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How does pelvic pain spread?

Photo by Wesley Tingey on Unsplash

Pelvic pain is a common condition affecting millions of women worldwide. The pelvic area specifically refers to the bowel, bladder and reproductive organs. The pain is generally felt in the lower area of the torso and can affect either a small part or the whole area. The type of pain that experienced can vary and has been described in different ways, from being sharp, stabbing, burning, to a dull or heavy ache or cramping and throbbing. When this pain lasts for 6 months or more, it is defined as chronic pelvic pain (CPP). CPP can be viewed as a single condition, but it is also a cluster of symptoms that overlap with other health conditions such as endometriosis, urinary tract infections, pelvic myofascial pain, vulvodynia, bladder pain syndrome and irritable bowel syndrome. The most common reason for referrals to women’s health services is CPP, making up approximately 20% of all outpatient appointments, with over £150 million spent annually by the NHS for pelvic pain treatment and management [1]. Yet, chronic pelvic pain disorders that disproportionately affect women, are not well understood and so often are inadequately managed.

For many women, pain in the pelvic region can be a complex experience that is difficult to make sense of. It has an impact on several aspects of a woman’s life including mental wellbeing, relationships, sexual function, and work. Pain is not always physiologically observed in the body, which can be discouraging for both patients as well as specialists involved in their care. Sometimes the level of pain experienced is greater than the expected severity and doesn’t necessarily match up as far as tissue damage and inflammation are concerned. Pain can also spread to nearby regions in the pelvis which is not always observable in tests or scans. For example, endometriosis sufferers report pelvic pain with varying bowel and bladder symptoms, but these don’t seem to correspond to the location and extent of the disease [2]. Experiencing debilitating symptoms to then be told that tests and scans show nothing is physiologically wrong is scary and demotivating, whilst leaving ambiguity around management and treatment. Much of the time, biomedical treatment approaches rely on observable changes and dysfunction in the body. Uncertainty around what is causing or contributing to pain usually means no label or diagnosis for the symptoms, and without a diagnosis appropriate treatment may be delayed. This can be extremely frightening and unsettling, how can you control or take action to treat and manage something when you don’t have a clear picture of what is going on?

Pain is a multifaceted sensory, cognitive, and emotional experience that engages several brain regions and neural networks. Pain signals are transmitted between the brain and body via the spinal cord through specialised nerve cells (neurotransmitters). In the presence of long-term pain, nerve pathways and signals can end up changing and becoming highly sensitive in response. Below we discuss how pain processes can change and alter the pain experience.

Central sensitisation

One way that pain modifies the way the nervous system works is by altering the way that pain is processed within the central nervous system via a mechanism known as central sensitisation. Central sensitisation is when the nervous system moves into a state of reactivity and the body becomes hypersensitive to pain signals. Due to the reactivity, the threshold for what causes pain is lowered so a small tweak could cause pain even if previously it wasn’t painful or something that was already painful before, causes more pain than it should or is expected.

Let’s think of a pain signal as a ringing doorbell. You ring the doorbell once or a few times and it rings and stops. Ring the doorbell constantly without letting go of the button and it can lead to it malfunctioning. Even when you’ve let go of the doorbell and you’re not pressing anymore, it might continue to ring, ring faster or louder. Applying the same logic to pain, the trigger/damage may no longer be there (i.e., we’re not pressing the bell anymore) but the pain continues to be experienced. For many people, central sensitisation explains the discrepancy between observed physiological damage and the degree of pain reported. A recent systematic review found that there is significant evidence for the presence of central sensitisation in urogynaecological chronic pelvic pain [3].

Peripheral sensitisation

Peripheral sensitisation is a reduction in pain threshold and an amplification in the responsiveness of pain receptors. The pain signals do not necessarily result in more pain than usual, but rather the threshold for pain signals to fire is lower.

Consider when you’ve had a stressful day and several different things have been piling up and adding on to your frustration. Your baseline level of stress and frustration is higher than it usually is. You come home at the end of the day and see that someone has eaten your favourite chocolate bar and that tips you over the edge - you lose it and snap. All it took was one small thing for the frustration to reach a critical level, even though this wouldn’t bother you or result in the same reaction on a day where the baseline level of frustration was lower.

Similarly, all nerves have a baseline level of activity but generally the nerves won’t fire or be activated unless a certain threshold is reached. Many different factors can influence the baseline level of activity in your nerves, including but not limited to stress, changes in environment, mood, movement, and pressure. Normally it takes quite a significant input to get the nerves to fire and to go from baseline to threshold. In many people with chronic pain, the baseline level of activity is higher in the nerves and so it only takes a small stimulus to reach threshold and for pain signals to fire.

Cross organ sensitisation

Whilst we can become more sensitive to pain signals overall, the pain can also become more widespread. Symptoms spread beyond where the pain started to other areas of the pelvis and local organs. This is known as cross-sensitisation.

Think of a Wi-Fi router you have at home with multiple devices connected. If one device has a virus, it could spread to other devices via the router (e.g., your phone, iPad, laptop), because they share the same software and receive similar signals from the router. What started off as one infected device has led to several devices malfunctioning. However, you notice that you have other devices that are connected to the Wi-Fi and they haven’t been affected (e.g., TV, games console, alarms). This is because they have a different operating software and receive different signals from the Wi-Fi router.

