A neuroimmune hypothesis linking chronic cervical inflammation to systemic symptoms: the role of the vagus-NTS axis

Chronic pain syndromes in women often present with symptoms that do not fully correspond to the anatomical site of detectable pathology. Dyspareunia, vulvar pain, bladder discomfort, glossodynia, headache, dizziness, gastrointestinal symptoms, palpitations, insomnia, and musculoskeletal pain may coexist, suggesting shared neuroimmune and autonomic mechanisms rather than isolated local disease alone. This hypothesis was motivated by two preliminary clinical observations presented at meetings of the Taiwan Association of Obstetrics and Gynecology. The first series, presented in March 2024, involved 28 women with dyspareunia in whom the anatomical location of pain did not consistently correspond to the presumed pathological origin, with symptomatic improvement observed after targeted endocervical treatment. The second series, presented in March 2026, involved 28 women with intractable glossodynia, several of whom had coexisting vulvovaginal or cervical inflammatory findings and reported improvement after gynecologic treatment. These observations are not presented as definitive evidence of causality, but as hypothesis-generating clinical signals. We propose that chronic cervical inflammation may act as a hidden peripheral inflammatory source capable of modulating vagal afferent signaling to the nucleus tractus solitarius. Through interactions with autonomic, hypothalamic, limbic, and cortical networks, persistent cervical inflammatory input may contribute to neuroimmune amplification and systemic symptoms beyond the anatomical location of pain. This model is testable through prospective studies evaluating cervical inflammatory markers, heart rate variability, vagal tone, cytokine profiles, central sensitization indices, and symptom changes after targeted cervical treatment. Pain location may not necessarily indicate pathological origin, and chronic cervical inflammation may represent an underrecognized contributor to systemic neuroimmune symptoms through the vagus-NTS axis.