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Retinal nerve fiber layer
Retinal nerve fiber layer
Retinal nerve fiber layer
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Retinal nerve fiber layer
Section of retina. (Stratum opticum labeled at right, second from the top.)
Plan of retinal neurons. (Stratum opticum labeled at left, second from the top.)
Details
Identifiers
Latinstratum neurofibrarum retinae
TA98A15.2.04.017
FMA58688
Anatomical terminology

The retinal nerve fiber layer (RNFL) or nerve fiber layer, stratum opticum, is part of the anatomy of the eye.

Physical structure

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The RNFL formed by the expansion of the fibers of the optic nerve; it is thickest near the optic disc, gradually diminishing toward the ora serrata.

As the nerve fibers pass through the lamina cribrosa sclerae they lose their medullary sheaths and are continued onward through the choroid and retina as simple axis-cylinders.

When they reach the internal surface of the retina they radiate from their point of entrance over this surface grouped in bundles, and in many places arranged in plexuses.

Most of the fibers are centripetal, and are the direct continuations of the axis-cylinder processes of the cells of the ganglionic layer, but a few of them are centrifugal and ramify in the inner plexiform and inner nuclear layers, where they end in enlarged extremities.

Measurement

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RNFL measurement can be made by Optical coherence tomography.[1]

Relation with diseases

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RNFL reduction

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Retinitis pigmentosa

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Patients with retinitis pigmentosa have abnormal thinning of the RNFL which correlates with the severity of the disease.[2] However the thickness of the RNFL also decreases with age and not visual acuity.[3] The sparing of this layer is important in the treatment of the disease as it is the basis for connecting retinal prostheses to the optic nerve, or implanting stem cells that could regenerate the lost photoreceptors.

Asymmetric RNFL

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RNFL asymmetry is the difference between the RNFL of the left and right eyes. In healthy patients, one study (2008, n=109) found asymmetry to be typically between 0-8μm, but occasionally higher, with average asymmetry of c.3μm at age 25 rising to 5μm at age 60.[4] A 2011 study (n=284) concluded that RNFL asymmetry exceeding 9μm may be considered statistically significant and may be indicative of early glaucomatous damage.[5] A 2023 study of 4034 children found mean RNFL of 106μm with SD of 9.4μm.[6]

Optic neuritis

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RNFL asymmetry has been proposed as a strong indicator of optic neuritis,[7][8] with one small study proposing that asymmetry of 5–6μm was "a robust structural threshold for identifying the presence of a unilateral optic nerve lesion in MS."[9] Optic neuritis is often associated with multiple sclerosis, and RNFL data may indicate the pace of future development of the MS.[10][11]

Glaucoma

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RNFL asymmetry may be produced by glaucoma.[12][13][14][15] Glaucoma is a lead cause of irreversible blindness. Resesrch in RNFL and optic nerve head (ONH) abnormalities may enable early detection and diagnosis of glaucoma.[2]

Fibromyalgia

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One small study found that fibromyalgia patients had decreased RNFL thickness[16] but another found no difference.[17]

Correlation with ethnicity

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RNFL may vary with ethnicity.[18][19]

Other factors affecting RNFL

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Some processes can excite RNFL apoptosis. Harmful situations which can damage RNFL include high intraocular pressure, high fluctuation on phase of intraocular pressure, inflammation, vascular disease and any kind of hypoxia. Gede Pardianto (2009) reported 6 cases of RNFL thickness change after the procedures of phacoemulsification.[20] Sudden intraocular fluctuation in any kind of intraocular surgeries maybe harmful to RNFL in accordance with mechanical stress on sudden compression and also ischemic effect of micro emboly as the result of the sudden decompression that may generate micro bubble that can clog micro vessels.[21]

Pattern of retinal nerve fibers

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Retinal nerve fiber layer

View on Grokipedia
from Grokipedia
The retinal nerve fiber layer (RNFL) is the innermost layer of the , consisting primarily of unmyelinated axons from retinal cells that converge toward the to form the , thereby transmitting visual signals from the to the . This layer lies adjacent to the inner limiting membrane and above the cell layer, forming an arcuate pattern across the while being notably absent at the fovea due to the displacement of inner retinal structures. Composed of these axons intermixed with and processes of Müller glial cells, the RNFL maintains the topographic organization of visual information, with thicker regions in areas of higher cell density, such as near the . Functionally, the RNFL serves as the final conduit for processed visual data in the , where axons from magnocellular and parvocellular cells bundle together before exiting the eye at the , preserving spatial relationships essential for central visual processing. It contains radial peripapillary capillaries that supply nutrients, supporting the layer's metabolic demands despite the absence of myelination within the itself. Clinically, the RNFL is a critical for neurodegenerative conditions; for instance, progressive thinning occurs in due to elevated damaging these axons, leading to retinal cell death and irreversible vision loss. Similarly, measurable RNFL atrophy is observed in , often quantified using (OCT) to assess disease progression and treatment efficacy. These changes underscore the RNFL's vulnerability and its role in early of optic neuropathies.

