Introduction
Glaucoma is a chronic, progressive optic neuropathy that can cause irreversible visual loss and requires lifelong monitoring and treatment. Visual impairment can restrict reading, mobility, driving, independence, and quality of life. Long-term therapy and repeated testing add further burden.1–5 Anxiety and depressive symptoms are also common in people with glaucoma, although reported prevalence varies across settings.6–14 Previous reviews have addressed psychiatric burden, management of anxiety and depression, and physiological and psychological stress in glaucoma.15–17 Proposed links between anxiety, depression, and glaucoma include hypothalamic–pituitary–adrenal (HPA) axis activation, cortisol changes, autonomic and vascular responses, inflammation, and sleep disturbance, although their effects on long-term glaucoma progression remain uncertain.17 Our review builds on these findings by comparing both directions of association, separating short-term IOP and VF effects from longitudinal structural outcomes, integrating observational studies with genetic evidence, and examining whether interventions demonstrate disease modification.
This distinction matters clinically because anxiety and depression may impair quality of life, adherence, and treatment engagement even if they do not alter glaucoma progression.
This review examines two directions of association. First, we assess how glaucoma, visual impairment, and treatment burden may contribute to anxiety and depression. Second, we assess whether anxiety or depression affects intraocular pressure (IOP), visual field (VF) outcomes, retinal nerve fiber layer (RNFL) loss, glaucoma conversion, or long-term progression.
We separate transient physiological or test-related changes from sustained structural or functional progression and consider genetic causal analyses and intervention studies. Our aim is to clarify the strength of evidence in each direction, the limits of causal inference, and the implications for clinical care.
Methods
This structured narrative review used reproducible search and screening procedures followed by critical synthesis. A narrative approach was chosen because the evidence spans prevalence studies, longitudinal cohorts, acute experiments, intervention trials, and genetic causal analyses. These study types address different questions and cannot be meaningfully combined into a single pooled estimate.
This was not a systematic review or meta-analysis, and we did not perform formal certainty-of-evidence grading. We evaluated evidence separately for glaucoma as a contributor to anxiety and depression and for anxiety or depression as a potential influence on glaucoma outcomes. We considered literature published from 1 January 2010 to 31 July 2026, while retaining earlier landmark sources needed to define glaucoma outcomes, psychometric instruments, and measurement principles.
Causal interpretations required clear temporality, control of confounding, and reliable longitudinal outcomes.
PubMed, Web of Science Core Collection, China National Knowledge Infrastructure (CNKI), Wanfang Data, and VIP Database were searched. Google Scholar was used as a supplementary source to identify potentially relevant reports missed by the five primary databases; reference lists and citing articles were also checked. Primary database searches combined glaucoma terms with anxiety/depression terms (Table 1).
For each Google Scholar query, all displayed results were screened consecutively in batches of up to 50 records.Table 1Database Search StrategyDatabase/sourceSearch Strategy and Source-Specific UsePubMed#1 Disease/subtype terms: (glaucoma*[Title/Abstract] OR glaucomatous[Title/Abstract])#2 Anxiety/depression terms: (anxiety[Title/Abstract] OR anxious[Title/Abstract] OR depression[Title/Abstract] OR depressive[Title/Abstract])Final set: #1 AND #2Web of Science Core Collection#1 Disease/subtype terms: TS=(glaucoma* OR glaucomatous)#2 Anxiety/depression terms: TS=(anxiety OR anxious OR depression OR depressive)Final set: #1 AND #2CNKI#1 Subject terms: glaucoma OR green-wind internal obstruction (traditional Chinese-medicine term; English translation)#2 Terms: anxiety OR depressionExecuted using the Chinese-language equivalents and the original database field/operator syntax.Wanfang Data#1 Disease terms: glaucoma OR green-wind internal obstruction (English translations)#2 Psychological terms: anxiety OR depressionCombined with AND in the original Chinese-language search.VIP Database#1 Title/topic or keyword fields: glaucoma OR green-wind internal obstruction (English translations)#2 Title/topic or keyword fields: anxiety OR depressionFinal combination: #1 AND #2; original queries were entered in Chinese.Google Scholar,reference-listscreening, andcitation trackingSupplementary title-restricted Google Scholar searches were used to check for relevant reports not found through the five indexed databases. Queries: allintitle: glaucoma anxiety; allintitle: glaucoma depression; allintitle: glaucomatous anxiety; allintitle: glaucomatous depression; allintitle: glaucoma anxious; allintitle: glaucoma depressive. For each query, all displayed results were screened in successive batches of up to 50 records.
