Overview
Optical coherence tomography, or OCT, is a noninvasive imaging test that provides high-resolution cross-sectional views of the retina and choroid. In inflammatory eye diseases, OCT helps clinicians see whether tissue damage is active or inactive, and it can reveal structural clues that are not obvious on routine examination.
This article focuses on inactive multifocal choroiditis with panuveitis and punctate inner choroidopathy, commonly grouped as MFCPU/PIC. These conditions are part of the same clinical spectrum and can leave behind pale, atrophic scars in the retina and choroid after inflammation has quieted down. The study compared OCT features of these lesions with scars caused by other inflammatory or infectious eye diseases that can look similar on examination.
Why this study matters
Distinguishing MFCPU/PIC from its mimickers is important because the diagnosis affects prognosis, follow-up, and treatment decisions. When inflammation is no longer active, the eye may show only old scars. At that stage, it can be difficult to know whether the lesion came from MFCPU/PIC, sarcoidosis, tuberculosis, syphilis, serpiginous choroiditis, acute posterior multifocal placoid pigment epitheliopathy, birdshot chorioretinopathy, or ocular toxoplasmosis.
The investigators wanted to identify OCT biomarkers that are especially characteristic of inactive MFCPU/PIC lesions. If certain imaging patterns are strongly associated with this disease, they could improve diagnostic confidence even when there is no active inflammation to guide the diagnosis.
Study design and patient group
This was a cross-sectional observational study conducted at Luigi Sacco Hospital in Milan, Italy. The researchers evaluated 59 patients with inactive chorioretinal atrophic lesions.
The group included:
– 27 patients with MFCPU/PIC, accounting for 57 lesions
– 32 patients with non-MFCPU/PIC causes, accounting for 49 lesions
The comparison group included lesions related to sarcoidosis, tuberculosis, syphilis, serpiginous choroiditis, APMPPE, birdshot chorioretinopathy, and ocular toxoplasmosis.
To ensure a thorough assessment, the investigators used multimodal imaging, including:
– Color fundus photography
– Near-infrared reflectance imaging
– Fundus autofluorescence
– Spectral-domain OCT (SD-OCT)
– High-resolution OCT (HR-OCT) in selected cases
Lesions were randomly sampled, with a maximum of three per eye, to reduce clustering bias. Statistical models were adjusted for the fact that several lesions could come from the same patient.
Key OCT measurements
The study evaluated both quantitative and structural OCT findings.
The main quantitative parameters were:
– Retinal pigment epithelium atrophy size, or RPE-AS: a measure of how large the atrophic area is in the RPE layer
– Bruch’s membrane defect size, or BrM-HS: a measure of the horizontal extent of breaks or defects in Bruch’s membrane
– Choroidal thickness coefficient, or CTC: an indicator related to the thickness and involvement of the choroid
The authors also graded structural changes in the retinal layers, including whether there was herniation or displacement of inner retinal tissue through defects in the outer retinal support layers.
Main findings
The most striking result was the frequency of Bruch’s membrane disruption in MFCPU/PIC lesions. Bruch’s membrane disruption was present in 94.7% of MFCPU/PIC lesions, compared with only 6.1% of control lesions. This difference was highly significant statistically.
Importantly, this finding remained strongly associated with MFCPU/PIC even after accounting for age and the size of RPE atrophy. In other words, the presence of a Bruch’s membrane break was not just a consequence of a larger scar; it appeared to be a disease-specific feature.
Another notable feature was inner nuclear layer herniation. This means that inner retinal tissue extended or protruded into the area of focal choroidal excavation, which was much more common in MFCPU/PIC lesions than in controls: 57.9% versus 4.3%.
RPE atrophy was present in all lesions in both groups, showing that atrophic scarring is a shared endpoint across these diseases. However, the Bruch’s membrane defects in MFCPU/PIC were generally smaller and were located concentrically within the area of RPE atrophy. This pattern suggests a localized destructive process rather than diffuse tissue loss.
