The Usefulness of Nerve Conduction Studies in Objectively Assessing Oxaliplatin-Induced Peripheral Neuropathy

Abstract

We read with great interest the recently published paper in your distinguished journal by Wang et al. [1], on the effect of oral glutamine in preventing oxaliplatin-induced peripheral neuropathy. The authors, among others, demonstrated an inconsistency between the electrophysiological findings and the subjective manifestations reported by patients. They report that, despite the clinical difference, the neurophysiological investigation did not show statistically significant differences between treatment groups. They also mention that, although sensory nerve conduction may be affected significantly after oxaliplatin-based treatment, the severity of clinical sensory neuropathy does not always correlate with findings of nerve conduction studies. Cascinu et al. [2] reached the same conclusion, demonstrating that sensory nerve conduction was significantly affected by oxaliplatin only in patients receiving placebo, but not in those receiving glutathione. The results of these studies raise the issue of whether nerve conduction studies are useful in objectively assessing chemotherapy-induced peripheral neuropathy (CIPN). In contrast to the results of Wang et al. [1], in our recently published study on the efficacy of oxcarbazepine in preventing oxaliplatin neurotoxicity, it was demonstrated that between-group (patients receiving oxcarbazepine versus control patients) longitudinal comparison of the median changes in amplitude of sensory action potentials (a-SAP) during chemotherapy revealed significant differences in two of the three sensory nerves tested, thereby favoring oxcarbazepine administration [3]. In line with existing knowledge on the topic of CIPN [4], the severity of clinical symptoms and signs correlated with our electrophysiological findings [5]. Furthermore, another study conducted by our group evidenced a significant longitudinal decrease in all the a-SAPs examined during therapy with the formal FOLFOX-4 regimen [5]. In our opinion, Wang et al. [1] should provide further explanation to justify this inconsistency. Their claim that the non–placebo controlled, unblinded study design might be the cause of this discrepancy is not sufficient. In their study, a subgroup of approximately one third of the patients underwent neurophysiological investigations; neither the technique nor the quantitative outcomes of the investigations were provided. In any case, we strongly support the view that nerve conduction studies are useful and capable of objectively assessing the extent of peripheral nerve damage secondary to chemotherapy administration and may also facilitate the identification of patients that manifest subclinical peripheral neuropathy prior to the onset of clinically significant neurotoxicity [6]. Our experience showed that a precise clinical evaluation, combined with a detailed electrophysiological assessment, could provide data regarding the characteristics of peripheral neuropathy during chemotherapy and may also predict the final neurological outcome of CIPN [7]. It is acknowledged that