Heterogeneity in nerve recovery patterns despite symptomatic improvement in paclitaxel-induced neuropathy: A longitudinal analysis.

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a common and potentially persistent toxicity of paclitaxel. This prospective study aimed to characterize longitudinal changes in paclitaxel-induced CIPN by integrating serial neurophysiological and clinical assessments. Twenty-six patients receiving paclitaxel-based chemotherapy for breast, ovarian, or endometrial cancer were prospectively enrolled. Assessments were scheduled at baseline (T0), completion of chemotherapy (T1), 3 months posttreatment (T2), and 1 year posttreatment (T3) and included nerve conduction studies (NCS), the self-reported Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS), and Common Terminology Criteria for Adverse Events (CTCAE) grading. Fourteen patients with available longitudinal outcome data were included in the analytic cohort. Longitudinal changes were analyzed using linear mixed-effects models, and associations between NCS parameters and clinical measures were explored using repeated-measures correlation. S-LANSS scores increased from 1.29 ± 4.81 at T0 to 14.29 ± 4.23 at T1 and subsequently decreased to 4.86 ± 5.88 at T3 (overall P < .001), although they remained higher than baseline (P = .008). NCS amplitudes showed heterogeneous recovery patterns. Sural SNAP amplitude markedly decreased at T1 but recovered thereafter and was not significantly different from baseline at T3. In contrast, ulnar SNAP amplitude remained significantly reduced at T3 (P < .001), whereas tibial compound motor action potential amplitude was no longer significantly different from baseline (P = .060). NCS amplitudes were inversely associated with clinical measures, with the strongest association observed between ulnar SNAP amplitude and CTCAE grade (r = -0.720, P < .001). Paclitaxel-induced peripheral neuropathy showed substantial symptomatic improvement after chemotherapy but heterogeneous electrophysiological recovery across peripheral nerves. Persistent abnormalities in selected nerves despite symptom improvement highlight the complementary roles of patient-reported outcomes and objective neurophysiological assessment in characterizing the longitudinal course of CIPN.