Natural History of Chemotherapy-Induced Peripheral Neuropathy in Paclitaxel-Treated Patients: A Prospective Analysis Using Nerve Conduction Studies and S-LANSS Questionnaires

Purpose Chemotherapy-induced peripheral neuropathy (CIPN) is a common and debilitating toxicity of paclitaxel that can compromise treatment adherence and survivorship. We aimed to prospectively characterize the natural history of paclitaxel-induced peripheral neuropathy by integrating objective neurophysiological assessments with patient-reported outcomes. Methods In this prospective study, 26 patients scheduled to receive paclitaxel-based chemotherapy for breast, ovarian, or endometrial cancer were enrolled. Serial evaluations were performed at baseline (T0), immediately post-chemotherapy (T1), three months after completion (T2), and one-year post-treatment (T3). Nerve conduction studies (NCS) of sensory and motor nerves, the self-reported Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS) questionnaire, and Common Terminology Criteria for Adverse Events (CTCAE) grading were conducted at each time point. Correlations between subjective and objective measures were analyzed. Results Fourteen patients who completed serial assessments up to T2 were included in the final analysis. At T1, S-LANSS scores increased significantly from baseline (1.29 ± 4.81 to 14.29 ± 4.23, p < 0.0001), with partial improvement at T2 and T3, though not fully returning to baseline. While distal latencies showed no significant changes, amplitudes of all studied nerves decreased immediately after chemotherapy. Partial recovery was observed in sural, median, and superficial radial sensory nerve action potentials (SNAPs), whereas tibial compound motor action potential (CMAP) and ulnar SNAP showed minimal recovery and remained significantly impaired at one year. Correlation analyses showed significant associations between patient-reported symptoms and NCS parameters, particularly for ulnar SNAP (r = –0.523, p < 0.0001) and tibial CMAP (r = –0.467, p = 0.0005). Analysis of ≥30% SNAP reductions revealed heterogeneity in recovery trajectories, with early sural involvement showing partial recovery, while median and ulnar nerve impairments persisted. Conclusion Paclitaxel-induced peripheral neuropathy persists long after treatment and demonstrates heterogeneous recovery patterns across nerves. Reliance solely on CTCAE grading may underestimate neuropathy burden; integration of patient-reported outcomes and NCS provides a more comprehensive evaluation. Early identification of high-risk patients through longitudinal monitoring may guide proactive management strategies and mitigate the long-term impact of CIPN.