL thinning of 69 μm and GC-IPL thinning of 60 μm have been reported ²⁾.
• Mechanism of visual field defects: RNFL thinning preferentially occurs in the inferior arcuate fibers, resulting in inferior arcuate scotomas. Enlarging cysts may also damage the superior inner retinal layers and impede axonal flow ²⁾.
• Development of RAPD: Due to effects on optic nerve fibers, a RAPD of 1.5 log units may occur ²⁾.

In a case of a 55-year-old man reported by Belamkar et al. (2022), the main complaint was progressive visual decline over 3 years. Examination confirmed RAPD of 1.5 log units, RNFL thinning of 69 μm, and GC-IPL thinning of 60 μm ²⁾. The inferior arcuate scotoma progressed over 16 months of follow-up, indicating that PICC can be a direct cause of visual field defects.

Progression of posterior staphyloma in high myopia causes worsening of fundus changes including macular atrophy over time ³⁾. PICC is positioned as part of these structural changes in high myopia.

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7. Latest Research and Future Perspectives (Research-stage Reports)

For patients: Please read this

The following content is currently at the research stage or under clinical trial, and is not standard treatment available at general hospitals. It is reference information for professionals regarding future medical developments.

Longitudinal Confirmation of Visual Field Progression

Belamkar et al. (2022) recorded progression of inferior arcuate scotoma to the superonasal area during a 16-month follow-up, suggesting that PICC may be directly involved in the progression of visual field defects ²⁾. Whether PICC itself is the cause or a secondary change of optic neuropathy associated with high myopia remains unclear, and accumulation of prospective long-term follow-up studies is needed.

Limitations of Multicolor Imaging and Choice of Imaging Modality

Venkatesh et al. (2021) reported a case in which PICC was detectable on fundus color photography but not on multicolor imaging ¹⁾. They attributed this to the inability of short-wavelength light to reach the area and the loss of infrared reflection due to lack of melanin. This finding suggests the importance of modality selection in screening for PICC, and there is a risk of missing PICC when relying on multicolor imaging ¹⁾.

Neuroprotective Agents such as Brimonidine

For visual field impairment associated with PICC, drugs with neuroprotective effects such as brimonidine tartrate have been proposed ²⁾. However, at present, clinical trial data targeting PICC are scarce, and efficacy has not been established.

Association with Fundus Changes in High Myopia

Carlà et al. (2025) analyzed 1228 eyes with high myopia (mean axial length 31.6 mm) and showed that posterior staphyloma and macular atrophy progress over time ³⁾. Further long-term follow-up studies are needed regarding the association between peripapillary lesions including PICC and macular changes.

Q Will effective treatments be developed in the future?

A

Currently, research is progressing in relation to neuroprotective agents (e.g., brimonidine) and axial length control treatments for high myopia (e.g., low-dose atropine, orthokeratology). However, evidence for treatments directly targeting PICC is still lacking ²⁾, and results from long-term follow-up studies are awaited.

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8. References

1. Venkatesh R, Sinha S, Nayak S, et al. Peripapillary intrachoroidal cavitation: why is it visible on fundus photography but not on multicolour imaging? BMJ Case Rep. 2021;14:e246837.
2. Belamkar AV, Kohli C, Bhola R, et al. Peripapillary intrachoroidal cavitation presenting as progressive visual field defect. Neuro-Ophthalmology. 2022;46(4):254-257.
3. Carlà MM, Boselli F, Giannuzzi F, et al. Longitudinal Progression of Myopic Maculopathy in a Long-Term Follow-Up of a European Cohort: Imaging Features and Visual Outcomes. Ophthalmol Retina. 2025;9(8):774-786. doi:10.1016/j.oret.2025.02.015. PMID:40010496.