Reference lists and forward citations were also checked.Time span (index date)1 January 2010–31 July 2026; final search update: 31 July 2026.Notes: #1 and #2 indicate database-specific search blocks. CNKI, Wanfang and VIP terminology is shown here in English translation as required by the journal; the original searches used the corresponding Chinese characters and sourcespecific field operators. The English renderings are explanatory rather than executable English queries.
Eligible evidence included human clinical studies with validated anxiety/depression measures or documented diagnoses. We also included systematic reviews and meta-analyses, Mendelian randomization and shared-genetics analyses, human acute-stress experiments relevant to glaucoma measurements, measurement-validation studies, and intervention trials. Studies of glaucoma suspects were included only if they assessed conversion or longitudinal glaucoma outcomes.
Nonhuman and purely mechanistic studies were not treated as core evidence. We excluded reports limited to procedural anxiety or routine nursing without specific anxiety/depression assessment, mixed populations without separable glaucoma data, ineligible publication types, and reports with insufficient clinical or methodological detail. Acute stress and general distress were treated as related but distinct constructs and were discussed only when relevant to physiology, measurement, or screening.
We defined objective glaucoma outcomes using repeated or longitudinal IOP measures, VF progression, and RNFL thickness or thinning rates.1–5 A single IOP or VF measurement was not considered evidence of progression. Disease modification required sustained slowing of structural or functional deterioration, such as a lower prespecified VF or RNFL progression rate, rather than a transient change in IOP or test performance.
Two authors independently screened records. They extracted study design, glaucoma subtype and severity, psychological measure or diagnosis, sample size, unit of analysis, handling of paired-eye data when relevant, follow-up, IOP, VF and RNFL outcomes, confounder adjustment, intervention characteristics, and limitations relevant to directional or causal interpretation. Disagreements were resolved by discussion.
Review-level estimates and primary studies were interpreted at their respective evidence levels; primary studies already included in a cited review or meta-analysis were not counted as independent replication.
The five databases yielded 3364 records: PubMed (n = 507), Web of Science Core Collection (n = 636), CNKI (n = 363), Wanfang Data (n = 999), and VIP Database (n = 859). After 1430 duplicates were removed, 1934 unique database records remained. Supplementary Google Scholar and citation searches produced 196 displayed results, from which 29 non-duplicate records were added.
This yielded 1963 records for title/abstract screening. We excluded 1846 records and assessed 117 full texts. Of these, 21 were excluded for insufficient methodological detail (n = 7), an ineligible population or intervention (n = 5), failure to address the stated directional question (n = 4), or secondary, duplicate, or unverifiable reports (n = 5).
The final narrative synthesis included 96 sources (Figure 1).Figure 1Study-selection flow diagram.Flowchart sequence: Identification, Screening, Eligibility, Included, with counts from 3364 records to 96 included.Flowchart sequence: Records identified through database searching, Duplicates removed, Database records after duplicates removed, Additional records identified from Google Scholar or reference checking, Titles or abstracts screened, Records excluded, Full text articles assessed, Full text articles excluded, Records included in final structured narrative synthesis. Text shown: Records identified through database searching, n equals 3,364. PubMed, n equals 507.
Web of Science, n equals 636. CNKI, n equals 363. Wanfang, n equals 999.
