Geographic Atrophy OCT Imaging: Key Retinal Insights

Geographic atrophy (GA), an advanced form of age-related macular degeneration, leads to progressive vision loss due to retinal cell degeneration. Optical coherence tomography (OCT) is a crucial tool for assessing GA, providing detailed cross-sectional images of retinal structures.

By analyzing OCT scans, clinicians can track disease progression and evaluate structural changes. Understanding key imaging features enhances diagnosis and monitoring.

Hallmarks on OCT Scans

Geographic atrophy presents distinct structural alterations on OCT that aid in identification and monitoring. A key feature is the loss of external retinal layers, particularly the retinal pigment epithelium (RPE) and overlying photoreceptors. This results in increased signal transmission into the choroid due to the absence of the RPE, which normally limits light penetration. The resulting hypertransmission signal helps differentiate atrophic regions from intact retina.

Thinning of the neurosensory retina in atrophic areas is another characteristic. Spectral-domain OCT (SD-OCT) studies show progressive loss of the outer nuclear layer (ONL) and ellipsoid zone (EZ), correlating with visual impairment. Greater ONL loss predicts faster progression. Atrophic lesion margins often contain residual RPE cells in a patchy distribution, creating a jagged transition between healthy and degenerated tissue.

Beyond atrophic zones, hyperreflective foci within the retina may indicate migrating RPE cells or lipid deposits. These have been linked to increased lesion expansion risk, as shown in longitudinal studies published in Ophthalmology and Investigative Ophthalmology & Visual Science. Additionally, the choroid beneath atrophic regions appears more prominent due to the loss of overlying structures, further emphasizing the contrast between affected and unaffected areas.

Retinal Layers Affected

Geographic atrophy disrupts multiple retinal layers, with the outer retina experiencing the most damage. The RPE is among the first to deteriorate, leading to a loss of its supportive functions, including nutrient transport and photoreceptor maintenance. As the RPE degenerates, the overlying photoreceptors—particularly cones and rods—atrophy due to the lack of metabolic support. OCT reveals this as thinning or complete loss of the ellipsoid zone (EZ), a key marker of photoreceptor integrity.

Beneath the damaged RPE, the ONL, which houses photoreceptor cell bodies, undergoes significant thinning. SD-OCT studies show a direct correlation between ONL thickness and visual function, with greater thinning linked to more severe impairment. The external limiting membrane (ELM), which separates photoreceptor cell bodies from their inner segments, often becomes disrupted in atrophic areas, further compromising retinal integrity.

GA also affects deeper structures like the choriocapillaris. OCT angiography (OCTA) reveals reduced choriocapillaris density beneath atrophic lesions, indicating declining vascular support. This exacerbates retinal degeneration, as the choriocapillaris supplies oxygen and nutrients to the RPE and photoreceptors. Thinning of Bruch’s membrane, a key interface between the retina and choroid, suggests structural changes extend beyond initially affected layers.

Hyperreflective Versus Hyporeflective Areas

OCT imaging of GA shows a contrast between hyperreflective and hyporeflective regions, each offering insights into disease progression. Hyperreflective areas correspond to structures that reflect more light, such as residual RPE cells, fibrotic changes, or lipid deposits. These often appear at lesion margins, where surviving RPE cells may be migrating or clustering. Their presence has been linked to increased lesion expansion rates in longitudinal studies, indicating ongoing cellular stress and remodeling.

Hyporeflective areas, by contrast, signify tissue loss or structural voids where OCT signals are absorbed or scattered. In GA, these appear in zones of complete RPE and photoreceptor atrophy, where the absence of reflective layers allows deeper light penetration into the choroid, producing a characteristic hypertransmission signal. Hyporeflective spaces may also occur within the choroid itself, particularly where choriocapillaris atrophy reduces vascular density.

The contrast between hyperreflective and hyporeflective regions evolves over time as GA progresses. Longitudinal OCT studies show that hyperreflective deposits often precede new atrophic zones, reinforcing their role as potential precursors to disease advancement. These shifting patterns highlight the heterogeneous nature of GA, where cellular and extracellular changes shape the structural landscape. Understanding these evolving features is critical for clinical trials assessing potential treatments.

Photoreceptor Disruption

Photoreceptor degeneration in GA is a major contributor to vision loss, with OCT providing a detailed view of structural alterations. In early stages, subtle disruptions in the ellipsoid zone (EZ) appear as localized thinning or discontinuities, often preceding more extensive atrophy. As GA advances, complete EZ collapse signifies irreversible damage. Spectral-domain OCT (SD-OCT) imaging highlights this deterioration, with the disappearance of the external limiting membrane (ELM) further underscoring photoreceptor breakdown.

The rate of photoreceptor loss varies by lesion location and size, with foveal involvement leading to more severe impairment. Adaptive optics scanning laser ophthalmoscopy (AOSLO) studies show progressive cone photoreceptor loss in parafoveal regions before central involvement. This aligns with microperimetry findings, which reveal corresponding declines in retinal sensitivity. Identifying early OCT biomarkers may help predict visual outcomes, particularly in patients with extrafoveal atrophy where central vision remains temporarily intact.

Retinal Pigment Epithelium Changes

The RPE undergoes significant alterations in GA, playing a central role in disease progression. As RPE cells degenerate, their ability to support photoreceptors diminishes, leading to widespread structural and functional consequences. OCT imaging captures these changes in detail, showing areas of RPE loss as increased light penetration into the choroid. This hypertransmission signal clearly demarcates atrophic regions, enabling clinicians to track lesion expansion. Atrophy borders often contain hyperreflective foci, indicating residual RPE cells attempting migration or reorganization.

Beyond complete atrophy, the RPE exhibits early pathological changes such as focal thickening and hyperreflectivity, which may signal stress responses like increased melanin production or lipid accumulation. OCT and autofluorescence studies show that hyperreflective RPE changes often precede lesion enlargement, making them a potential biomarker for progression. Additionally, sub-RPE deposits, or drusen, sometimes persist in GA. While more common in earlier macular degeneration stages, large confluent drusen in GA are linked to a higher likelihood of RPE atrophy. These dynamic changes illustrate the complexity of RPE involvement in GA.

Measurement Parameters for Lesion Size

Quantifying lesion size in GA is essential for clinical assessment and research. OCT provides multiple parameters for measuring atrophic regions, with en face and cross-sectional analyses offering complementary insights. The most widely used metric is the area of hypertransmission, which reflects RPE loss by measuring increased light penetration into the choroid. This parameter strongly correlates with fundus autofluorescence (FAF) findings, where hypoautofluorescent regions signify atrophy. Combining OCT and FAF data improves lesion border delineation and tracking over time.

Retinal thickness measurements further evaluate GA severity. Progressive thinning of the ONL and EZ can indicate lesion expansion before complete atrophy occurs. Automated segmentation algorithms enhance measurement precision, allowing objective tracking of structural deterioration. Another key metric is lesion margin irregularity, as jagged or scalloped edges are associated with faster progression. Longitudinal studies show lesion growth rates vary, averaging 1.5 to 2.5 mm² per year, depending on factors like baseline size and location. These quantitative assessments aid prognosis and serve as critical endpoints in clinical trials evaluating therapies to slow disease advancement.