Anatomy and Development

Histological Structure

The retinal nerve fiber layer (RNFL) constitutes the innermost layer of the neurosensory , positioned immediately adjacent to the internal limiting membrane and the overlying vitreous humor. This superficial location allows the RNFL to form the interface between the neural and the vitreous cavity, facilitating the convergence of visual signals toward the . The primary cellular component of the RNFL consists of unmyelinated axons originating from retinal ganglion cells, which extend from the ganglion cell layer to the head. These axons are organized into parallel bundles that course across the inner retinal surface, supported structurally by processes of Müller glial cells that wrap and insulate the bundles, preventing mechanical damage and maintaining axonal integrity. Additionally, , a specialized type of macroglia, envelop the axonal bundles, providing metabolic support, regulating ion homeostasis, and contributing to the within the RNFL. Together, these elements form a compact, organized tissue devoid of myelination, which distinguishes the RNFL from the myelinated beyond the lamina cribrosa. Regionally, the RNFL exhibits distinct organizational patterns adapted to the topographic distribution of projections. In the superior and inferior quadrants, axons form prominent arcuate bundles that arch around the , creating a characteristic "hourglass" pattern that funnels fibers toward the . Nasally, the papillomacular bundle predominates, comprising a denser aggregation of axons from ganglion cells near the that project directly to the head, supporting high-acuity central vision. These variations in bundling reflect the functional specialization of visual pathways, with arcuate bundles serving peripheral fields and the papillomacular bundle emphasizing foveal input. The axons within the RNFL remain unmyelinated throughout their intra-retinal course, only acquiring sheaths upon entering the head at the lamina cribrosa, which optimizes signal conduction while minimizing retinal bulk. In adults, the RNFL exhibits an average thickness of approximately 100-120 μm, with notable quadrant-specific differences: the superior and inferior regions are thicker (often exceeding 130 μm) compared to the thinner nasal and temporal quadrants, reflecting the higher axonal density in arcuate areas.

Embryological Development

The embryological development of the retinal nerve fiber layer (RNFL) begins with the differentiation of retinal ganglion cells (RGCs) from retinal progenitor cells in the inner neuroblastic zone of the . In humans, RGC neurogenesis initiates around the 7th gestational week, marking the first neuronal to emerge in the . These cells rapidly extend axons toward the , with initial axonogenesis occurring before 10 weeks of gestation in the central . By 8 weeks, axons begin populating the , and extension continues progressively, reaching the chiasm by approximately 10-12 weeks. Axonogenesis is precisely guided by molecular cues, including netrins and semaphorins, which direct RGC during . Netrin-1, expressed at the head, acts as a chemoattractant to facilitate exit from the , triggering local protein synthesis in within minutes via receptors like DCC. Semaphorin 3A, conversely, promotes repulsion and collapse in distal regions, with responsiveness emerging as axons advance into the ; this involves cytoskeletal reorganization and . Concurrently, astroglial precursors invade the nascent RNFL from the , establishing supportive networks essential for . Müller cells, derived from retinal progenitors via Notch signaling and factors like , play a critical role in early RNFL assembly by providing structural support for bundling. During weeks 12-20 of , their endfeet delimit and stabilize emerging bundles within the RNFL, contributing to layer thickening as the inner neuroblastic zone matures. A well-defined RNFL is evident by 18 weeks, comprising about one-fourth of the inner zone thickness, with progressive expansion thereafter. During this period, RGC axons undergo significant overproduction, peaking at approximately 3.7 million axons in the around 16-17 weeks , followed by elimination of about 70% (resulting in ~1.2 million axons by birth) through apoptotic processes that refine the RNFL's axonal composition. RNFL maturation involves continued thickening that peaks postnatally, transitioning from a biphasic around 38 weeks postmenstrual age, after which minor thinning occurs as the layer stabilizes. Myelination of RGC axons commences in the late fetal period at the , progressing anteriorly from the lateral geniculate body but halting posterior to the lamina cribrosa near birth, ensuring the RNFL remains unmyelinated. Recent studies emphasize that the development of astroglia, including Müller cells and RNFL-specific , is vital for RNFL structural integrity, as these cells integrate neuronal and vascular elements through VEGF-mediated patterning and mechanical support.