VIP, n equals 859. Duplicates removed, n equals 1,430. Database records after duplicates removed, n equals 1,934.
Additional records identified from Google Scholar or reference checking, n equals 29. Titles or abstracts screened, n equals 1,963. Records excluded, n equals 1,846.
Not relevant to glaucoma anxiety or depression; procedural anxiety or routine nursing; mixed or non glaucoma population; ineligible publication type; or insufficient clinical information. Full text articles assessed, n equals 117. Full text articles excluded, n equals 21.
Insufficient methodological detail, n equals 7. Wrong population or intervention, n equals 5. No glaucoma anxiety or depression relationship, n equals 4.
Secondary or duplicate or unverifiable coverage, n equals 5. Records included in final structured narrative synthesis, n equals 96.
The evidence included prevalence studies, longitudinal associations, acute experiments, interventions, and genetic causal analyses. We therefore used critical narrative synthesis rather than quantitative pooling. No de novo meta-analysis or formal certainty grading was performed.
We reserved stronger causal interpretations for studies with clear temporality, adequate confounder control, and reliable longitudinal endpoints.
Evidence That Glaucoma Contributes to Anxiety and Depression
Epidemiological Magnitude and Heterogeneity
Across meta-analyses, clinic cohorts, national databases, and population studies, anxiety and depressive symptoms are common in glaucoma, but estimates vary widely by setting and instrument. Groff et al pooled 45 studies and estimated anxiety in 25% (95% CI, 21%–30%) and depression in 19% (95% CI, 16%–23%) of patients with glaucoma.6 Yin et al reported higher pooled risks than in control populations (relative risk, 2.99 for anxiety and 5.92 for depression), with substantial heterogeneity.7 Clinic and population studies include both positive and null adjusted associations,8,9,11–13,18,19 and other reports show wide variation in prevalence and associated clinical factors.20–42 Overall, the literature indicates greater psychological burden at the population level, not universal psychiatric morbidity.
Psychological burden may differ by glaucoma subtype. Primary open-angle glaucoma (POAG) often has an insidious course, whereas primary angle-closure glaucoma (PACG) may present with acute symptoms, although both can be chronic. In a study comparing 50 patients with PACG and 50 with POAG, anxiety was reported in 66% vs 44% and depression in 56% vs 40%, respectively.
These single-center findings may not generalize to other populations.28
Visual Impairment and Disease Severity
The strongest evidence that glaucoma contributes to anxiety and depression relates to visual impairment and disease severity. Binocular or better-eye VF status and progression are associated with limitations in reading, mobility, driving, independence, and vision-related quality of life.43–46 A prospective cohort found that faster VF progression preceded later depressive symptoms.47 A nationwide South Korean cohort found a higher subsequent risk of depression in patients with glaucoma and visual impairment.11 Studies from Taiwan, Japan, and Croatia also linked greater glaucoma burden or damage with depressive or anxiety symptoms.18,19,48 In a 2026 Chinese tertiary-center study, greater visual impairment among adults with glaucoma-related blindness was associated with higher PHQ-9 scores and poorer vision-related quality of life.14 Other studies also link visual disability with psychological symptoms,49–51 although these associations may be weaker in early or preperimetric disease.52
Treatment and Monitoring Burden
Long-term treatment and monitoring can add psychological burden even when objective progression is stable. Contributing factors include lifelong topical therapy, repeated perimetry and OCT, laser or surgical decisions, treatment costs, uncertainty about target IOP, and fear of blindness.53–60 Anxiety and depressive symptoms have also been associated with poorer adherence and lower activation for glaucoma self-management.61–64 These findings support education, adherence support, and mental-health referral when needed.
Psychotropic medications may have ocular effects relevant to glaucoma care. Tricyclic antidepressants have anticholinergic effects, while some selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs) may affect pupil size or IOP, potentially increasing angle-closure risk in susceptible eyes. Topiramate can cause secondary angle closure through ciliochoroidal effusion and forward displacement of the lens–iris diaphragm.65–67 Topical timolol has also been associated with depressive symptoms, although causality remains uncertain.58 These considerations support individualized treatment rather than routine avoidance of appropriate psychiatric care.
