Persistent pelvic pain (PPP) presents challenges above and beyond those suffered by others living with chronic pain. In the past, patients have been reluctant to present to healthcare providers as their pain has embarrassing gender, fertility and sexual health overtones. Their reluctance has been reinforced by their experiences of frequently being dismissed, downplayed or normalised as ‘just period pain’, blamed on their mental health or straight disbelief by healthcare providers based on unhelpful stereotypes and inadequate training to provide the comprehensive assessment and care these patients need. Patients have often had myriad unsuccessful treatments or no treatment at all so that they eventually avoid and even distrust healthcare practitioners. This situation has been exacerbated by poor understanding of the mechanisms contributing to chronic pain in general and PPP in particular.

However, there are glimmers of light for PPP sufferers in 2019. Pain medicine is a rapidly evolving discipline with exciting new frontiers now being explored in the science of neuro-immune interactions and the social and psychological disciplines. Pain medicine was recognised as a medical specialty by the Australian Medical Council in 2005, and endorsed as a scope of practice in New Zealand in 2012. This recognised the importance of the problem of unrelieved pain in the community and the need for a comprehensive medical response through education, training and practice. The Faculty of Pain Medicine (FPM) of the Australian and New Zealand College of Anaesthetists (ANZCA) was established in 1998 to address these needs.

Sources of PPP include disorders of the gynaecologic, urologic, gastro-intestinal and neurological systems, either as the sole or, more commonly, multi-factorial aetiology. Genetic and environmental influences, gender-specific mechanisms, including the role of sex hormones, as well as changes related to pregnancy may also contribute. The unique neuroanatomical features of the lumbo-sacral nerve plexus, a predilection for somatic referral and an ability to provoke strong emotional responses add to the complexity of the PPP phenotype.

Known mechanisms of PPP include pelvic organ and somatic causes of nociception (including inflammation) and neuropathic pain. Persistent or cyclical nociceptive inputs from the periphery to the spinal cord can lead to increased membrane excitability, synaptic facilitation and disinhibition resulting in reduced thresholds for activation, spontaneous activity and enlargement of receptive fields whereby spinal cord neurons now respond to noxious and innocuous stimuli. In addition, recent research in the contribution of immune mechanisms to persistent pain show that the neuronal processes involved in conducting heightened nociception are triggered by anatomically distributed immune signals.¹ These signals arise from glia, immune-like cells, distributed throughout the nervous system exhibiting bidirectional communication between peripheral immune, spinal immune and brain immune systems. Glia, particularly microglia, engulf the synapses and control neurotransmitter release both pre- and post-synaptically. Normally glia maintain neuronal reactivity; however, they can amplify neuronal signalling sufficiently to create persistent pain states through fundamental reorganisation with recruitment of maladaptive microcytic and glial processes as well as T-cell involvement, changing trophic support and releasing pro-inflammatory cytokines that modify the pre- and post-synaptic terminals permanently. Together this suggests that the pathology of persistent pain resides in the glial component, but is expressed by adaptations in the neuronal system, namely peripheral and central sensitisation and cross sensitisation between organs.²

These neuro-immune changes can be triggered by end-organ dysfunction anywhere in the body. In PPP, multiple organ systems appear to be involved either as the primary pathology generates a secondary response to pain in other tissues or as a result of viscero-somatic or viscero-visceral convergence with expansion of the receptive fields of spinal cord neurons. So, it is not surprising that PPP is often described as multiple pains in several different sites, commonly associated with a range of other somatic and autonomic symptoms.

Changes extend to the brain where characteristic alterations in brain morphology, commonly decreases in regional grey matter, can be seen on functional MRI scans suggesting altered neuronal activity at the brain level as well as affecting the ‘top-down regulatory pathways’.³ Multiple areas, including the ventro-medial thalamus, parabrachial amygdala, somatosensory pathways and the periaqueductal grey, are involved. The ventro-medial prefrontal cortex is particularly important in pain appraisal, driving aversive behaviours. Neuroplastic changes in these areas lead to changes in the appraisal of pain, altering descending modulation and avoidance learning, underpinning the emotional and behavioural responses to pain. The extent of these changes is modulated by genetic factors, brain development throughout childhood, particularly adverse childhood events, and past pain experiences. Much depends on the language used to communicate pain experiences. The language of pain and the influence of cultural contexts are relatively new, but very important, areas of pain research. Pain is a subjective and very personal experience that is communicated to others through language and behaviours. Women with PPP frequently report unsatisfactory conversations with healthcare practitioners and not surprisingly feel misunderstood.

