Clinical and etiological profile of patients with bitemporal optic disc pallor visiting at a tertiary eye hospital

Abstract

Background

Bitemporal optic disc pallor may result from chiasmal compression as well as bilateral toxic, nutritional, hereditary, or inflammatory optic neuropathies. Data describing its clinical and etiological profile in Nepal are limited. This study was conducted with the aim to describe the clinical and etiological profile of patients with bitemporal optic disc pallor and to evaluate the relationship between clinical, visual-field, neuroimaging, and OCT findings.

Methods

A hospital-based prospective, cross-sectional study was conducted among patients with clinically documented bitemporal optic disc pallor presenting to Biratnagar Eye Hospital, Nepal. The minimum calculated sample size was 49, and 50 participants were included in the final analysis. Demographic and clinical findings, Humphrey visual-field patterns, neuroimaging findings, optical coherence tomography-derived retinal nerve fibre layer (RNFL) and macular ganglion cell analysis (GCA) measurements, and relevant blood investigations were evaluated. Data were summarized using frequencies, percentages, means, and standard deviations.

Results

The mean age of participants was 38.58 ± 15.20 years, and 58.0% were male. Diminution of vision was the predominant presenting complaint (88.0%). Central scotoma was the most common visual-field defect (48.0%), followed by cecocentral scotoma (26.0%) and bitemporal hemianopia (20.0%). Nutritional optic neuropathy was the most frequent etiology (26.0%), followed by toxic optic neuropathy (20.0%); Leber hereditary optic neuropathy and inflammatory optic neuropathy each accounted for 18.0%. Pituitary macroadenoma was present in 16.0% and Rathke cleft cyst in 2.0%. Bitemporal hemianopia was predominantly associated with sellar lesions. The combined pituitary macroadenoma/Rathke cleft cyst group had the lowest mean RNFL thickness (67.4 ± 10.7 μm). Temporal RNFL thinning was more prominent in toxic optic neuropathy and Leber hereditary optic neuropathy, with mean temporal RNFL values of 39.5 and 40.8 μm, respectively.

Conclusions

Bitemporal optic disc pallor demonstrated a diverse etiological spectrum. Sellar lesions were predominantly associated with bitemporal hemianopia and greater overall RNFL loss, whereas non-sellar optic neuropathies were more frequently associated with central or cecocentral scotomas and temporal RNFL thinning. Combined clinical examination, visual-field assessment, neuroimaging, and optical coherence tomography may assist in differentiating the underlying causes.

Introduction

Bitemporal optic disc pallor is an important neuro-ophthalmic finding that may indicate involvement of the optic chiasm or bilateral optic nerves. Because the optic chiasm lies immediately above the pituitary gland within the sellar region, it is particularly vulnerable to compression from sellar, parasellar and suprasellar lesions. Pituitary adenomas are among the most common causes of chiasmal compression, while other lesions, including craniopharyngiomas, meningiomas, and other sellar, parasellar or suprasellar masses, may also cause optic chiasmal compression. Non-compressive causes, including nutritional, toxic, inflammatory, and ischemic optic neuropathies, may also produce bilateral optic disc pallor [1, 2].

Chronic compression or injury of the afferent visual pathway can result in irreversible axonal degeneration and optic atrophy [2]. Visual-field examination is therefore an important component of evaluation, with bitemporal hemianopia being the characteristic defect associated with optic chiasmal involvement. Visual-field loss can substantially affect functional vision and quality of life, emphasizing the importance of early recognition and appropriate investigation [3]. Previous studies have also reported better visual outcomes with early diagnosis and timely treatment of compressive lesions, whereas delayed presentation may result in permanent visual impairment [4].

The evaluation of patients with bitemporal optic disc pallor requires correlation of clinical findings with functional and structural investigations. Humphrey automated perimetry helps characterize the pattern and severity of visual-field loss, while magnetic resonance imaging or computed tomography of the sellar, parasellar, and suprasellar regions can identify compressive or infiltrative lesions [1, 5]. Optical coherence tomography (OCT), including retinal nerve fibre layer (RNFL) and macular ganglion cell analysis (GCA), provides an objective assessment of retinal ganglion-cell axonal loss and may further characterize the pattern of optic neuropathy.

Despite the clinical importance of this condition, there is limited published information from Nepal regarding the etiological spectrum, clinical presentation, visual-field patterns and relationship between optic disc findings and neuroimaging in patients with bitemporal optic disc pallor. The present study was therefore undertaken with aim to describe the clinical and etiological profile of patients with bitemporal optic disc pallor presenting to Biratnagar Eye Hospital, Nepal, and to evaluate the relationship between clinical, visual-field, neuroimaging and OCT findings.