Evidence That Anxiety and Depression May Influence Glaucoma-Related Outcomes
Most acute-stress studies do not assess chronic anxiety or depressive disorders. We therefore treat them as evidence of short-term physiological or measurement effects, not as direct evidence that anxiety or depression accelerates glaucoma progression.
Acute Physiological Responses and IOP
Evidence for IOP effects is strongest for acute stress. In a within-subject study of 36 patients with open-angle glaucoma (72 eyes), induced mental stress increased IOP and produced a short-term tendency toward worse VF mean deviation.68 A randomized acute-stress experiment in 39 patients with POAG found an IOP rise of about 4 mmHg.69 In a simulated clinical setting, higher anxiety was associated with transient IOP elevation consistent with a possible white-coat effect, although the participants were healthy volunteers.70 Perceived academic stress was also associated with higher IOP in a small study that included juvenile-onset open-angle glaucoma.71
These findings support short-term autonomic or neuroendocrine reactivity, but they do not show that chronic anxiety or depression increases sustained IOP exposure. One glaucoma study associated anxiety with features of the IOP profile,72 and medication-related findings further complicate interpretation.58,73 Behavioral pathways, such as poor adherence, may affect disease management without directly accelerating retinal ganglion cell loss. Overall, evidence supports acute state-related effects more strongly than chronic anxiety or depression causing sustained IOP dysregulation.
Visual-Field Performance and Longitudinal Progression
VF performance can vary with attention, fatigue, fixation, response behavior, and test-retest effects. Acute stress produced a short-term tendency toward worse mean deviation in one experiment, although immediate retesting and learning complicated interpretation.68 A prospective study found test-related anxiety but no significant association with conventional VF reliability indices.74 Standard reliability indices do not capture all psychophysical variability.75–81
A worse VF result during anxiety or depression may reflect underlying glaucoma, a transient measurement effect, or shared confounding. Current evidence does not show that chronic anxiety or depression independently accelerates VF decline. Progression should be based on reproducible longitudinal change and concordant structural and functional evidence, not on a single discordant field.
Structural Progression and Glaucoma Conversion
In a retrospective study of 251 eyes with open-angle glaucoma followed for at least two years, mean RNFL thinning was faster in the high-anxiety group than in the low-anxiety group (−1.96 ± 2.23 vs −0.68 ± 1.39 μm/year; P = 0.021). The difference should be interpreted cautiously because of substantial variability and the observational study design.72 Cross-sectional analyses provide weaker evidence. Serum neuropeptide Y was associated with psychological symptoms and glaucoma severity,82 and a 2025 PACG study linked anxiety/depressive scores with RNFL thickness and cup-to-disc ratio.13 No study has shown that improvement in anxiety or depression reverses established RNFL loss.
