Purpose: Chemotherapy-induced painful peripheral neuropathy (CIPPN) affects up to 90% of cancer patients treated with chemotherapy agents. Despite the fact that it is relatively common, the underlying pathophysiology is still unclear and its treatment remains generic. Mechanisms of CIPPN are multifactorial, dependent on the specific chemotherapeutic agent used, and include multiple patient-related factors, including genetic factors that may predispose patients to either develop or not develop CIPPN. The purpose of this article is to review mechanisms, clinical signs and symptoms, diagnosis, treatment options, and prognosis for patients who develop CIPPN. We also offer research considerations for this complex and unpredictable phenomenon.
Principal findings: Chemotherapeutic agents can damage the peripheral nervous system, including the nerve terminals, axons, cell body, and myelin sheath of sensory nerves. Herein, we describe some of the anatomical and functional changes that are thought to take place at various levels of the nervous system. On a clinical level, patients with CIPPN report multiple symptoms. It is essential to obtain an accurate history from the patient and to perform a thorough physical examination in order to obtain the patient's subjective perspective. Additionally, objective measurements may be needed in order to articulate clearly the effects of this complex syndrome and to ensure an accurate diagnosis, treatment, and prognosis.
Conclusions: The management of CIPPN remains a clinical challenge for pain practitioners. As more research is being carried out to elucidate its pathophysiology and therapy, the innovative use of several non-traditional categories of drugs seems promising in the management of this complex phenomenon. Studies addressing predictability and possible genetic predisposition are necessary not only for preventive measures but also for targeted treatments.