Burning, Stinging, Tenderness: Sensory Profiling of Vulvar Pain in Chronic Discomfort — A DATRIV Study Perspective

Background: Chronic vulvar discomfort (CVD) affects up to 28% of women but remains diagnostically challenging due to overlapping symptoms and limited application of structured sensory profiling. Objective: To delineate qualitative sensory profiles in women with vulvar dermatoses and vulvodynia, identify dominant pain descriptors, and explore internal sensory hierarchies using comparative statistical methods. Methods: A total of 328 women were enrolled in the prospective DATRIV study. All participants underwent structured pain assessment, Three-Rings Vulvoscopy (TRIV), and targeted vulvar biopsy with histopathologic confirmation. Pain descriptors were categorized according to putative neurophysiological mechanisms (C-fiber vs. A-delta fiber input). Statistical analyses included frequency comparisons, co-occurrence matrices, and data visualization through heatmaps and radar plots. Results: Dull pain was nearly universal (>98%). In vulvar dermatoses, itching (96.2%) and stinging (77.4%) predominated, reflecting C-fiber-mediated pruriceptive pathways. In contrast, vulvodynia demonstrated a significantly higher prevalence of sharp pain, particularly stabbing (45.5%) and knife-like sensations (54.5%), indicating A-delta fiber hyperexcitability. Heatmap analysis revealed distinct internal sensory hierarchies: clustering of pruritic descriptors in dermatoses and a more heterogeneous, dispersed pattern in vulvodynia. Conclusion: Women with chronic vulvar discomfort display distinct sensory phenotypes that align with underlying neurophysiological mechanisms. Sensory profiling distinguishes between inflammatory C-fiber–mediated and neuropathic A-delta–mediated patterns, as well as mixed profiles reflecting contributions from both fiber types, and non-specific or minimal input lacking clear descriptor dominance. Notably, a subset of patients with histologically confirmed dermatoses also displayed A-delta–dominant features, suggesting overlapping neuropathic components. These findings indicate that vulvodynia and vulvar dermatoses may represent interconnected conditions along a shared pathophysiological continuum, where untreated or prolonged vulvodynia may evolve toward inflammatory dermatoses. Recognizing these trajectories may enhance diagnostic precision and support personalized, mechanism-based therapeutic strategies.