Longitudinal database studies extend the reverse hypothesis from progression to disease development. Among 3259 glaucoma suspects, anxiety and combined anxiety/depression diagnoses were associated with conversion during follow-up (adjusted hazard ratios, 1.16 and 1.27).83 A nationwide cohort also reported higher glaucoma incidence across depression-related categories.84 However, Mendelian randomization analyses did not establish robust direct causal effects in either direction.85–87 Genetic correlation, bidirectional MR, and colocalization likewise found no evidence that common negative emotional traits causally affect glaucoma.88 Thus, current observational signals do not establish anxiety or depression as independent glaucoma risk factors (Table 2).Table 2Representative Studies Informing the Two Directional Questions and Causal InterpretationDirection / DomainRepresentative Study / DesignKey FindingInterpretation / Main LimitationGlaucoma contributing to anxiety/depressionGroff et al, 2023;6 systematic review/meta-analysis, 45 studiesPooled anxiety prevalence was 25% (95% CI, 21%–30%) and depression prevalence was 19% (95% CI, 16%–23%).Supports increased psychological burden at the population level; instruments and settings were heterogeneous.Glaucoma contributing to anxiety/depressionWu et al, 2022;8 cross-sectional, 446 glaucoma patientsAnxiety and depressive symptoms were associated with vision-related quality of life and visual-function indices.Cross-sectional association; causal direction cannot be established.Glaucoma progression and later depressive symptomsDiniz-Filho et al, 2016;47 prospective cohort, 102 patients (204 eyes)Faster VF progression was associated with subsequent depressive symptoms.Supports temporality from glaucoma progression to later depressive symptoms; residual confounding remains possible.Severe visual impairment and depressive burdenLuo et al, 2026;14 cross-sectional, 110 adults with glaucoma-related blindness and caregiversGreater visual impairment was associated with higher depressive-symptom scores and poorer vision-related quality of life.Severe tertiary-center cohort; cross-sectional design.Acute stress and IOP/VFKeren et al, 2022;68 within-subject experiment, 36 OAG patients (72 eyes)Induced stress produced a modest IOP rise and a short-term tendency toward worse VF mean deviation.Acute state effect; does not establish chronic glaucoma progression.Acute stress and IOPFerreira et al, 2024;69 randomized acute-stress experiment, 39 POAG patientsIOP increased by approximately 4 mmHg during experimentally induced stress.Acute physiological response only; no longitudinal VF or RNFL endpoint.Testing anxiety and VF reliabilityMaheshwari et al, 2025;74 prospective comparative study, 300 patientsAnxiety was not significantly associated with conventional VF reliability indices.Test-related anxiety does not necessarily produce abnormal reliability indices or indicate progression.Anxiety and RNFL thinningShin et al, 2021;72 retrospective longitudinal study, 251 OAG eyes, follow-up ≥2 yearsHigh- vs low-anxiety RNFL thinning: −1.96 ± 2.23 vs −0.68 ± 1.39 μm/year (P = 0.021).Retrospective structural association; wide variability, confounding and lack of independent replication.Anxiety/depression and glaucoma conversionBerchuck et al, 2021;83 registry cohort, 3259 glaucoma suspectsAnxiety and combined anxiety/depression diagnoses were associated with glaucoma conversion (adjusted HRs 1.16 and 1.27).Administrative diagnoses and residual confounding; association does not establish causality.Depression and glaucoma incidenceJung et al, 2021;84 nationwide cohort, 922,769 adults aged 66 yearsDepressive symptoms/disorder were associated with higher subsequent glaucoma incidence.Large longitudinal association; administrative definitions and residual confounding limit causal inference.Shared genetics and causal inferenceZhang et al, 2024;86 observational, shared-genetics, and MR analysesShared genetic signals were identified, but MR did not establish a robust direct causal effect.Genetic overlap is not direct causation; instrument and ancestry assumptions apply.Genetic causal inferenceQi et al, 2025;88 UK Biobank/FinnGen genetic correlation, bidirectional MR, and colocalizationNo evidence of a causal relationship between common negative-emotion traits and glaucoma was identified.Constrains strong causal claims but does not exclude short-term physiological or behavioral effects.Abbreviations: CI, confidence interval; HR, hazard ratio; IOP, intraocular pressure; MD, mean deviation; MR, Mendelian randomization; OAG, open-angle glaucoma; POAG, primary open-angle glaucoma; RNFL, retinal nerve fiber layer; VF, visual field.
Psychological and Behavioral Interventions
Psychological and Patient-Centered Outcomes
Psychological and behavioral interventions can improve symptoms and patient-centered outcomes, but durable effects on glaucoma progression have not been shown. An eight-week Baduanjin randomized trial improved HADS anxiety/depression scores, sleep quality, and selected quality-of-life domains.89 A multicenter glaucoma-education trial reduced anxiety and improved knowledge over short follow-up.90 Neither trial assessed longitudinal VF or RNFL progression.