Function and Physiology

Role in Visual Signal Transmission

The retinal nerve fiber layer (RNFL) comprises the unmyelinated axons of retinal cells (RGCs), which serve as the final output neurons of the , integrating and relaying processed visual information from upstream retinal circuits to the . These axons originate from RGC somata in the ganglion cell layer, course superficially through the in bundled arcuate trajectories, and converge at the to exit the eye as the (cranial nerve II). Upon leaving the eye, the optic nerve contains approximately 1.2 million axons that conduct action potentials toward the (LGN) of the , passing through the where nasal fibers partially decussate and then continuing via the optic tract. This pathway integration ensures the transmission of spatially organized visual signals from the to higher visual centers. Within the RNFL, action potentials propagate along these unmyelinated axons at conduction velocities typically ranging from 0.5 to 1.7 m/s, enabling the relay of neural signals despite the absence of sheaths in the intraretinal segment. Myelination begins just posterior to the lamina cribrosa in the head, accelerating conduction beyond the eye, but the RNFL's slower velocity contributes to the overall timing of visual processing. Conduction velocities vary spatially across the RNFL, with peripheral axons propagating faster than foveal ones (up to three times higher) to compensate for longer paths and synchronize signals at the LGN. Glial support is crucial for maintaining this transmission: , primarily located in the RNFL, provide metabolic support to axons by regulating nutrient supply and waste removal, while also ensheathing blood vessels to stabilize the local microenvironment. Complementarily, Müller cells span the retinal thickness, their processes interfacing with the RNFL to maintain ionic balance—particularly —during repetitive firing, preventing disruptions in signal propagation. The RNFL's role is fundamentally important for conveying feature-specific visual data, such as contrast sensitivity, motion detection, and color opponency, encoded by distinct RGC subtypes whose axons form the layer. This selective transmission preserves the fidelity of retinal computations, allowing the brain to reconstruct coherent visual scenes. Damage to RNFL axons, such as from injury or degeneration, compromises this relay, resulting in reduced signal amplitude and desynchronized arrival times at the LGN, which manifests as visual field defects.

Normal Thickness Characteristics

The retinal nerve fiber layer (RNFL) in healthy adults exhibits a mean global thickness ranging from 97 to 110 μm, reflecting the bundled unmyelinated axons of retinal ganglion cells that converge toward the . This thickness varies by quadrant, following the ISNT rule (inferior > superior > nasal > temporal), with typical values of approximately 120 μm in the superior and inferior quadrants, 80 μm in the nasal quadrant, and 70 μm in the temporal quadrant. Age-related thinning of the RNFL is a physiological process, with an annual reduction of 0.2-0.4 μm observed after age 20, accelerating to higher rates after age 50 due to progressive axonal loss. In healthy individuals, inter-eye symmetry is high, with typical differences in average RNFL thickness less than 5-10 μm, supporting the use of bilateral comparisons in clinical assessments. Minor diurnal fluctuations in RNFL thickness, on the order of 2-5 μm, occur in healthy eyes, primarily attributable to variations in throughout the day. Normative reference databases, such as those derived from large cohorts like the , provide age- and sex-adjusted percentiles for RNFL thickness, enabling percentile-based evaluations in populations exceeding 20,000 individuals.
QuadrantApproximate Normal Thickness (μm)Source
Superior~120Knighton et al., 2012
Inferior~120Knighton et al., 2012
Nasal~80Bendsen et al., 2017
Temporal~70Bendsen et al., 2017

