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Letter To The Editor

letter

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

^aDepartment of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery, London, United Kingdom; ^bDepartment of Neurology – EMG Laboratory, University of Patras Medical School, Rion-Patras, Greece

Correspondence: Andreas A. Argyriou, M.D., Ph.D., Department of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery, WC1N3BG, London, United Kingdom. Telephone: +30 2610999485; Fax: +30 2610993949; e-mail: andargyriou{at}yahoo.gr

Received May 7, 2007; accepted for publication September 25, 2007.

Disclosure: No potential conflicts of interest were reported by the authors, planners, reviewers, or staff managers of this article.

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 electrophysiological examination is not always available in the general oncology practice; however, oncologists should be aware that, particularly, the estimation of vibration perception, deep tendon reflexes, and sural sensory action potential is mandatory in the follow-up course of CIPN [7].

	REFERENCES

Top References

 

1. Wang WS, Lin JK, Lin TC et al. Oral glutamine is effective for preventing oxaliplatin-induced neuropathy in colorectal cancer patients. The Oncologist 2007;12:312–319.[Abstract/Free Full Text]
2. Cascinu S, Catalano V, Cordella L et al. Neuroprotective effect of reduced glutathione on oxaliplatin-based chemotherapy in advanced colorectal cancer: A randomized, double-blind, placebo-controlled trial. J Clin Oncol 2002;20:3478–3483.[Abstract/Free Full Text]
3. Argyriou AA, Chroni E, Polychronopoulos P et al. Efficacy of oxcarbazepine for prophylaxis against cumulative oxaliplatin-induced neuropathy. Neurology 2006;67:2253–2255.[Abstract/Free Full Text]
4. Quasthoff S, Hartung HP. Chemotherapy-induced peripheral neuropathy. J Neurol 2002;249:9–17.[CrossRef][Medline]
5. Argyriou AA, Polychronopoulos P, Iconomou G et al. Incidence and characteristics of peripheral neuropathy during oxaliplatin-based chemotherapy for metastatic colon cancer. Acta Oncol 2007 Jun 21 [Epub ahead of print; doi: 10.1080/02841860701355055].
6. Chaudhry V, Rowinsky EK, Sartorius SE et al. Peripheral neuropathy from taxol and cisplatin combination chemotherapy: Clinical and electrophysiological studies. Ann Neurol 1994;35:304–311.[CrossRef][Medline]
7. Argyriou AA, Polychronopoulos P, Koutras A et al. Peripheral neuropathy induced by administration of cisplatin- and paclitaxel-based chemotherapy. Could it be predicted? Support Care Cancer 2005;13:647–651.[CrossRef][Medline]

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