Short-Term IOP Responses to Stress-Reduction Interventions
Short-term mindfulness and breathing trials reported lower IOP together with changes in stress biomarkers, autonomic measures, or trabecular-meshwork gene expression.91–93 These findings suggest short-term physiological effects. They do not show that improvement in anxiety or depression mediates sustained IOP reduction or alters long-term VF or RNFL progression.
Short-Term Visual-Field Change vs Disease Progression
A randomized eye-yoga study in 27 patients with POAG reported small one-month changes in IOP, retinal vascular measures, and selected VF outcomes.94 Interpretation is limited by the small sample, short follow-up, possible retest effects, lack of validated psychological mediation, and a reported potential conflict of interest. Short-term VF change should not be interpreted as slower longitudinal VF progression.
Evidence for Modification of Glaucoma Progression
No identified intervention trial showed reversal of established RNFL loss, slower RNFL thinning, or slower prespecified VF progression.89–94 Current intervention evidence therefore supports psychological or short-term physiological benefit, not durable modification of glaucoma progression (Table 3).Table 3Representative Intervention Studies: Psychological Outcomes, Short-Term Physiological Responses, and Long-Term Glaucoma ProgressionStudyDesign / PopulationIntervention / Follow-UpMain OutcomesMain Interpretive LimitationZeng et al, 202689RCT; 112 enrolled, 102 completed; primary glaucomaBaduanjin; 8 weeksImproved HADS anxiety/depression scores, sleep quality, and selected quality-of-life domainsNo IOP, VF-progression, or RNFL endpointSkalicky et al, 201890Multicenter RCT; 101 newly diagnosed glaucoma patientsPatient-centered education; 4 weeksReduced anxiety and improved knowledge; no significant between-group difference in treatment satisfactionPatient-centered benefit; no longitudinal VF or RNFL progression endpointDada et al, 201891RCT; 90 POAG patients (180 eyes)Mindfulness meditation; 21 daysLower short-term IOP and stress biomarkers; improved quality of lifeShort duration; no longitudinal VF or RNFL progression endpointDada et al, 202192Parallel-arm, single-masked RCT; 60 medically uncontrolled POAG patientsMindfulness; 3 weeksGreater short-term IOP reduction, altered diurnal IOP, and trabecular-meshwork gene-expression changesNo validated anxiety/depression mediation; no VF or RNFL progression slopeDada et al, 202493RCT; 80 POAG patients365-breathing technique; 6 weeksLower mean IOP and serum cortisol; altered autonomic measuresShort-term physiological response; no longitudinal VF or RNFL endpointZhou et al, 202594Exploratory RCT; 27 POAG patientsEye yoga; 1 monthSmall short-term changes in IOP, retinal vascular measures, and selected VF outcomesVery small sample, short follow-up, possible retest effects, no psychological mediation, and reported potential conflict of interestAbbreviations: HADS, Hospital Anxiety and Depression Scale; IOP, intraocular pressure; POAG, primary open-angle glaucoma; RCT, randomized controlled trial; RNFL, retinal nerve fiber layer; VF, visual field.
Discussion
Overall Interpretation of the Evidence
Evidence is asymmetric. The direction from glaucoma to anxiety and depression is supported by prevalence data, severity gradients, functional associations, and longitudinal observations.6,7,11,14,43,47 The reverse direction is less certain. Acute or perceived stress can alter IOP and may affect VF performance,68–71 while observational studies link psychological factors with RNFL thinning, glaucoma conversion, incidence, or structural markers.13,72,82–84 These findings lack independent replication with repeated validated psychological assessments and prespecified progression endpoints.
Importantly, the volume of literature should not be confused with the strength of causal evidence. Most studies describe prevalence, burden, or cross-sectional associations; only a small subset directly addresses temporality, longitudinal progression, or causality.
