Introduction

Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating complication of neurotoxic chemotherapeutic agents, primarily manifesting as dose-dependent peripheral nerve injury with sensory disturbances (eg, numbness, tingling, pain) and, in some cases, motor and autonomic dysfunction. The prevalence of CIPN varies widely, with estimates suggesting it affects nearly half of patients who received chemotherapy, peaking above 68% in the first month post-treatment and persisting in about 60% at three months and about 30% at six months. However, these estimates are based on studies conducted over a decade ago, with limited sample sizes (31 studies, 4179 patients), underscoring the need for updated, comprehensive analyses.1

Given the rising global cancer burden, expanding chemotherapy options, and increasing survivorship, CIPN prevalence is expected to rise.2 Additionally, there is a lack of comprehensive analyses exploring the global prevalence of chronic CIPN, defined as symptoms persisting for three months or longer post-completion of chemotherapy, and the factors that contribute to its development. Chronic CIPN contributes to significant disability, increased healthcare costs up to $1425 per patient monthly,3,4 and potential treatment modifications that may impact prognosis. Additionally, disparities in CIPN prevalence by socioeconomic and demographic factors remain underexplored. Beyond overall prevalence, the severity and symptom burden of CIPN are critical yet less well characterized. Recent evidence2 suggests that among patients with chronic CIPN, nearly half experience moderate-to-severe or painful neuropathy, highlighting a substantial subgroup with clinically significant morbidity refractory to conventional medical management.5,6 These burdensome forms of CIPN are particularly prevalent among patients receiving taxanes and platinum-based therapies and in cancers such as breast cancer and lung cancer, underscoring the heterogeneity of patient experiences and the importance of stratified evaluation.2

This study aims to evaluate the global prevalence of chronic CIPN and examine key moderators, including chemotherapy type, cancer type, socioeconomic and demographic factors, and methodological considerations.

Materials and Methods

We conducted a meta-analysis that was compliant with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines, as well as systematic review guidelines specific to the field of pain medicine.7–11 We prospectively registered the protocol in the International Prospective Register of Systematic Reviews (PROSPERO ID CRD42024584154).8 The study was deemed exempt from institutional board review.

Search Strategy

We conducted a search strategy in collaboration with a medical librarian (L.J.P). The search was performed on May 31, 2025 without date restrictions, identifying studies that described the development of CIPN among patients who received chemotherapy. We queried electronic databases including Ovid MEDLINE® and Epub Ahead of Print, Ovid Embase, Ovid Cochrane Central Register of Controlled Trials, and Scopus. A controlled vocabulary supplemented with keywords was used; the specific search strategy is reported in e-Box 1.

Study Selection

Inclusion criteria for this meta-analysis were studies that: (1) implemented any design including randomized clinical trials (RCTs) and observational studies (smaller series were selected only if ≥10 patients received chemotherapy); (2) reported the prevalence of chronic CIPN in a cohort of cancer survivors (≥18 years old) who received chemotherapy; and (3) described the process for identifying CIPN via clinical assessment or a screening tool. We specifically considered studies that provided the following two numbers: cases of chronic CIPN and total number of patients who received chemotherapy. We defined chronic CIPN as peripheral neuropathy attributed to neurotoxicity following chemotherapy, and persisting for ≥3 months after completion of chemotherapy. This threshold was selected to distinguish persistent from acute post-treatment neurotoxicity and does not imply that symptoms are irreversible, as recovery may continue beyond 3 months.

Exclusion criteria consisted of articles that: (1) were conference abstracts or non-published; (2) were unavailable in the English language; (3) evaluated treatment outcomes to prevent or treat CIPN; (4) reported on children and adolescents; (5) reported on patients receiving ongoing chemotherapy.

Study Screening

Two authors (S.W. and Y.F.H) independently screened all titles and abstracts using the Covidence online software (Veritas Health Innovation, Melbourne, Australia). Subsequently, two authors (S.W. and Y.F.H) independently reviewed full-text versions of eligible citations for final inclusion. All discrepancies were adjudicated by a third author (R.S.D).