Objectives

General objective:

To describe the clinical and etiological profile of patients with bitemporal optic disc pallor presenting to Biratnagar Eye Hospital, Nepal.

Specific objectives:

1. To describe the patterns of visual-field defects in patients with bitemporal optic disc pallor.

2. To correlate clinical findings with MRI/CT imaging findings in patients with bitemporal optic disc pallor.

3. To correlate optic disc pallor with retinal nerve fiber layer (RNFL) thickness and macular ganglion cell analysis (GCA).

Methods

Study design and setting

This hospital-based prospective, cross-sectional study was conducted in the Department of Pediatric and Neuro-ophthalmology at Biratnagar Eye Hospital, Nepal, a tertiary referral eye-care center serving patients from eastern Nepal and neighboring regions.

Study population and sample size

The study population comprised patients presenting to Biratnagar Eye Hospital with clinically documented bitemporal optic disc pallor. The minimum sample size was calculated using the standard formula for estimation of a single population proportion: n = Z²p(1 − p) / d², where Z = 1.96 for a 95% confidence level, p = 0.50 as a conservative estimate in the absence of local prevalence data, and d = 0.14 as the allowable margin of error.

Thus, n = (1.96² × 0.50 × 0.50) / (0.14²) ≈ 49. Therefore, the minimum required sample size was 49 participants. A total of 50 participant records fulfilling the eligibility criteria were available for the final analysis.

Sampling and eligibility criteria

Purposive sampling was used. Patients aged 18 years or older with a clinical diagnosis of bitemporal optic disc pallor and who were willing to participate were eligible. Patients with media opacity preventing adequate optic disc evaluation and those unwilling to participate were excluded.

Data collection and clinical assessment

Demographic and clinical information was collected prospectively from patients presenting to Biratnagar Eye Hospital with clinically documented bitemporal optic disc pallor using a structured clinical proforma. Data were collected at the time of presentation and clinical assessment. Variables included age, sex, presenting complaints, visual acuity, pupillary reaction, color vision, visual-field findings, OCT parameters, neuroimaging findings, and relevant blood investigations. Best-corrected visual acuity was assessed using a Snellen chart. Visual-field testing was performed using Humphrey automated perimetry, and reliable examinations were included. Optic disc and OCT images were initially reviewed by one author. In cases of diagnostic doubt or uncertainty, both authors independently reviewed the images and a consensus opinion was documented.

OCT, neuroimaging and laboratory investigations

OCT was used to assess peripapillary RNFL thickness and macular GCA. OCT was performed using the ZEISS CIRRUS HD-OCT 5000 (Carl Zeiss Meditec, Dublin, CA, USA). Peripapillary RNFL thickness was assessed using the Optic Disc Cube 200 × 200 protocol, and macular ganglion cell analysis (GCA) was obtained from the macular cube scan. MRI or CT of the sellar and suprasellar region was reviewed to identify structural causes such as pituitary adenoma or other compressive/infiltrative lesions. Relevant blood investigations included hemoglobin, vitamin B12 and serum folate where available.

Data analysis

Data were entered into Microsoft Excel and analyzed using Statistical Package for the Social Sciences (SPSS) version 20. Categorical variables were summarized as frequencies and percentages, while continuous variables were summarized using means and standard deviations. Etiology-wise RNFL and GCA measurements and visual-field patterns were compared descriptively. No inferential statistical testing was performed.

Ethical considerations

The study was conducted in accordance with the Declaration of Helsinki. It was conducted after appropriate ethical approval and informed consent. Participant confidentiality was maintained, participation was voluntary, and participants could withdraw without affecting their medical care. The study was approved by the Institutional Review Committee (IRC) of Biratnagar Eye Hospital, affiliated with the Nepal Health Research Council (NHRC), under approval number BEH-IRC-151/2026. Ethical approval was granted on 3 February 2026. No funding was received for this study.

Diagnostic criteria for etiological classification

The etiological diagnosis was established based on the clinical assessment and relevant ancillary investigations. Nutritional optic neuropathy was diagnosed when patients had a compatible bilateral optic neuropathy characterized by bilateral optic disc pallor with predominantly central or ceco-central visual-field involvement, together with clinical evidence of nutritional deficiency or relevant biochemical abnormalities where available, after consideration of alternative causes [6]. Toxic optic neuropathy was diagnosed when a compatible bilateral optic neuropathy was present, typically with central or ceco-central visual-field involvement and bilateral optic disc pallor, in the setting of a documented exposure to a recognized neurotoxic agent and after consideration of other potential causes [6].

