Aetiology

The underlying aetiology is unclear. Studies indicate that the anterior cingulate gyrus, insular cortex, and amygdala have increased activity in many chronic pain syndromes, including those seen in chronic pelvic pain.[10] Sexual abuse or trauma at a susceptible age also leads to dysregulation of these brain structures.

Pain seems to spread from one organ system to another by a process of centrally mediated allodynia without end-organ pathology. These features indicate that dysregulation of the limbic lobe may be responsible for many of the features of chronic pelvic pain.

The aetiology of the associated diagnoses is similarly poorly understood. Pain may arise from one or more organs, and the actual presentation and pathophysiology affecting each organ system may be variable. One definition of chronic pelvic pain is dysmenorrhoea lasting for at least 6 months, which causes limitation of activity. This type of cyclic gynaecological pain may represent adenomyosis or fibroids, both of which are disorders of the uterus itself.

Endometriosis is frequently considered to be the result of retrograde menstruation, but the stage of endometriosis does not correlate with the severity of pain.[11][12] A newer hypothesis is that stressors lead to neuro-immune dysregulation, allowing the normal process of retrograde menstruation to develop into sensory innervated endometriosis implants via peritoneal nerve growth factor production.

Adenomyosis is a variant of endometriosis, and may also occur due to abnormal nidation of endometrial tissue through unknown transport mechanisms, or at the time of pregnancy.[13]

Pathophysiology

The pathophysiology underlying the development of chronic pain is unknown. The hypothesis of limbic-associated pelvic pain is designed to account for many of the features seen in these patients.

This syndrome represents a state of hypervigilance for pain due to overactivity of limbic structures, specifically the amygdala and anterior cingulate. This leads to focused attention on one (or more) sites in the pelvis (typically a muscle or muscular organ), which respond by generating pain. This induces the limbic system to increase pain vigilance in the area, which reinforces the pain and can spread to adjacent organs.[14]

Most organs involved in pain generation do not have significant or detectable pathological change.[10]

For some of the associated conditions, end-organ pathological changes are demonstrable.

  • Endometriosis is defined as the presence of endometrial glands and stroma outside of the uterine lining.

  • Adenomyosis is defined as the presence of endometrial glands and stroma inside the uterine wall.

  • In interstitial cystitis there may be breakages in the glycosaminoglycan layer of the bladder, exposing the underlying mucosa to the urine. A number of other changes can inconsistently be demonstrated in the bladder epithelium and bladder wall.[15]

  • Irritable bowel syndrome may represent dysregulation of the enteric neural plexus, potentially involving serotonin receptors.[16]

  • Fibromyalgia and vulvodynia do not demonstrate consistent pathological findings but appear to have a disordered local neural milieu.[17]

  • In pelvic congestion syndrome, excess blood flow to the uterus produces a feeling of heaviness. Whether this exists as a separate entity is controversial.[18]

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