Measurement Methods

Optical Coherence Tomography

(OCT) serves as the gold standard for imaging and quantification of the retinal nerve fiber layer (RNFL), providing high-resolution cross-sectional views of retinal structures through low-coherence . This technique employs near-infrared light to generate interference patterns, enabling precise measurement of tissue reflectivity and thickness with axial resolutions of 3-5 μm. Modern OCT systems primarily utilize spectral-domain OCT (SD-OCT), which achieves scan speeds of 20,000-40,000 A-scans per second at wavelengths of 800-870 nm, or swept-source OCT (SS-OCT), offering even higher speeds up to 400,000 A-scans per second with longer wavelengths (1050-1060 nm) for improved penetration through ocular media. These advancements allow for detailed RNFL assessment without the need for contact or dilation, making OCT essential for evaluating RNFL integrity. The standard procedure for RNFL evaluation involves a peripapillary circular scan with a of 3.4 centered on the , capturing 360-degree thickness measurements around the nerve fiber bundle. Automated algorithms then segment the RNFL boundaries by identifying the internal limiting membrane and posterior RNFL limits, generating quantitative data in real time. This non-contact process typically requires the patient to fixate on a target for mere seconds per eye, minimizing discomfort. OCT outputs include comprehensive RNFL thickness maps, which display average and sectoral values compared against age-matched normative databases to highlight deviations from normal ranges (typically 90-110 μm globally). Clock-hour analysis further divides the peripapillary region into 12 sectors, facilitating detection of focal thinning or defects in specific quadrants. These visualizations aid in longitudinal monitoring by quantifying subtle changes over time. Key advantages of OCT for RNFL imaging include its non-invasive nature, rapid acquisition (under 5 seconds per eye), and high reproducibility, with test-retest variability often below 2 μm in healthy subjects. These features enable reliable, objective assessments that surpass traditional methods in sensitivity and consistency. Despite its strengths, OCT is susceptible to signal artifacts from media opacities, such as cataracts, which can degrade image quality and segmentation accuracy. Recent advances from 2024-2025 incorporate for enhanced segmentation, using models to automate boundary detection, reduce errors in real-time, and accelerate analysis of RNFL thickness in large datasets. These AI integrations have demonstrated improved efficiency and precision in tissue quantification.

Alternative Imaging Techniques

Scanning polarimetry (SLP) is a non-OCT technique that assesses the retinal nerve fiber layer (RNFL) by measuring its , which arises from the organized arrangement of within retinal ganglion cell axons. In SLP, a polarized low-coherence beam scans the peripapillary , and the phase retardation of the light after passing through the RNFL is quantified to estimate thickness; this method is particularly sensitive to early axon loss in due to its ability to detect structural changes before visible defects appear. Commercial devices such as the GDx Nerve Fiber Analyzer (now GDx-VCC or enhanced versions) automate this process, providing reproducible quantitative maps of RNFL thickness with a resolution of approximately 10 μm, though it is generally less precise than (OCT) for overall thickness measurement. SLP's utility shines in cases where corneal compensation is optimized, making it a valuable adjunct for monitoring progression in early suspects. Confocal scanning laser ophthalmoscopy (CSLO) offers qualitative visualization of RNFL bundles through high-resolution confocal of the fundus, typically using a 670 nm diode laser to produce three-dimensional reconstructions of the head and peripapillary region. Devices like the Heidelberg Retina Tomograph (HRT) enable red-free-like that highlights nerve fiber bundles by reducing scattered light, allowing clinicians to detect localized defects or wedge-shaped losses without quantitative thickness metrics. While historical in origin, CSLO remains adjunctive for its non-invasive nature and ability to provide en face views of RNFL architecture, though it lacks the axial resolution of OCT and is more operator-dependent for interpretation. Fundus photography, particularly with red-free or blue filters, provides a straightforward, non-quantitative method for gross estimation of RNFL thickness and defect identification by enhancing contrast against the darker background of inner retinal layers. Stereoscopic red-free captures specular reflections from RNFL bundles, enabling visual assessment of arcuate patterns or focal thinning, and serves as a portable, cost-effective tool for longitudinal comparison in clinical settings. Its limitations include subjective interpretation and poor precision for subtle changes, restricting it to adjunctive roles rather than primary diagnostic measurement. Emerging techniques include polarization-sensitive OCT (PS-OCT) variants, which extend standard OCT by incorporating polarization analysis to detect in the RNFL, as myelinated segments alter light retardation differently from unmyelinated axons. PS-OCT enables depth-resolved mapping of , offering insights into axonal integrity and beyond mere thickness, with applications in distinguishing inflammatory from degenerative changes. In cases of opaque ocular media, such as cataracts or vitreous hemorrhage, B-scan ultrasonography provides gross anatomical evaluation of the and peripapillary structures, though it cannot resolve fine RNFL details due to its lower resolution (around 150-200 μm). These alternatives complement OCT, the gold standard, by addressing specific niches like birefringence sensitivity or media opacities.