Genetic analyses further weaken strong reverse-direction claims. Mendelian randomization did not establish a robust direct causal relationship in the tested directions,85–87 and genetic correlation, bidirectional MR, and colocalization found no evidence that common negative emotional traits cause glaucoma.88 UK Biobank analyses reported reciprocal observational associations but did not demonstrate direct modification of glaucoma progression.95
IOP-independent pathways involving autonomic, neuroendocrine, vascular, and inflammatory processes may contribute to retinal ganglion-cell vulnerability. However, demonstrating neuroprotection requires evidence of sustained slowing of VF or RNFL progression; improvements in psychological symptoms or short-term IOP alone are insufficient.17,96
These distinctions matter clinically. Psychological benefit, short-term physiological or measurement effects, and durable modification of glaucoma progression are not equivalent. Relief of anxiety or depression is valuable even if objective progression is unchanged.
Evidence of disease modification would require sustained slowing of VF or RNFL progression after the intervention.
Clinical Implications
Current evidence supports targeted psychological screening rather than assuming psychiatric morbidity in all patients with glaucoma. Screening is most relevant when worry is persistent, mood symptoms impair functioning, visual loss is substantial, or long-term management disrupts treatment engagement.31,33,48,57 HADS, GAD-7, and PHQ-9 can quantify anxiety and depressive symptoms.97–99 In 300 patients with POAG, the Distress Thermometer performed well as a brief screen against HADS, although it measures general distress rather than a psychiatric diagnosis.100 Positive screens require clinical interpretation and referral when appropriate. Psychological symptoms should not be assumed to explain an isolated abnormal test result, nor should a single discordant test prompt treatment escalation.
When VF results conflict with OCT, optic-disc, or IOP trends, test reliability and repeatability should be reviewed before concluding that progression has occurred.75–81 Reproducible structural and functional decline should be managed according to glaucoma evidence regardless of coexisting anxiety or depression.
Severe depression warrants attention to suicidal ideation and self-harm risk, particularly in patients with advanced visual loss. A population-based study reported an association between glaucoma and suicidal ideation, without establishing causality.27 Patients at risk should receive timely mental-health assessment.
Mental-health care should complement, not replace, evidence-based IOP-lowering treatment. The lack of proven effects on glaucoma progression does not reduce the value of symptom relief, better quality of life, adherence support, and treatment engagement. Anxiety and depressive symptoms have been associated with poorer adherence,61–63 and greater depressive symptom burden with lower activation for glaucoma self-management.64 They should therefore be managed as clinically important comorbidities on the basis of symptom burden, functioning, and treatment engagement, independent of any unproven effect on glaucoma progression.
The evidence base remains limited by heterogeneous psychological measures and glaucoma definitions, few longitudinal reverse-direction studies, and residual confounding.
As a narrative review, this work focused on anxiety- and depression-related evidence, synthesized findings qualitatively, and did not include a formal risk-of-bias assessment. Future trials should consider 2–3 years of follow-up, prespecified VF and RNFL progression endpoints, repeated validated psychological assessments, and mediation analyses. Until then, psychological factors should be considered potential but unproven influences on glaucoma progression.
Conclusions
Current evidence supports an asymmetric association. Glaucoma-related visual loss, functional limitation, uncertainty, and long-term management are consistently linked to anxiety and depressive symptoms. Evidence that anxiety or depression accelerates glaucoma is much weaker.
Reverse-direction evidence remains heterogeneous and does not establish independent acceleration of glaucomatous neurodegeneration. Acute stress can transiently affect IOP and test performance, and observational studies report structural or clinical associations. However, intervention trials have not shown sustained slowing of prespecified VF or RNFL progression after improvement in anxiety or depressive symptoms.
Anxiety and depression are therefore important comorbidities in glaucoma, but they are not established modifiers of glaucoma progression. Psychological assessment, education, adherence support, and mental-health treatment should remain part of comprehensive glaucoma care alongside objective monitoring and evidence-based IOP-lowering therapy.