In a similar fashion, when one area in the pelvic region starts to experience pain, pain can also arise in normal tissue/organs that are close in proximity to the original pain site as a result of shared neural pathways (i.e. receive signals from the same pathway or ‘router’). Although this phenomenon is still unclear, it is believed to be a contributor to why people with pelvic pain often have multiple issues with pelvic organs e.g., bowel and bladder pain. Research has shown that bladder pain syndrome and chronic pelvic pain are related to other chronic illnesses such as irritable bowel syndrome and vulvodynia [4].

Increased sensitivity to pain in addition to symptoms spreading to other areas can make it difficult to feel that there is a way out or to be positive about the future. When pain becomes chronic and we’re not given the information we need to make sense of our experience, it can feel like a never-ending cycle and be a significant source of stress. Evidence suggests that stress can exacerbate the reactivity of the nervous system and contribute to cross-sensitisation by affecting nervous system functioning and making it highly sensitive [5].

Knowing about pain helps pain

The good news is that an increased understanding of the neural mechanisms involved in pelvic pain can inform treatments that focus on reducing nerve reactivity. In addition, eliminating the confusion around what is occurring in the body when experiencing pelvic pain takes away the additional layer of uncertainty and provides a sense of clarity.

Pain is typically considered more threatening when we’re not sure what’s really going on. Naturally if you’re experiencing pain, you would be hypervigilant and anticipating situations that haven’t happened yet to protect yourself. Previous studies have shown that the expectation of intense pain can make pain feel worse while the expectation of milder pain can make it hurt less. Anticipation of pain increases the perception of threat and activates brain regions involved in both the sensory and emotional intensity of pain, priming a stronger initial pain response [6].

Pain education also enables you to change how you think about pain and replaces fear and uncertainty with reassurance and confidence. Pain is considered threatening and activates threat systems/the fight-or-flight response which serves to increase inflammation and activate nociceptors, the sensors of the pain pathway. Inflammation and greater pain sensitivity amplifies pain perception, adding to the fear and uncertainty and thus keeps people stuck in a chronic pain cycle [7]. Subsequently, catastrophic thoughts and less adaptive coping strategies such as avoidance and isolation are likely to take place and interfere with daily life and limit functioning. Reducing fear and anxiety can dampen pain by diminishing activation of threat systems and unhelpful coping mechanisms.

Where do I get started?

Coping with pelvic pain and the impact it has on different areas of life is challenging but there are some tips you can apply to get you started.

As highlighted above, the anticipation of pain alters sensory experiences. Although not easy, reducing hypervigilance and refocusing attention where possible helps to decrease physical tension and stress, both of which are associated with increased pain experience. Refocusing attention might look like focusing on your breathing, using the 5 senses to shift your attention to the present moment, connecting with nature, or doing something completely different as distraction.

Seek support from those around you and/or people with similar experiences. Navigating pain and its consequences can feel lonely and isolating. Shared experiences and support is a powerful tool; research shows that social isolation can change the way pain is perceived and that maintaining connections results in feeling better equipped to deal with pain [8].

Pain is threatening and frightening. One of our first automatic responses to it, whether that is physically or emotionally is resistance and trying to ward it off (naturally when it’s uncomfortable). Resistance contributes to tension and the perception of threat. Acknowledging and naming how it makes you feel helps with resistance and can create some space between ourselves and our emotions – “I’m feeling scared right now”; “It’s unfair that I have to put in so much effort to cope”. Think about how you would approach a loved one who is experiencing the same thing, usually we are kinder and more compassionate, which can really help when we’re in pain.

The links below are a good place to start:

Pelvic Pain Support Network:

The Pain Toolkit:


[1] Latthe, P., Latthe, M., Say, L., Gülmezoglu, M., & Khan, K. S. (2006). WHO systematic review of prevalence of chronic pelvic pain: a neglected reproductive health morbidity. BMC public health, 6(1), 1-7.

[2] Monten, L., Forman, A., & Andersson, K. E. (2018). Pelvic organ cross-talk: A new paradigm for endometriosis-related pelvic pain?. Journal of Endometriosis and Pelvic Pain Disorders, 10(4), 208-215.

[3] Kaya, S., Hermans, L., Willems, T., Roussel, N., & Meeus, M. (2013). Central sensitization in urogynecological chronic pelvic pain: a systematic literature review. Pain physician, 16(4), 291-308.

[4] Majima, T., & Sassa, N. (2021). Organ cross-sensitization mechanisms in chronic diseases related to the genitourinary tract. Journal of Smooth Muscle Research, 57, 49-52.

[5] Belda, X., Fuentes, S., Daviu, N., Nadal, R., & Armario, A. (2015). Stress-induced sensitization: the hypothalamic–pituitary–adrenal axis and beyond. Stress, 18(3), 269-279.

[6] Borkum, J. M. (2010). Maladaptive cognitions and chronic pain: epidemiology, neurobiology, and treatment. Journal of Rational-Emotive & Cognitive-Behavior Therapy, 28(1), 4-24.

[7] Schlereth, T., & Birklein, F. (2008). The sympathetic nervous system and pain. Neuromolecular medicine, 10(3), 141–147.

[8] Karayannis, N. V., Baumann, I., Sturgeon, J. A., Melloh, M., & Mackey, S. C. (2019). The impact of social isolation on pain interference: a longitudinal study. Annals of Behavioral Medicine, 53(1), 65-74.


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