Photobiomodulation Therapy for Chemotherapy-Induced Peripheral Neuropathy: Targeted Mechanisms and Optimized Strategies for Sensory Symptom Relief

Chemotherapy-induced peripheral neuropathy (CIPN) is a widespread and often disabling effect of neurotoxic cancer therapies. Patients frequently experience sensory abnormalities such as numbness, tingling, heightened sensitivity to mechanical or cold stimuli (allodynia), and disrupted proprioception. These symptoms can persist long after treatment, significantly impairing daily function and quality of life. Photobiomodulation (PBM), which uses specific wavelengths of low-level red or near-infrared light, has recently emerged as a viable non-pharmacologic option for reducing these sensory disruptions. Evidence from both laboratory and clinical research shows that PBM can enhance mitochondrial activity, facilitate axonal repair, and suppress oxidative stress and inflammatory responses within nervous tissue. In particular, PBM administered in the 780–850 nm wavelength range with fluences between 3 and 48 J/cm² has demonstrated the ability to relieve allodynia mediated by transient receptor potential (TRP) channels and restore proprioceptive function via nerve regeneration. Clinical implementation is hampered by inconsistencies in reported treatment parameters such as wavelength, dosage, and session frequency, making it challenging to replicate findings or compare studies. Furthermore, many existing PBM protocols do not tailor treatments to specific sensory symptoms or differentiate by chemotherapy type. This review consolidates current mechanistic and clinical data, evaluates PBM’s effects across various CIPN symptom categories, and highlights the need for standardization and patient-specific protocol development. Future progress should include the integration of biomarkers for response prediction, the use of quantitative sensory testing (QST), and rigorous long-term safety assessments. Adopting an approach that matches PBM parameters to sensory symptom patterns and underlying chemotherapeutic mechanisms may significantly enhance its therapeutic impact in treating CIPN.