Functional pain syndromes are disorders characterized by pain and often accompanied by dysfunction originating in an organ without evidence of organic disease. As such, these disorders are largely diagnosed by patient-reported symptomology and after ruling out other potential disease- or infection-based diagnoses. The vast majority of chronic pain conditions involving pelvic/visceral structures can be categorized as functional pain disorders, including irritable bowel syndrome, non-Hunner’s interstitial cystitis/painful bladder syndrome, chronic prostatitis/chronic pelvic pain syndrome, and vulvodynia.
Oftentimes patients are diagnosed with more than one of these disorders, suggesting common underlying mechanisms. Animal models of functional pelvic pain syndromes have been developed, using direct organ stimulation or non-invasive methods of initiating pelvic hypersensitivity, to determine potential underlying mechanisms and to test pharmacological and non-pharmacological interventions. Clinical studies have investigated changes in both the affected organ or tissue, as well as higher order structures involved in pain signaling. Both basic science and translational approaches are critical to furthering our understanding of the etiology of these disorders and to identifying potential novel therapeutic strategies for their prevention and treatment.
Functional pelvic pain disorders are highly prevalent and difficult to treat due to a poor understanding of the underlying etiology. Clinical studies have shown evidence of increased nociceptive processing both at the site of pain and in higher order structures within the neural axis. What remains unknown is whether and how symptoms are correlated with peripheral and central changes and how predisposing factors, such as genetic alterations and environmental stressors, influence the onset and/or intensity of pain and functional impairment.
Clinical studies investigating these correlations are needed to understand how best to treat symptoms. Likewise, animal models with high face validity are necessary for fully investigating underlying mechanisms, including identifying potential therapeutic targets.
• The objective of this research topic is to identify neural, immune, and metabolic changes that underlie pain and comorbidity in animal models of and clinical populations with functional pelvic pain disorders. Submissions can include original research papers and review articles that cover the following aims:
• Examine how the nervous and immune systems interact in the initiation and maintenance of functional pelvic pain disorders.
• Determine changes in structure and function within higher order pain processing centers that drive symptoms of functional pelvic pain disorders.
• Identify peripheral and central changes that drive comorbidity in functional pelvic pain disorders.
• Explore how genetic and environmental factors contribute to the development, severity, and comorbidity of functional pelvic pain disorders.
Functional pain syndromes are disorders characterized by pain and often accompanied by dysfunction originating in an organ without evidence of organic disease. As such, these disorders are largely diagnosed by patient-reported symptomology and after ruling out other potential disease- or infection-based diagnoses. The vast majority of chronic pain conditions involving pelvic/visceral structures can be categorized as functional pain disorders, including irritable bowel syndrome, non-Hunner’s interstitial cystitis/painful bladder syndrome, chronic prostatitis/chronic pelvic pain syndrome, and vulvodynia.
Oftentimes patients are diagnosed with more than one of these disorders, suggesting common underlying mechanisms. Animal models of functional pelvic pain syndromes have been developed, using direct organ stimulation or non-invasive methods of initiating pelvic hypersensitivity, to determine potential underlying mechanisms and to test pharmacological and non-pharmacological interventions. Clinical studies have investigated changes in both the affected organ or tissue, as well as higher order structures involved in pain signaling. Both basic science and translational approaches are critical to furthering our understanding of the etiology of these disorders and to identifying potential novel therapeutic strategies for their prevention and treatment.
Functional pelvic pain disorders are highly prevalent and difficult to treat due to a poor understanding of the underlying etiology. Clinical studies have shown evidence of increased nociceptive processing both at the site of pain and in higher order structures within the neural axis. What remains unknown is whether and how symptoms are correlated with peripheral and central changes and how predisposing factors, such as genetic alterations and environmental stressors, influence the onset and/or intensity of pain and functional impairment.
Clinical studies investigating these correlations are needed to understand how best to treat symptoms. Likewise, animal models with high face validity are necessary for fully investigating underlying mechanisms, including identifying potential therapeutic targets.
• The objective of this research topic is to identify neural, immune, and metabolic changes that underlie pain and comorbidity in animal models of and clinical populations with functional pelvic pain disorders. Submissions can include original research papers and review articles that cover the following aims:
• Examine how the nervous and immune systems interact in the initiation and maintenance of functional pelvic pain disorders.
• Determine changes in structure and function within higher order pain processing centers that drive symptoms of functional pelvic pain disorders.
• Identify peripheral and central changes that drive comorbidity in functional pelvic pain disorders.
• Explore how genetic and environmental factors contribute to the development, severity, and comorbidity of functional pelvic pain disorders.