There was also a positive correlation between the size of the RPE atrophy and the size of the Bruch’s membrane defect. As the atrophic area became larger, the defect in Bruch’s membrane tended to increase as well.
MFCPU/PIC lesions showed lower choroidal thickness coefficient values and more frequent focal choroidal excavation, suggesting greater choroidal involvement or remodeling in this disease.
Agreement between standard OCT and high-resolution OCT
The researchers also compared SD-OCT with HR-OCT. The agreement between the two modalities was good, with a kappa value of 0.60. In practical terms, this means standard SD-OCT was usually sufficient to identify the key abnormalities.
High-resolution OCT did not provide a meaningful additional diagnostic yield in this study. This is clinically relevant because it suggests that routine OCT imaging may be enough in many cases, making the diagnostic process more accessible and efficient.
Interpretation of the findings
The study supports a distinctive OCT pattern for inactive MFCPU/PIC. The combination of Bruch’s membrane disruption, inner retinal layer herniation, and focal choroidal excavation appears highly characteristic.
These imaging features suggest that MFCPU/PIC may involve a particular lytic inflammatory process affecting the outer retina, Bruch’s membrane, and the choroid. “Lytic” in this context implies tissue breakdown or destruction, leaving behind a structural defect rather than just a pigmented scar.
This is important because many inflammatory and infectious chorioretinal scars can look similar clinically, but they may not share the same underlying structural pattern. Identifying a disease-specific OCT signature can therefore improve diagnostic accuracy, especially when active inflammation is absent and laboratory testing is noncontributory.
Clinical significance
For retina and uveitis specialists, these findings may help in several ways:
– Supporting the diagnosis of inactive MFCPU/PIC when only old scars are visible
– Distinguishing MFCPU/PIC from infectious or systemic inflammatory mimickers
– Improving confidence in historical diagnosis when prior active episodes were not documented
– Providing a structural marker that may help in long-term disease characterization and research
In everyday clinical practice, this could matter for a patient who presents with stable white chorioretinal scars, no current inflammation, and an unclear past history. If OCT shows Bruch’s membrane rupture with inner retinal herniation into a focal excavation, MFCPU/PIC becomes more likely.
Practical background on MFCPU and PIC
MFCPU and PIC are inflammatory disorders primarily affecting the choroid and outer retina. They are often seen in young to middle-aged patients and may be associated with visual symptoms such as blurred vision, floaters, metamorphopsia, or central scotoma. One major complication is choroidal neovascularization, which can cause further vision loss and may require treatment with anti-VEGF injections.
When the disease is active, inflammation may be evident on examination or imaging. However, once the episode has resolved, the remaining lesions may appear as atrophic scars. At that stage, diagnosis relies heavily on imaging patterns and clinical history.
Although this study focused on inactive lesions, it reinforces an important point: not all old inflammatory scars are the same. The way tissue is lost or remodeled can reflect the original disease process.
Limitations to keep in mind
As with any observational study, there are some limitations. The sample size was modest, and the work was performed at a single center. In addition, the analysis focused on inactive lesions, so the findings may not fully capture the appearance of active MFCPU/PIC.
Another practical point is that while the OCT pattern was highly suggestive, imaging alone should not replace clinical judgment. Diagnosis still depends on the full context, including age, symptoms, prior inflammatory episodes, laboratory evaluation, and exclusion of infectious causes when appropriate.
Conclusion
This study shows that Bruch’s membrane disruption and inner retinal layer herniation into focal choroidal excavation are highly characteristic OCT features of inactive MFCPU/PIC lesions. Compared with common inflammatory and infectious mimickers, these lesions showed a much higher rate of Bruch’s membrane breaks, more frequent inner nuclear layer herniation, and greater choroidal involvement.
The results suggest that standard OCT can provide powerful diagnostic clues even when inflammation is no longer active. In clinical practice, recognizing this pattern may help ophthalmologists distinguish MFCPU/PIC from other causes of chorioretinal atrophy and better understand the disease’s underlying destructive mechanism.
