Chronic primary pelvic pain syndrome (CPPPS) is a heterogeneous disease with unknown pathogenesis and a lack of distinct pathological features, which complicates diagnosis and therapy and has a significant impact on patients' daily life. Because pharmacological management is ineffective and long-term use may result in additional system damage, developing a more effective treatment is critical. Neuromodulation has advanced rapidly over the last few decades, and various types of neuromodulations have demonstrated efficacy in the treatment of CPPPS. In this article we discuss the evolution of neuromodulation technology in the treatment of chronic pelvic pain, its application to various subtypes of chronic pelvic pain, and the comparison of relevant efficacy and parameter differences, as well as assess the relative advantages and disadvantages of sacral neuromodulation, percutaneous tibial nerve stimulation , transcutaneous electrical nerve stimulation, electroacupuncture, and pudendal neuromodulation. Furthermore, it was noted that chronic pelvic pain should be evaluated in terms of pain, associated symptoms, psychological problems, and quality of life. Although neuromodulation approaches have been shown to be effective in treating chronic pelvic pain, more extensive multicenter trials are required to confirm this.

Interstitial cystitis/bladder pain syndrome (IC/BPS) represents a chronic, non-infectious inflammatory bladder disorder, predominantly affecting women. Primary symptoms include ongoing pelvic pain, frequent urination, and urgency, often accompanied by functional somatic pain syndromes and psychological health disturbances. The severity of IC symptoms significantly impairs patients’ quality of life, highlighting the necessity for research on the pathogenesis, progression, and treatment of IC/BPS. Although the exact etiology of IC remains unclear, and there is no simple or definitive diagnostic method, current clinical treatments primarily focus on symptom relief rather than a cure. In recent years, extensive experimental studies on the etiology and pathophysiology of IC have identified a multitude of signaling pathways involved in the disease’s initiation, progression, and self-repair mechanisms. This study focuses on IC-related signaling pathways, analyzing the role of key molecular signals in the onset and progression of IC. By integrating clinical symptoms and signs with molecular biology insights, we provide a comprehensive overview and comparative analysis of IC’s etiology and pathophysiological activities. The goal is to establish a theoretical foundation for the development of more efficient diagnostic tools, drug therapies, treatment evaluations, and preventive strategies for IC.