|dc.contributor.author||Peters, Kathleen Mary||-|
|dc.description.abstract||Endometriosis, the growth of endometrial-like tissue at sites outside the uterus, may affect up to 10% of reproductively-aged women. Endometriosis-associated pain (EAP), the predominant symptom, is often refractory to treatment, and places a considerable economic and social burden on these women and wider society. Reducing this burden is a vital undertaking. However, the underlying pain mechanisms in women with EAP are yet to be fully determined. Understanding these pain mechanisms is crucial to delivering expanded mechanism-targeted pain management, thereby reducing the pain-related burden for women with EAP.
This study aimed to apply the biopsychosocial model of pain assessment to the identification of endometriosis-associated pain mechanisms, in order to generate a sensory phenotype and psychosocial profile of EAP.
We hypothesised that the sensory phenotypes and psychosocial profiles of women with endometriosis would differ from women without endometriosis, reflecting that underlying neuropathological pain mechanisms contribute to EAP.
Quantitative sensory testing (QST), a psychophysical method of testing sensory function, was used to identify normal and pathological pain processing mechanisms in women with endometriosis (n = 20), women with EAP and suspected undiagnosed endometriosis (n = 9), and pain-free women without endometriosis (n = 14). QST, as prescribed by the German Research Network on Neuropathic Pain (DFNS), allows the development of sensory phenotypes. The same women completed psychosocial evaluations which were conducted with well-established pain-related questionnaires that capture core outcome domains for pain severity and emotional and cognitive functioning, as recommended by the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT).
Sensory phenotypes and psychosocial profiles differed between women with and without EAP. Increased pain sensitivity to noxious pinprick stimuli was observed at the primary EAP referral sites (back and abdomen) for women with EAP compared with pinprick pain sensitivity at the same location for EAP-free women without endometriosis. In women with endometriosis, the biopsychosocial functioning revealed that lower pain severity at the primary EAP referral sites and at the distant test site (hand) was associated with higher pain-related self-efficacy and lower levels of catastrophising. In contrast, at the same test locations, higher pain severity was associated with higher levels of catastrophising.
This study examined the complete sensory pathway of potential, pathological pain mechanisms in women with endometriosis. The algesiogenic potential of endometriosis itself appears to contribute to increased viscero-visceral pain sensitivity (hyperalgesia), with the key findings indicating that the primary referral region for EAP is the site of multiple mechanistic contributions to hyperalgesia. Additionally, centrally-driven amplification of hyperalgesia appears to spread pain sensitivity beyond the referral site of the primary pathology. Nevertheless, at the primary referral region for EAP, lower pain severity is associated with higher psychosocial functioning and vice versa. This may be due to the neuroplasticity of the same underlying, centrally-driven pain mechanisms, which offers the tantalising opportunity for the use of centrally-acting interventions, including those targeting psychosocial aspects, to reduce pain sensitivity and improve pain-related outcomes for women with EAP.||en_AU|
|dc.publisher||University of Sydney||en_AU|
|dc.publisher||Sydney Medical School||en_AU|
|dc.publisher||Department of Obstetrics, Gynaecology and Neonatology||en_AU|
|dc.rights||The author retains copyright of this thesis. It may only be used for the purposes of research and study. It must not be used for any other purposes and may not be transmitted or shared with others without prior permission.||en_AU|
|dc.title||The Biopsychosocial Assessment of Pain Mechanisms in Women with Endometriosis||en_AU|
|dc.type.pubtype||Doctor of Philosophy Ph.D.||en_AU|
|dc.description.disclaimer||Access is restricted to staff and students of the University of Sydney . UniKey credentials are required. Non university access may be obtained by visiting the University of Sydney Library.||en_AU|
|Appears in Collections:||Sydney Digital Theses (University of Sydney Access only)|