Data Extraction

Two independent reviewers (S.W. and Y.F.H) extracted data into an Excel spreadsheet (Microsoft Excel 2016), and a third reviewer (R.S.D) resolved disagreements. The authors extracted the following data: number of patients diagnosed with chronic CIPN (≥3 months), total number of patients who received chemotherapy, duration of time elapsed since completion of chemotherapy, country, continent, drug class(es) of chemotherapy regimen, primary cancer diagnosis, location of CIPN (upper extremity, lower extremity, both), study design (RCT, prospective observational study, retrospective observational study), human development index (HDI) of the respective country, and year of publication. Studies were not restricted or stratified according to diagnostic modality; CIPN ascertainment was accepted as reported using clinical assessment or screening tools. HDI is a composite measure that includes life expectancy, income per capita, and education,12 with each component normalized on a 0–1 scale. Subsequently, the composite score (0–1) is derived from the geometric mean. A score of ≥0.800 indicates a very high HDI, 0.700–0.799 indicates a high HDI, 0.550–0.699 indicates a medium HDI, and <0.550 indicates a low HDI.

Outcomes of Interest, Subgroup Analysis, and Meta-Regression

The primary outcome was the global prevalence of chronic CIPN (defined as neurologic symptoms persisting ≥3 months since completion of chemotherapy) among patients who received and completed chemotherapy. We conducted subgroup analysis of chronic CIPN prevalence based on time elapsed since completion of chemotherapy, country, chemotherapy regimen, primary cancer type, and study design. Only subgroups with ≥2 study entries were included. Further, in terms of the subgroup analysis based on time elapsed since completion of chemotherapy, we stratified this into three subgroups: within a year of chemotherapy completion (≥3 months to <12 months), after the first year of chemotherapy completion (≥12 months to <24 months), and long-term at 24 months and later (≥24 months). Additionally, we performed meta-regression analysis to assess if select covariates moderated the observed variations between studies. We explored the following variables as covariates in the meta-regression analysis: time elapsed since completion of chemotherapy, HDI, and year of manuscript publication.

Statistical Analysis

We calculated the pooled estimate of prevalence of chronic CIPN with 95% confidence interval (CI) using MetaXL software 5.3 (EpiGear International, Queensland, Australia). We transformed estimates from each study using the Freeman-Tukey transformation (double-arcsine transformation). The rationale for choosing this transformation was two-fold: (1) to address CIs outside of 0–100%; and (2) to manage impact of variance instability on the pooled estimate from studies with extreme estimates (eg, 0 or 100%).13 We pooled the transformed point estimates with 95% CI using a random effects model. We also conducted a cumulative meta-analysis to characterize temporal trends and assess the stability of prevalence estimates over time. Statistical significance was set at p<0.05. We conducted meta-regression analysis using IBM SPSS Statistics version 29.0 (IBM Corp., Armonk, N.Y., USA). We utilized a random effects model and associated weights. Further, we calculated robust standard errors, using the HC1 function in SPSS, which is a degrees-of-freedom adjustment.

Appraisal of Bias and Certainty in Prevalence Estimates

We assessed small-study effects using the Luis Furuya-Kanamori (LFK) index and constructing Doi plots, which quantify asymmetry.14 LFK values beyond ±1 signify asymmetry. We assessed statistical heterogeneity using the I2 statistic with a cut-off of 75% signifying substantial heterogeneity.

We appraised risk of bias using a tool15 comprised of four questions used in prior meta-analyses.16,17 Two reviewers (S.W. and Y.F.H) assessed if included studies completed (yes/no binary response) each of the following four questions, with a third reviewer (R.S.D) adjudicating any discrepancies:

Selection Bias: Do(es) the patient(s) represent the whole experience of the investigator (center) or is the selection method unclear to the extent that other patients with similar presentation may not have been reported? Ascertainment of Exposure: Was the exposure (chemotherapy) adequately ascertained? Ascertainment of Outcome: Was the outcome (chronic CIPN) adequately ascertained? Reporting Bias: Is the case(s) described with sufficient details to allow other investigators to replicate the research or to allow practitioners make inferences related to their own practice?