Treating patients with PPP therefore requires a sound understanding of the language of pain, the social context in which patients experience pain and the psychological impact of the pain in addition to knowledge of pelvic organ pathology and neuroanatomy in order to develop a comprehensive management plan. The most complex patients are best served by a multidisciplinary team working in an interdisciplinary environment using a sociopsychobiomedical paradigm.⁴ Discipline-specific training is required to address the wide range of biomedical contributions to PPP. Additional training in pain medicine addresses the sociopsychological dimensions, changing attitudes and behaviours while enhancing the knowledge and skills required to manage the more challenging PPP conditions. However, not every gynaecologist will wish to or be able to undertake an additional training program in pain medicine. Simple steps such as raised awareness of the potential complexity of the patient’s presentation of PPP and altering lines of inquiry when taking the history, considering different approaches to investigations, preoperative preparation and postoperative pain relief can make a real difference. Engaging early with a pain medicine specialist and allied health practitioners with pain training can be useful.

Gynaecologists are in a prime position to set expectations for the patient and their other healthcare providers regarding recovery times and opioid analgesic tapering. The language used in history taking is critically important. Not infrequently, the language used has inadvertent high threat value for patients. Reframing information into less threatening language can help. Judicious use of adjuvant analgesics, such as low-dose amitriptyline, from the first night postoperatively through to the follow up visit can be a useful strategy for reducing opioid use. Learning about pain has been shown to empower patients to manage pain more effectively. Gynaecologists can assist by directing patients to reputable online resources such as the Pelvic Pain Foundation of Australia website⁵ or the New South Wales Agency for Clinical Innovation website, the Pain Management Network.⁶

For gynaecologists wishing to learn more about persistent pain, the FPM offers two options; a series of online learning modules and a specialist training program. There are 12 one-hour modules in the Better Pain Management⁷ program. Participants may choose to do one, a few or all 12 modules. For gynaecologists wanting more immersive learning, the faculty’s specialist training pathway leads to the qualification of specialist pain medicine physician. The FPM was the first multidisciplinary medical academy in pain medicine in the world. The two-year fellowship is an additional fellowship to a primary specialist or general practice qualification. The faculty’s 2015 curriculum and training program reflects the sociopsychobiomedical paradigm and is based on the CanMEDs structure. It consists of workplace-based clinical supervision with in-training progressive feedback and targeted summative assessments. A range of resources are available on the faculty’s e-learning platform to support learning. They include modules introducing nine essential topic areas for the core training stage (first year) of which visceral pain is one. The practice development stage (second year) provides an opportunity for trainees to develop expertise in topic areas of their choice. PPP is one option for which learning outcomes have been defined.⁸

Gynaecologists face many challenges in looking after women with PPP. It takes a lot of time and emotional resilience. Currently, the remuneration structures in private practice are grossly inadequate and indeed there are perverse incentives for gynaecologists providing long consultations. In the public sector, there are high demands on outpatient clinics and pressures on surgical waiting lists. Limited access to pelvic physiotherapists, pain trained psychologists and specialist pain clinics across both sectors also contributes to less-than-optimal care. As individual physicians, we may feel we cannot do much about these problems; however, persistent pain is finally being recognised as a major public health issue and federal government funding is now targeting specific pain conditions, especially endometriosis, and by association PPP. We can lobby our respective professional organisations, RANZCOG and FPM ANZCA, to work together and strongly advocate for change. Our patients are depending on us.

1. KN Dodds, EAH Beckett, SF Evans, MR Hutchinson. Spinal Glial Adaptations Occur in a Minimally Invasive Mouse Model of Endometriosis: Potential Implications for Lesion Etiology and Persistent Pelvic Pain. Reprod Sci. 2019;26(3):357-69.
2. CA Von Hehn, R Baron, CJ Woolf. Deconstructing the neuropathic pain phenotype to reveal neural mechanisms. Neuron. 2012;73(4):638-52.
3. A/Prof Tor Wager presentation, FPM Refresher Course Day, May 2018
4. DB Carr, YS Bradshaw. Time to flip the pain curriculum? Anesthesiology. 2014;120(1):12-14.
5. Pelvic Pain Foundation of Australia. www.pelvicpain.org.au.
6. Pain Management Network. www.aci.health.nsw.gov.au/chronic-pain.
7. Better Pain Management program. www.fpm.anzca.edu.au/resources/better-pain-management.
8. Faculty of Pain Medicine 2015 training program www.fpm.anzca.edu.au/training/2015-training-program.