Ultraweak photon emission (UPE) refers to spontaneous, low-intensity photon release from biological systems, generated largely through oxidative metabolic reactions involving reactive oxygen species, lipid peroxidation, mitochondrial activity, and electronically excited molecular intermediates. Because the nervous system is highly metabolically active and vulnerable to oxidative stress, hypoxia, excitotoxicity, inflammation, and mitochondrial dysfunction, UPE may offer a noninvasive optical window into neural physiology and disease. In this narrative review, we examine experimental and translational evidence linking UPE to nervous system function, with emphasis on neuronal excitation, glutamate-mediated activity, ischemia-reperfusion injury, stroke, neurodegeneration, mental-state and anesthesia paradigms, photobiomodulation, demyelinating disease, Parkinson disease, amyotrophic lateral sclerosis, and neuro-oncology. Across these domains, UPE appears most consistently associated with redox metabolism, mitochondrial function, oxidative stress, and excitation–metabolism coupling, whereas evidence that endogenous photons mediate functional neural signaling remains preliminary. Current data suggest that UPE may be most promising as a preclinical biomarker of tissue metabolic state, delayed post-ischemic dysfunction, and early neurodegenerative change, particularly when integrated with electrophysiology, perfusion imaging, molecular assays, and other physiologic measures. However, clinical translation is limited by low photon flux, limited temporal and spectral resolution, difficulty localizing signals from deep tissue, heterogeneous experimental protocols, and incomplete source attribution. Overall, UPE represents a promising but still early-stage framework for studying nervous system metabolism and disease, with future progress dependent on standardized methods, multimodal validation, and disease-specific investigation.