We assessed the certainty of chronic CIPN prevalence estimates following the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) criteria.18 This appraisal considered the following five domains: risk of bias, inconsistency, indirectness, publication bias, and imprecision. Based on these criteria, we categorized the overall certainty as high (indicating that further research is very unlikely to alter confidence in the prevalence estimate of chronic CIPN), moderate (suggesting that additional research may influence confidence in the estimate and may potentially modify the prevalence estimate of chronic CIPN), low (indicating a high likelihood that further research will impact confidence and alter the prevalence estimate of chronic CIPN), or very low (reflecting considerable uncertainty in the prevalence estimate of chronic CIPN).

Results Identification of Studies

Of 1935 studies, 497 articles were obtained for full-text review, of which 300 were excluded (Figure 1). A total of 197 articles published between 1980–2025 were included in the final analysis, comprising a total of 72,794 participants who had received chemotherapy worldwide (36 countries), of whom 26,258 had chronic CIPN.

Figure 1 PRISMA diagram. Flowchart demonstrates the study selection process. PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-Analyses.

Study Characteristics

Study characteristics are described in eTable 1. Studies were conducted across 36 countries, with the highest number conducted in the United States (53 studies [26.90%]), followed by Japan (15 studies [7.61%]) and the Netherlands (15 studies [7.61%]). Most studies were retrospective observational studies (86 studies [43.65%]), followed by prospective observational studies (67 studies [34.01%]), and RCTs (44 studies [22.34%]). Most studies focused on breast cancer (44 studies [22.34%]), colorectal cancer (28 studies [14.21%]), multiple myeloma (25 studies [12.69%]), and ovarian cancer (14 studies [7.11%]). Most studies (93 studies [47.21%]) reported patients with CIPN in both the upper and lower extremities. The most common chemotherapy regimen included taxanes in 36 studies (18.27%), followed by platinum-based agents in 20 studies (10.15%), platinum-based agents plus taxanes in 14 studies (7.11%), bortezomib in 13 studies (6.60%), and vinca alkaloids in 8 studies (4.06%). A total of 165 studies (83.76%) were conducted in countries with a very high HDI, followed by 26 studies (13.20%) conducted in countries with a high HDI, and six studies (3.04%) conducted in countries with a medium HDI.

Outcomes of Interest and Subgroup Analysis

Of patients who received chemotherapy, the pooled prevalence estimate of chronic CIPN from 197 studies (n = 72,794) was 44.50% (95% CI 40.77–48.25) with evidence for substantial between-study heterogeneity (I2 = 99%, p<0.01; eFigure 1). When assessing prevalence rates based on time elapsed since completion of chemotherapy, subgroup analysis revealed that chronic CIPN prevalence was 54.37% (95% CI 48.24–60.45) at 3–12 months post-treatment, 37.12% (95% CI 30.15–44.26) at 12–24 months post-treatment, and 40.36% (95% CI 34.72–46.08) at ≥24 months post-treatment (eFigure 2). Visual inspection of the cumulative meta-analysis forest plot suggests that pooled prevalence estimates of chronic CIPN have increased over time from 1980 to 2025 (eFigure 3).

Prevalence rates by country are summarized in a graph (Figure 2) and forest plot (eFigure 4), although meaningful subgroup analysis was unable to be performed as several countries were represented by only two studies (countries represented by only one study were omitted from subgroup analysis). A heat map signifying chronic CIPN prevalence by country is displayed in Figure 3 across 22 countries (14 countries represented by only one study were omitted). Among countries (eFigure 4), India had the highest prevalence of chronic CIPN at 60.82% (95% CI 44.99–76.07), followed by Tunisia at 58.39% (95% CI 46.62–69.91), and Japan at 55.99% (95% CI 39.65–72.00). Portugal had the lowest pooled prevalence of chronic CIPN at 19.92% (95% CI 14.66–25.55).