Laboratory assessment included haemoglobin, serum vitamin B12 and serum folate where available. These investigations were interpreted in conjunction with the clinical findings rather than used in isolation to establish the diagnosis.

Results

After application of the inclusion and exclusion criteria, 50 participant records were available for analysis, exceeding the calculated minimum sample size by one participant.

Demographic characteristics

Participants were aged 18–70 years, with a mean age of 38.58 ± 15.20 years. There were 29 males (58.0%) and 21 females (42.0%). The largest age group was 18–30 years (38.0%), followed by 31–45 years (30.0%). The age distribution of the study participants is presented in Table 1.

Table 1.

Age distribution of study participants

Age group (years)	Frequency	Percentage
18–30	19	38.0%
31–45	15	30.0%
46–60	10	20.0%
> 60	6	12.0%
Total	50	100.0%

Presenting complaints

Diminution of vision was the predominant presenting complaint. It occurred alone in 44 participants (88.0%), with headache in 5 (10.0%), while 1 participant (2.0%) reported headache alone.

Results

Visual-field findings

Humphrey visual-field testing demonstrated several patterns. Central scotoma was the most frequently recorded pattern (48.0%), followed by ceco-central scotoma (26.0%) and bitemporal hemianopia (20.0%). Three participants (6.0%) could not complete or did not have a usable visual-field result. These three participants were included in the overall study analysis but were excluded from visual-field pattern-specific analysis because no usable visual-field result was available. The distribution of visual-field patterns is presented in Table 2.

Table 2.

Visual-field patterns

Visual-field pattern	Frequency	Percentage
Bitemporal hemianopia	10	20.0%
Central scotoma	24	48.0%
Cecocentral scotoma	13	26.0%
Could not be done	3	6.0%
Total	50	100.0%

Etiological profile

Nutritional optic neuropathy was the most frequent recorded etiology (26.0%), followed by toxic optic neuropathy (20.0%). Leber hereditary optic neuropathy and inflammatory optic neuropathy each accounted for 18.0%. Pituitary macroadenoma accounted for 16.0% and Rathke cleft cyst for 2.0%. The etiological distribution of the study participants is presented in Table 3.

Table 3.

Etiological distribution

Etiology	Frequency	Percentage
Pituitary macroadenoma	8	16.0%
Rathke cleft cyst	1	2.0%
Nutritional optic neuropathy	13	26.0%
Toxic optic neuropathy	10	20.0%
Leber hereditary optic neuropathy	9	18.0%
Inflammatory optic neuropathy	9	18.0%
Total	50	100.0%

Neuroimaging findings

Neuroimaging was reported as within normal limits in 36 participants (72.0%). Pituitary macroadenoma was reported in 8 (16.0%), Rathke cleft cyst in 1 (2.0%), prominent optic nerves in 3 (6.0%), and thinning of optic nerves in 2 (4.0%).

OCT findings

The OCT-derived RNFL and macular GCA measurements are presented in Table 4.

Table 4.

OCT-derived RNFL and macular GCA measurements

OCT parameter	Mean ± SD	Median	Range	Valid n
RNFL thickness – right eye	77.68 ± 14.91 μm	79.0	50–106	50
RNFL thickness – left eye	75.94 ± 16.83 μm	77.5	23–106	50
Macular GCA – right eye	58.74 ± 11.03 μm	58.0	33–81	50
Macular GCA – left eye	58.54 ± 13.75 μm	59.0	12–82	50

Hematologic investigations

Mean hemoglobin was 12.86 ± 1.62 g/dL, vitamin B12 was 346.26 ± 210.62 pg/mL, and serum folate was 6.43 ± 5.20 ng/mL. Using the stated reference intervals, haemoglobin was below 12 g/dL in 17 participants (34.0%), vitamin B12 was below 192 pg/mL in 19 participants (38.0%), and serum folate was at or below 5.21 ng/mL in 28 participants (56.0%).

Relationship between etiology and visual-field pattern

The relationship between etiology and visual-field pattern is presented in Table 5.

Table 5.

