Endometriosis is a systemic, estrogen dependent neuroinflammatory-mediated disease affecting approximately 10–15% of women of reproductive age. Clinical manifestations include chronic pelvic pain (CPP), dysmenorrhea, dyspareunia, dyschezia, dysuria, and infertility. Endometriosis-associated pain is multifactorial and comprises overlapping nociceptive, neuropathic, and nociplastic pain phenotypes driven by persistent inflammation, neuroangiogenesis, peripheral nerve involvement, and central sensitization (CS). These mechanisms may sustain pain beyond lesion excision, highlighting the importance of pelvic nervous system (PNS) involvement. This narrative review examines the role of neuropelveology (NP) in endometriosis, focusing on pain mechanisms, diagnostic implications, and surgical decision making. NP integrates pelvic neuroanatomy and neurophysiology into structured neurological assessment, pain mapping, symptom localization, and nerve sparing surgery. Current evidence suggests that NP may complement conventional evaluation in selected patients with refractory pain, neuropathic symptoms, discordance between symptom severity and imaging findings, or suspected involvement of the sacral plexus or sciatic nerve. Recognizing distinct pain phenotypes may support individualized treatment planning by balancing lesion excision with neural preservation and identifying patients who may benefit from multidisciplinary pain management, rehabilitation, neurolysis, or neuromodulation. Although current evidence remains limited, NP should be considered a complementary framework rather than a replacement for established endometriosis management. Prospective multicenter studies using standardized diagnostic criteria and long-term functional outcomes are needed to define its clinical utility.

Endometriosis is a systemic, estrogen dependent neuroinflammatory-mediated disease affecting approximately 10-15% of women of reproductive age. Clinical manifestations include chronic pelvic pain (CPP), dysmenorrhea, dyspareunia, dyschezia, dysuria, and infertility. Endometriosis-associated pain is multifactorial and comprises overlapping nociceptive, neuropathic, and nociplastic pain phenotypes driven by persistent inflammation, neuroangiogenesis, peripheral nerve involvement, and central sensitization (CS). These mechanisms may sustain pain beyond lesion excision, highlighting the importance of pelvic nervous system (PNS) involvement. This narrative review examines the role of neuropelveology (NP) in endometriosis, focusing on pain mechanisms, diagnostic implications, and surgical decision making. NP integrates pelvic neuroanatomy and neurophysiology into structured neurological assessment, pain mapping, symptom localization, and nerve sparing surgery. Current evidence suggests that NP may complement conventional evaluation in selected patients with refractory pain, neuropathic symptoms, discordance between symptom severity and imaging findings, or suspected involvement of the sacral plexus or sciatic nerve. Recognizing distinct pain phenotypes may support individualized treatment planning by balancing lesion excision with neural preservation and identifying patients who may benefit from multidisciplinary pain management, rehabilitation, neurolysis, or neuromodulation. Although current evidence remains limited, NP should be considered a complementary framework rather than a replacement for established endometriosis management. Prospective multicenter studies using standardized diagnostic criteria and long-term functional outcomes are needed to define its clinical utility.

The relationship between the gut microbiota and the central nervous system has gained attention as a biological axis that may influence the development of several neurological disorders. Recent evidence integrating genomic, neurobiological, and microbiota research shows how bacterial composition, host genetic variability, and the mechanisms of the microbiota-gut-brain axis interact in conditions such as autism spectrum disorder, epilepsy, and schizophrenia. These interactions function through neural, metabolic, and immunological related pathways involving intestinal and blood-brain barrier permeability. Genome-wide association studies (GWAS) and Mendelian randomization analyses highlight shared immunogenetic pathways that may shape both microbial profiles and neurological susceptibility. Consistent patterns of dysbiosis and alterations in neuroactive metabolites have also been reported, linking microbiota changes to neuroinflammation and disrupted neuronal signaling. This review synthesizes the current evidence supporting the integration of the microbiota-gut-brain axis and its underlying communication pathways. It also outlines the present therapeutic strategies for neurological disorders such as autism spectrum disorder, epilepsy, and schizophrenia, highlighting their potential to modulate neurological function. Additionally, it discusses the existing limitations in the field and offers insights into future research directions within this rapidly evolving area.