Figure 2 Graph Displaying Pooled Prevalence of Chronic Chemotherapy-induced Peripheral Neuropathy By Country. The graph displays pooled prevalence estimates (95% CI) of chronic chemotherapy-induced peripheral neuropathy by country. The grayed area represents the point estimate and 95% CI for all countries pooled together. From top to bottom, countries are arranged in descending order of pooled prevalence.

Figure 3 Heat Map of the Global Burden of Chronic CIPN. A Robinson projection of the world map was utilized. Prevalence rates for chronic CIPN are displayed among patients who received chemotherapy. The number of contributing studies varied by country; therefore, mapped prevalence estimates should be interpreted alongside the study counts and confidence intervals presented in Figure 2 and eFigure 4. Pts = patients.

Subgroup analysis based on chemotherapy regimen (Figure 4 and eFigure 5) revealed that patients who received thalidomide (67.70%; 95% CI 0–100.00), platinum (61.12%; 95% CI 43.08–78.37), or taxane (57.22%; 95% CI 49.99–64.35) reported the highest prevalence of chronic CIPN, while patients who received 5-fluorouracil plus platinum (6.52%, 95% CI 0–20.82) reported the lowest prevalence of chronic CIPN. Subgroup analysis based on primary cancer (Figure 4 and eFigure 6) revealed that patients with colorectal cancer (54.22%; 95% CI 41.50–66.80) and lung cancer (51.34%; 95% CI 45.18–57.49) reported the highest prevalence of chronic CIPN, while patients with cervical cancer (20.55%, 95% CI 8.96–33.60) reported the lowest prevalence of chronic CIPN. The following primary cancers were omitted because only one study reported rates of chronic CIPN: biliary, endometrial, esophageal, glioblastoma, hepatic, melanoma, prostate, renal, and skin (squamous cell carcinoma). There were no subgroup differences based on study design (Figure 4 and eFigure 7), with the chronic CIPN prevalence at 42.05% (95% CI 33.31–50.94) in RCTs, 46.30% (95% CI 39.53–53.10) in prospective observational studies, and 43.97% (95% CI 38.59–49.40) in retrospective observational studies. Despite the aforementioned subgroup analyses, statistical heterogeneity persisted within each subgroup.

Figure 4 Graph Displaying Pooled Prevalence of Chronic Chemotherapy-induced Peripheral Neuropathy By Various Subgroups. The graph displays pooled prevalence estimates (95% CI) of chronic chemotherapy-induced peripheral neuropathy by (A) chemotherapy regimen, (B) primary cancer type, (C) study design, and (D) time since stopping chemotherapy. The grayed area in each graph represents the point estimate and 95% CI for all studies pooled together. From top to bottom, within each graph, subgroups are arranged in descending order of pooled prevalence.

Meta-Regression Analysis

Time since completion of chemotherapy was a significant moderator of chronic CIPN prevalence (β = −0.003, 95% CI −0.005–0.000; t = −2.052; p = 0.042), with longer durations associated with lower prevalence estimates (eTable 2 and eFigure 8). The HDI (β = 0.147, 95% CI −0.999–1.292, t = 0.253, p = 0.801; eTable 2 and eFigure 9) and manuscript publication year (β = 0.009, 95% CI 0.000–0.018, t = 1.900, p = 0.059; eTable 2 and eFigure 10) were non-significant moderators for chronic CIPN prevalence.

Assessment of Risk of Bias and Certainty in Prevalence Estimate

The LFK index indicated major asymmetry in effect size for the primary outcome, indicating high likelihood of small-study effects (LFK index = 2.19; eFigure 11). Assessment of risk of bias domains (selection, ascertainment of exposure, ascertainment of outcome, and reporting) is displayed in eTable 3. Generally, there was a high rate of selection bias (106 studies; 53.81%) and reporting bias (61 studies; 30.96%). Table 1 provides a summary of the GRADE certainty appraisal for the primary outcome. The certainty in chronic CIPN prevalence was assessed to be very low due to high risk of bias in multiple domains (selection and reporting bias), high statistical heterogeneity, and publication bias (LFK = 2.19).