Clinical Applications

Assessment in Glaucoma

In , the retinal nerve fiber layer (RNFL) undergoes pathological thinning that typically begins in the superior and inferior sectors, reflecting the arcuate bundle distribution of axons. This progressive loss is characteristic of open-angle , where the average rate of RNFL thinning is approximately 1-2 μm per year, as observed in longitudinal cohorts using spectral-domain (SD-OCT). In primary open-angle (POAG), baseline RNFL thickness at tends to be relatively preserved compared to more advanced stages, allowing for earlier detection before widespread atrophy. Diagnostic assessment of RNFL in relies on comparing thickness measurements to age-matched normative databases, with thresholds typically set at the 5th for abnormality. Focal defects are identified when inter-eye exceeds 9-12 μm or when sector-specific thinning falls below this , enhancing sensitivity for early glaucomatous damage. These criteria, derived from SD-OCT, outperform disc photography in detecting pre-perimetric . Progression monitoring employs event-based analysis of serial OCT scans, where significant —such as a confirmed decrease of ≥5 μm in average RNFL or in two or more clock-hour sectors—indicates advancement. This approach correlates strongly with loss, as RNFL thinning in affected sectors often precedes corresponding perimetric defects by months to years. In POAG, event-based methods detect progression in up to 85% of clock-hour sectors when changes occur in adjacent areas. Glaucoma subtypes exhibit distinct RNFL patterns: POAG shows gradual thinning at 0.86-1.07 μm/year, while angle-closure features more rapid initial loss, particularly post-acute episodes, with global RNFL decreasing markedly within the first 3 months after intervention. In treated primary angle-closure , rates slow but remain higher than in stable POAG eyes. Longitudinal studies affirm RNFL thickness as an early biomarker in glaucoma, with thinning detectable up to 6 years before optic disc cupping or visual field progression in pre-perimetric cases. These findings, from cohorts followed for 5-10 years, underscore RNFL's role in predicting conversion from ocular hypertension to glaucoma.

Involvement in Neurodegenerative Disorders

The retinal nerve fiber layer (RNFL) undergoes significant alterations in (MS), particularly in association with (ON), where acute episodes lead to pronounced axonal loss. Following an acute ON episode in MS patients, RNFL thickness typically decreases by 20-40 μm within 3-6 months, reflecting irreversible neurodegeneration. This thinning is often asymmetric, with greater reduction in the affected eye compared to the fellow eye, and persists even after visual recovery. Moreover, RNFL thickness in MS correlates with global atrophy, as minimum RNFL measures predict up to 21% of the variance in brain parenchymal fraction, independent of prior ON history. In (AD), RNFL exhibits global thinning of approximately 10-15 μm compared to age-matched controls, a change detectable via (OCT) and indicative of widespread (RGC) degeneration. This thinning correlates with , where lower RNFL thickness associates with reduced performance on and executive function tests, serving as a potential early marker of disease severity. Additionally, AD involves selective loss of melanopsin-expressing RGCs, which contribute to non-image-forming visual functions and show abnormal morphology with amyloid-beta deposition, exacerbating circadian disruptions. Recent 2025 reviews highlight these RNFL changes as part of broader retinal neurodegeneration mirroring cortical . In (PD), RNFL thickness is reduced by approximately 10-12 μm globally compared to controls, with more pronounced thinning in the inferior quadrant (up to 15 μm), as measured by OCT in studies up to 2023. This axonal loss correlates with disease duration, Unified Parkinson's Disease Rating Scale (UPDRS) scores, and cognitive decline, positioning RNFL as a non-invasive for tracking neurodegeneration and motor/cognitive progression. Retinitis pigmentosa (RP), a hereditary photoreceptor , leads to secondary peripheral RNFL reduction due to transneuronal degeneration of RGCs driven by upstream photoreceptor loss. OCT studies reveal thinning predominantly in the inferior quadrant (up to 32% of affected eyes), with mean RNFL thickness averaging 97.6 μm versus thicker temporal sectors, reflecting vascular and structural remodeling in the inner . , characterized by central sensitization, is associated with subtle asymmetric RNFL thinning, particularly in temporal sectors (3-8 μm reduction), suggesting underlying neurodegenerative processes despite limited longitudinal evidence. This pattern, more evident in biologic fibromyalgia subgroups, supports retinal changes as a marker of hypersensitivity, though larger studies are needed to confirm causality. In mellitus (T2DM), RNFL thinning of 5-10 μm occurs early and associates with severity, independent of status. This reduction correlates with (MCI), as thinner RNFL in T2DM-MCI patients links to lower scores, highlighting retinal measures as indicators of systemic neural damage. Recent studies from 2024-2025 position RNFL thickness, assessed via OCT, as a non-invasive for AD progression, with baseline thinning predicting cognitive decline over five years and integrating with multimodal retinal imaging for early detection.

