Conclusion

VVS is a debilitating syndrome involving unexplained, localized vestibular pain on contact accompanied by minimal objective clinical findings. The etiology is unknown and possibly is multifactorial. The prevailing theory postulates that the syndrome is a neuropathic disorder of abnormal pain perception triggered by some form of chronic inflammation. Possible triggers include infectious agents, excessive use of irritating topical products or medications, prior laser or cryogenic treatments for HPV infection, and Type I hypersensitivity to seminal fluid. Mounting evidence suggests that VVS-afflicted women are predisposed genetically to chronic inflammatory responses or may have impaired immune defenses against infectious agents. Evidence also exists for physical (pelvic musculature dysfunction, vaginismus) and psychological contributing factors. Rigorous randomized prospective trials evaluating alternative therapeutic approaches are lacking. Conservative interventions with some evidence for efficacy are anesthetic symptom relief, pain modulation with low-dose tricyclic antidepressants, and electromyographic biofeedback. Antifungal or interferon therapy may be beneficial for selected subsets of patients. Surgical excision of afflicted portions of the vestibule produces relief but is reserved for chronic, recalcitrant cases when other treatments have failed. Patients with VVS benefit from supportive therapy; a multimodal treatment approach may be optimal to address both the physical symptoms and the psychological sequelae. More research is required to elucidate etiologic mechanisms and produce effective, evidence-based treatments for this complex disease.

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