Table 1 GRADE Evidence Profile and Summary of Findings Showing Certainty in Estimates for Primary Outcome

Discussion Overall Findings

This meta-analysis provides the most comprehensive assessment to date of the global prevalence of chronic CIPN, analyzing data from 197 studies conducted across 36 countries and including 72,794 participants. Our findings indicate that 44.50% of patients who have undergone chemotherapy experience chronic CIPN (defined as symptoms persisting ≥3 months post-treatment), with prevalence varying based on time since chemotherapy completion, country, primary cancer type, and chemotherapy regimen. These results underscore the significant burden of CIPN, which continues to affect a substantial proportion of cancer survivors. However, this finding was characterized by potential publication bias, statistical heterogeneity, and very low certainty according to GRADE criteria.

The pooled prevalence of chronic CIPN was highest (54.37%) within the first year after chemotherapy completion and showed a modest decline (37.12%) by the second year. Interestingly, the prevalence increased slightly to 40.36% among patients assessed at ≥24 months post-chemotherapy. These estimates represent pooled data from different study cohorts at each time interval rather than longitudinal follow-up of the same patients. Further, these findings suggest that while there may be partial recovery of CIPN, a significant subset of patients continues to experience persistent peripheral neuropathy, highlighting the chronic nature of CIPN in many cases. This aligns with prior studies1,2,19,20 that demonstrated only partial resolution of symptoms over time and the need for treatment options to attenuate long-term symptoms.

A prior meta-analysis by Seretny et al1 (31 studies, 4179 patients) was pivotal in quantifying CIPN prevalence over a decade ago. Our study expands on this with refined statistical methods and a near 20-fold larger sample (197 studies, 72,794 patients), incorporating a broader range of cancers and chemotherapy regimens for a more detailed analysis of chronic CIPN prevalence. While Seretny et al emphasized the need for standardized assessment tools, substantial heterogeneity persists. Notably, our findings suggest a lower rate of CIPN symptom resolution over time than that reported by Seretny et al, potentially due to improved detection or evolving treatment practices. These differences underscore the need for ongoing surveillance and standardized reporting.

Factors Influencing Chronic CIPN Prevalence

Subgroup analyses revealed several important trends. India exhibited the highest prevalence at 60.82%, followed closely by Tunisia at 58.39% and Japan at 55.99%. These differences may reflect a combination of cultural, genetic, clinical, and methodological factors. For example, a high prevalence may be influenced by heightened awareness and comprehensive reporting systems for chemotherapy-related adverse effects, alongside potential genetic predispositions to neuropathy in Asian populations.21,22 Further, limited access to early diagnostic tools and treatment interventions, as well as higher usage of neurotoxic chemotherapy agents due to differing cancer care protocols or limited resources, may contribute to the elevated prevalence. Regional disparities may also stem from differences in study design, sample characteristics, and methods of CIPN assessment. For instance, cultural norms in reporting pain and symptoms may influence prevalence rates, with underreporting potentially skewing results in some regions.23,24 Country-level differences should be interpreted cautiously given substantial between-study heterogeneity, uneven representation across countries, and variation in study populations and CIPN assessment methods; therefore, these estimates may not reflect true differences in national prevalence.

Taxane monotherapy, platinum-based monotherapy, and thalidomide were associated with the highest prevalences of chronic CIPN, consistent with their known neurotoxicity.25 Platinum-based agents induce neurotoxicity in dorsal root ganglia (DRG) sensory neurons through deoxyribonucleic acid binding, oxidative stress, mitochondrial dysfunction, and apoptosis, resulting in both non-length-dependent and length-dependent sensory neuropathies.26 Taxanes exacerbate DRG damage by disrupting ion channels, impairing axonal transport, and accumulating in central sensory neurons, further contributing to CIPN pathogenesis.27 These findings highlight the importance of exploring alternative dosing strategies or adjunctive therapies to mitigate neurotoxicity from these regimens.

