Our hypothesis is that Persistent Genital Arousal Disorder (PGAD) may involve neuropathic mechanisms reflected in abnormal sensory profiles and nerve fiber pathology. The aim of this exploratory and feasibility study was to assess somatosensory function in women with PGAD. Specifically, this study investigated whether PGAD is associated with alterations in peripheral sensory processing, central pain modulation, and small nerve fiber integrity.

This single-center case-control study was conducted between 2021 and 2023. Thirty women with a formal diagnosis of PGAD were compared with 30 age-decade-matched healthy female controls. Participants underwent a comprehensive assessment including quantitative sensory testing (QST) at extragenital (hand) and bilateral genital sites (location 1,2: lateral from clitoris, location 3,4: labium majora, location 5,6: at the level of ischial tuberosity), conditioned pain modulation (CPM) to evaluate central pain inhibition, and corneal confocal microscopy (CCM) to assess small nerve fiber morphology. Statistical analyses were performed to measure group differences; independent t-test, Fisher’s exact test and Mann-Whitney U test were used.

QST revealed no abnormalities at the control site (hand), suggesting no generalized sensory dysfunction. However, genital testing showed significant differences (table 1). PGAD participants exhibited thermal hyperalgesia, reflected by higher cold pain thresholds and lower heat pain thresholds. The detection-to-pain interval for cold stimuli was also reduced. Mechanical pain thresholds did not differ, but PGAD participants showed enhanced temporal summation, indicating increased sensitivity to repeated stimulation. Dynamic mechanical allodynia seems more frequent in PGAD , and statistically significant at location 4 and 5 (Figure 1A). The mean pain intensity ratings were significantly higher in PGAD (Figure 1B). 
CPM responses did not differ significantly between groups, indicating no consistent impairment in central pain inhibition.
CCM findings showed abnormalities in small nerve fiber parameters in a subset of PGAD participants, but differences were not statistically significant compared to controls.

The findings suggest that PGAD is associated with localized sensory abnormalities rather than a generalized somatosensory disorder. The presence of thermal hyperalgesia, increased pain ratings, and enhanced temporal summation supports the involvement of altered peripheral sensory processing and possible central amplification mechanisms. These results are consistent with a neuropathic component, potentially involving pudendal nerve dysfunction and small fiber pathology.
The absence of consistent differences in CPM indicates that impaired descending pain inhibition is not a universal feature of PGAD, although variability suggests heterogeneity among patients. Similarly, CCM results suggest that small fiber pathology may be present in a subset of patients but is not a defining characteristic for all.

This study supports the concept that PGAD has a multifactorial pathophysiology involving both peripheral and central sensory mechanisms. The feasibility of QST, CPM and CCM in women with PGAD, together with the observed abnormalities in sensory processing, indicates that these tools may help identify distinct sensory phenotypes within this population. Defining such phenotypes could facilitate more personalized diagnostic pathways and targeted interventions, underscoring the need for validation in larger cohorts.

Continence 19S (2026) 102530
DOI: 10.1016/j.cont.2026.102530