Oxaliplatin-Induced Peripheral Neuropathy

No drug or medical device currently has strong evidence for preventing OIPN. Agents such as vitamin B12, calcium-magnesium preparations, gabapentin, pregabalin, and goshajinkigan are sometimes used empirically but have insufficient efficacy evidence. Oxaliplatin-induced peripheral neuropathy occurs in a dose-dependent manner and is the drug's major limiting toxicity. Proposed CIPN mechanisms include mitochondrial dysfunction, oxidative stress, ion channel changes, neuroinflammation, and peripheral nerve structural changes. CIPN mechanisms can damage A-delta and C fibres and produce abnormal pain sensitivity. Acute OIPN symptoms such as cold dysesthesia and muscle cramps are typically transient and resolve within a few days. CIPN is a central concern because NACT can trigger stress responses and neuro-immune-endocrine effects that contribute to neuropathy. Chronic OIPN can substantially impair daily life and may force chemotherapy modification or discontinuation because it correlates with cumulative oxaliplatin exposure. CIPN often presents as evoked pain or hyperalgesia. Chronic OIPN may become irreversible once established, making prevention especially important.