Patients treated for colorectal cancer and lung cancer showed the highest rates of chronic CIPN, reflecting prolonged chemotherapy cycles and frequent use of neurotoxic agents such as taxanes and platinum-based drugs in these populations. Conversely, cancers with less reliance on these agents demonstrated lower prevalence rates. The majority of studies were conducted in countries with a very high HDI score, potentially reflecting disparities in research infrastructure and reporting. Limited data from countries with lower HDI scores may underestimate the global burden of CIPN, especially given differences in access to supportive care, chemotherapy protocols, and multimodal treatment options. Finally, publication year was not a statistically significant moderator of chronic CIPN prevalence (p=0.059). Although visual inspection of the cumulative meta-analysis forest plot suggested a possible increase in prevalence over time, this apparent trend should be interpreted cautiously. Together, these findings may reflect a lack of meaningful progress in preventing or managing CIPN-related neurological symptoms. Alternatively, this observation may be influenced by the increasing use of more potent chemotherapeutic agents with greater neurotoxic potential.

Strengths and Limitations

Strengths of this meta-analysis include its sample size, adherence to methodological standards (PRISMA guidelines, protocol registration, GRADE criteria), and statistical approaches to address heterogeneity. These findings are relevant to clinicians, researchers, and policymakers in developing strategies to mitigate the global burden of chronic CIPN.

However, several limitations exist. High between-study heterogeneity likely reflected differences in study design, populations, and assessment methods, with residual confounding despite subgroup analyses and meta-regression. Inclusion of studies with varying quality, including retrospective designs, may have introduced bias. Variability in CIPN diagnostic tools, ranging from clinician-reported measures to patient-reported outcomes, likely contributed to the substantial between-study heterogeneity and complicated data synthesis, highlighting the need for standardized criteria. Because diagnostic modality was not extracted, its influence could not be formally assessed. Most studies did not quantify CIPN severity, and apart from HDI, regional healthcare disparities were not assessed. Additionally, the risk-of-bias tool used was originally developed for case reports and case series and may not fully capture design-specific domains relevant to RCTs and cohort studies, including confounding, attrition, and blinding, which may limit the comprehensiveness of the quality assessment.

Pre-existing diabetes and diabetic peripheral neuropathy were inconsistently reported across studies, with some studies excluding patients with pre-existing diabetic neuropathy.28 Although studies that evaluated diabetes generally did not identify it as a significant predictor of treatment-related neuropathy,29–32 limited sample sizes33 and heterogeneous reporting precluded formal assessment of its influence on chronic CIPN prevalence.

Conclusion

This meta-analysis highlights the global burden of chronic CIPN, affecting over half of cancer survivors within the first year after chemotherapy, and approximately 40% experiencing persistent symptoms thereafter. However, the pooled prevalence estimate should be interpreted cautiously given the very high heterogeneity, evidence of small-study effects, and very low certainty according to GRADE. The findings underscore the need for improved detection, prevention, and management strategies, as well as further research into CIPN mechanisms. Variability across countries, chemotherapy regimens, and cancer types emphasizes the importance of personalized, patient-centered approaches to addressing this condition.

Data Sharing Statement

Data are available upon reasonable request to the corresponding author (RSD).

Ethics Approval Statement

As the current study uses data from previously published studies, ethical approval was deemed as exempt.

Acknowledgments

RSD received investigator-initiated research grant funding from Nevro Corp and Saol Therapeutics paid to his institution. AB has received consultancy fees from Medtronic and Bioventus. His institution has also received funding for studies to track outcomes of neuromodulation therapies from Medtronic.

Author Contributions

Ryan D’Souza (study conception, manuscript composition, data validation, data extraction and analysis, supervision of all aspects of the study). All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Disclosure

RSD received investigator-initiated research grant funding from Nevro Corp and Saol Therapeutics paid to his institution. AB has received consultancy fees from Medtronic and Bioventus. His institution has also received funding for studies to track outcomes of neuromodulation therapies from Medtronic. Other authors declare no conflict of interest.

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