Etiology-wise visual-field patterns

Etiology	Bitemporal hemianopia	Central scotoma	Cecocentral scotoma	*Could not be done	Total
Pituitary macroadenoma (n = 8)	7 (87.50%)	0 (0%)	0 (0%)	1 (12.50%)	8 (100%)
Rathke cleft cyst (n = 1)	1 (100%)	0 (0%)	0 (0%)	0 (0%)	1 (100%)
Nutritional optic neuropathy (n = 13)	2 (15.38%)	6 (46.15%)	5 (38.46%)	0 (0%)	13 (100%)
Toxic optic neuropathy (n = 10)	0 (0%)	6 (60.00%)	3 (30.00%)	1 (10.00%)	10 (100%)
Leber hereditary optic neuropathy (n = 9)	0 (0%)	5 (55.56%)	3 (33.33%)	1 (11.11%)	9 (100%)
Inflammatory optic neuropathy (n = 9)	0 (0%)	7 (77.78%)	2 (22.22%)	0 (0%)	9 (100%)

* These three participants were included in the overall study analysis but were excluded from visual-field pattern-specific analysis because no usable visual-field result was available

Etiology-wise OCT findings

The etiology-wise OCT findings are presented in Table 6. OCT measurements were obtained using the ZEISS CIRRUS HD-OCT 5000. RNFL measurements were derived from the Optic Disc Cube 200 × 200 protocol, and macular GCA measurements were obtained from macular OCT analysis.

Table 6.

Etiology-wise OCT findings

Etiology	n	Mean RNFL (µm), mean ± SD	Mean macular GCA (µm), mean ± SD
Pituitary macroadenoma / Rathke cleft cyst	9 (18%)	67.4 ± 10.7	56.2 ± 11.8
Toxic optic neuropathy	10 (20.0%)	81.0 ± 17.9	55.7 ± 12.1
Leber hereditary optic neuropathy	9 (18.0%)	80.2 ± 13.1	56.4 ± 9.9
Nutritional optic neuropathy	13 (26.0%)	79.3 ± 16.1	63.5 ± 11.3
Inflammatory optic neuropathy	9 (18.0%)	74.6 ± 13.3	59.6 ± 13.8

Sector-level OCT analysis demonstrated a generalized pattern of reduced RNFL thickness in the combined pituitary macroadenoma/Rathke cleft cyst group. Temporal RNFL thickness was particularly reduced in toxic optic neuropathy and Leber hereditary optic neuropathy, with mean temporal RNFL values of 39.5 μm and 40.8 μm, respectively. Nutritional and inflammatory optic neuropathies also demonstrated reduced temporal-sector RNFL thickness. These findings were descriptive; no inferential statistical testing was performed. The etiology-wise sectoral RNFL measurements, with device-specific normative reference values for contextual interpretation, are presented in Table 7

Table 7.

Etiology-wise sectoral RNFL findings

Etiology	Superior (µm)	Inferior (µm)	Nasal (µm)	Temporal (µm)
Pituitary macroadenoma / Rathke cleft cyst	82.8	85.2	57.4	43.0
Toxic optic neuropathy	109.8	113.7	61.9	39.5
Leber hereditary optic neuropathy	111.9	102.3	64.2	40.8
Nutritional optic neuropathy	108.9	101.6	60.9	43.6
Inflammatory optic neuropathy	96.5	93.1	57.6	41.4
Approximate published normal reference*	~ 110–115	~ 110–115	~ 65–75	~ 50–60

*Published normative reference values from the ZEISS CIRRUS HD-OCT normative database are provided for contextual interpretation of the sectoral RNFL measurements. All OCT examinations in the present study were performed using the same ZEISS CIRRUS HD-OCT 5000 platform. As this was a descriptive cross-sectional study without a separate healthy control group, the normative values were not used for statistical comparison

Discussion

In the present study, nutritional optic neuropathy was the most common etiology (26%), followed by toxic optic neuropathy (20%), while pituitary macroadenoma accounted for 16% of cases. This relatively broad etiological spectrum is consistent with the recognized causes of bilateral optic neuropathy, including nutritional, toxic, hereditary and compressive disorders.

Our finding of bitemporal hemianopia predominantly in pituitary macroadenoma is consistent with studies by Danesh-Meyer et al., who demonstrated the relationship between chiasmal compression and retinal nerve fibre layer loss, with visual-field defects reflecting the anatomical site of compression [7]. In our study, 7 of 8 (87.5%) patients with pituitary macroadenoma had bitemporal hemianopia, supporting the typical effect of chiasmal compression.