Modulating Factors

Demographic Influences

The thickness of the retinal nerve fiber layer (RNFL) varies significantly across ethnic groups, influenced by factors such as genetic predispositions and size. Individuals of African descent typically exhibit thicker RNFL measurements, with average values ranging from 110 to 115 μm, compared to 90 to 110 μm in those of Caucasian descent and 95 to 115 μm in those of Asian descent.31684-1/fulltext) These differences persist even after adjusting for area, suggesting underlying genetic contributions to axonal density and distribution. Multicenter studies, including the African Descent and Evaluation Study (ADAGES) conducted in 2010, have confirmed these ethnic variations through (OCT) assessments in healthy populations, emphasizing the need for ethnicity-specific normative databases to enhance diagnostic precision in conditions like . Age-related changes represent another key demographic influence on RNFL thickness, characterized by a progressive thinning that occurs linearly at an average rate of 0.3 μm per year across adulthood. This decline accelerates in older individuals, exceeding 2 μm per decade after age 60, particularly in the superior and inferior quadrants where axonal loss is more pronounced. Longitudinal and cross-sectional analyses in healthy cohorts have established this pattern, attributing it to physiologic axonal attrition rather than , though the exact mechanisms remain under investigation. Gender also exerts a subtle effect on RNFL thickness, with males generally showing slightly thicker layers by 2 to 5 μm compared to females, potentially linked to hormonal differences influencing axonal development or . This disparity is observed in average global thickness and specific quadrants, as documented in population-based OCT studies of healthy adults.00085-X/fulltext) Overall, these demographic influences—ethnicity, age, and —necessitate tailored reference ranges in to avoid misinterpretation of RNFL measurements and ensure accurate assessment of health.

Ocular and Systemic Variables

The retinal nerve fiber layer (RNFL) thickness is influenced by various ocular variables, including axial length, which shows a negative with peripapillary RNFL thickness (pRNFLT) in healthy populations, with longer axial lengths associated with thinner RNFL (decrease of approximately 1.02–2.2 μm per mm increase; P < 0.001). Similarly, modulates RNFL thickness, as hyperopia is linked to thicker RNFL compared to , with spherical equivalent positively correlating in multivariate analyses (increase of 0.62 μm per diopter; P < 0.001). Optic disc area also plays a role, exhibiting a positive association where larger disc areas correspond to thicker RNFL (increase of about 3.3 μm per mm²; P = 0.010). Other ocular factors include , with lower levels associated with thicker RNFL (P = 0.004), and central corneal thickness, where thinner corneas correlate with increased RNFL thickness (P = 0.02). Additionally, a history of is positively associated with temporal quadrant pRNFLT (increase of 4.30 μm; P < 0.001), potentially due to postoperative changes in or lens status. Systemic variables further modulate RNFL characteristics, with diabetes mellitus consistently linked to RNFL thinning across quadrants, reflecting axonal loss in retinal ganglion cells (decrease of 1.69 μm overall; P = 0.004). Hypertension similarly contributes to reduced pRNFLT, particularly in patients with , where longer disease duration exacerbates thinning (P < 0.001), and systemic elevates the risk of multiple RNFL defects (odds ratio 7.49; 95% CI: 1.96–17.45). shows a positive with overall RNFL thickness (increase of 0.19 μm per unit; P = 0.002), possibly related to metabolic influences on retinal . Shorter stature is associated with thicker RNFL in univariate analyses (P < 0.001), though this may reflect broader anthropometric effects. More severe systemic conditions, such as end-stage renal disease and , heighten the prevalence of multiple RNFL defects (odds ratios 73.70 and 26.60, respectively; P < 0.001), indicating vascular contributions to RNFL integrity. A history of is negatively correlated with temporal pRNFLT (decrease of 2.21 μm; P = 0.011).

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