Neurochemical and inflammatory mechanisms in head and neck nerve injury: implications for neuromonitoring and neuroprotection

Peripheral nerve injury in the head and neck region remains a critical cause of postoperative morbidity despite advances in microsurgery and intraoperative neuromonitoring. Beyond mechanical disruption, such injuries trigger complex neurochemical and inflammatory cascades that determine neuronal survival and functional recovery. This review synthesizes current evidence on the interplay between inflammatory signaling, oxidative stress, and neurotrophic modulation in peripheral nerve regeneration, emphasizing recurrent laryngeal and facial nerves. Experimental and molecular data reveal that Schwann cell–macrophage crosstalk, activation of NF-κB, MAPK, and PI3K/Akt pathways, and redox regulation via Nrf2 orchestrate the transition from degeneration to repair. Disruption of glutamatergic signaling, calcium homeostasis, and mitochondrial integrity further shapes the regenerative outcome. Translational research demonstrates that biomaterial scaffolds, photobiomodulation, and antioxidant or growth-factor therapies can enhance reinnervation, while clinical studies confirm that real-time electromyography monitoring predicts postoperative nerve function and reduces injury risk. Understanding these molecular–electrophysiological connections provides a foundation for developing predictive biomarkers and personalized neuroprotective strategies. The convergence of molecular neuroscience and precision surgery heralds a paradigm shift toward proactive, regenerative nerve care in head and neck surgery.