The lower mean RNFL thickness in the pituitary macroadenoma/Rathke cleft cyst group (67.4 ± 10.7 μm) compared with the non-sellar groups is consistent with the findings of Danesh-Meyer et al., who reported that OCT-derived RNFL thinning can reflect axonal loss in chiasmal compression [7]. Similarly, Monteiro et al. demonstrated structural retinal changes in patients with chiasmal compression, supporting the use of OCT as an objective marker of apparent visual pathway damage [8].

In contrast, our study demonstrated predominant temporal RNFL thinning in toxic optic neuropathy and Leber hereditary optic neuropathy, with temporal RNFL values of 39.5 μm and 40.8 μm, respectively. This finding is consistent with studies by Barboni et al., who described preferential involvement of the papillomacular bundle and corresponding retinal nerve fibre layer changes in Leber hereditary optic neuropathy [9, 10]. The predominance of central and ceco-central scotomas in these groups further supports this structure-function relationship.

Our findings of central and cecocentral scotomas in nutritional and toxic optic neuropathy are also consistent with the clinical pattern described in previous studies of toxic and nutritional optic neuropathies, where preferential papillomacular bundle involvement produces central visual dysfunction.¹ In our cohort, nutritional optic neuropathy was associated with 6 (46.2%) central and 5 (38.5%) ceco-central scotomas, while toxic optic neuropathy showed 6 (60.0%) central and 3 (30.0%) ceco-central scotomas.

Overall, our findings are consistent with previous studies demonstrating that compressive optic neuropathy produces generalized structural RNFL loss with characteristic bitemporal field defects, whereas toxic, nutritional and mitochondrial optic neuropathies preferentially affect the papillomacular bundle, producing temporal RNFL thinning and central or cecocentral scotomas. The present study therefore supports the complementary role of visual-field testing and OCT in differentiating the underlying etiologies of bitemporal optic disc pallor.

Strengths and limitations

The study provides a combined descriptive assessment of clinical findings, visual fields, neuroimaging, OCT and laboratory investigations across several etiological categories. However, the sample size was small, the study was hospital-based, and the cross-sectional design limits generalizability and assessment of longitudinal outcomes. Visual-acuity entries were heterogeneous, and no inferential statistical testing was performed; therefore, differences between etiological groups should be interpreted as descriptive rather than statistically significant associations.

Conclusions

Bitemporal optic disc pallor in this tertiary-care population demonstrated a diverse etiological spectrum, with nutritional and toxic optic neuropathies being the most frequent causes. Pituitary macroadenoma was the predominant sellar lesion and was strongly associated with bitemporal hemianopia. Non-sellar etiologies, particularly toxic, nutritional and Leber hereditary optic neuropathy, were more commonly associated with central or cecocentral scotomas and temporal RNFL thinning. OCT findings demonstrated reduced RNFL and macular GCA measurements, with greater overall RNFL loss in the sellar-lesion group. These findings highlight the complementary value of detailed visual-field assessment, neuroimaging and OCT in the evaluation and etiological differentiation of patients with bitemporal optic disc pallor. Further studies with larger samples and formal statistical analysis are warranted to validate these observed structure-function relationships.

Abbreviations

BEH

Biratnagar eye hospital

CT

Computed tomography

DOV

Diminution of vision

GCA

Ganglion cell analysis

Hb

Haemoglobin

LHON

Leber hereditary optic neuropathy

MRI

Magnetic resonance imaging

OCT

Optical coherence tomography

RAPD

Relative afferent pupillary defect

RNFL

Retinal nerve fibre layer

SD

Standard deviation

SPSS

Statistical package for the social sciences

WNL

Within normal limits

Author contributions

Both authors contributed to the conception and design of the study, clinical/data collection, interpretation of findings, manuscript preparation and critical revision, and final approval of the version to be submitted. Both authors agree to be accountable for all aspects of the work and to ensure that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Funding

No funding was received for this study.

Data availability

The underlying participant-level data are contained in the study master chart and are not publicly available because they contain potentially identifiable clinical information and are subject to institutional and ethical restrictions. De-identified data may be made available from the corresponding author on reasonable request, subject to approval by the Institutional Review Committee and applicable confidentiality requirements.

Declarations

Ethics approval and consent to participate

The study was approved by the Institutional Review Committee (IRC) of Biratnagar Eye Hospital, affiliated with the Nepal Health Research Council (NHRC), under approval number BEH-IRC-151/2026. The approval was granted on 3 February 2026. The study was conducted in accordance with the Declaration of Helsinki and the approved research protocol. Informed consent was obtained from participants in accordance with the approved protocol. Participant confidentiality was maintained throughout the study, and participation was voluntary; participants could withdraw without affecting their medical care.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.