Greater occipital neurectomy for refractory occipital neuralgia secondary to neurovascular compression: Anatomical Correlation, histopathological findings, and systematic review

Background: Occipital neuralgia (ON), or Arnold’s neuralgia, is a debilitating neuropathic pain disorder often attributed to muscular entrapment. However, increasing evidence suggests that neurovascular compression (NVC) by the occipital artery (OA) serves as a primary etiology in refractory cases. This study aims to evaluate the anatomical relationship between the greater occipital nerve (GON) and the OA through cadaveric morphometry, analyze clinical- histopathological correlation in surgical patients, and synthesize global evidence through a systematic review. Methods: We performed 18 cadaveric dissections using ImageJ morphometry to analyze the GON-OA complex at the superior nuchal line (1.39 mm mean distance). A clinical series of 25 pharmacoresistant patients was evaluated; three refractory cases underwent GON neurectomy with subsequent hematoxylin and eosin staining. Concurrently, a systematic review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines was conducted, integrating 21 core studies for qualitative synthesis. Results: Neurovascular contact was identified in 66% of cadaveric specimens, with a 27% prevalence of complex helical entanglement. Histopathological analysis of resected nerves revealed axonal distortion, perineural thickening, and focal myelin sheath dilation, confirming structural damage due to chronic pulsatility. The systematic review confirmed that surgical interventions addressing the vascular component significantly improve long-term clinical outcomes. Conclusion: Pulsatile NVC induces irreversible structural neuropathy, as evidenced by the axonal distortion found in our series. While decompression is viable in early stages, neurectomy of the third portion of the GON represents a definitive and justified therapeutic strategy for refractory Arnold’s neuralgia with established nerve damage.