Why does endometriosis hurt differently than it used to?

You used to only have period pain. Now the pain appears during ovulation, after sitting for a long time, after a walk, during intercourse, and sometimes for no apparent reason. Or the opposite: periods are less painful than they were years ago, but in their place there's a constant, dull discomfort that refuses to go away. Or the pain has moved from the lower abdomen to the hips, back, thighs, and has begun to radiate to places that seem unrelated to the uterus.

If you have endometriosis and recognize this description, you may be wondering if the disease is progressing, if you've missed something, or if the surgery didn't help as it should. The answer to these questions is complex and has a specific biological basis. Endometriosis pain changes over time, not always because the disease itself changes. Often, it's the way the nervous system processes pain that changes.

Pain as a signal and pain as a disease

To understand why endometriosis hurts differently than it used to, it's worth starting with a basic distinction that is fundamental in pain medicine.

Acute pain is a signal. It informs us of tissue damage, prompts us to protect the injured area, and subsides as the tissue heals. It is proportional to the stimulus and serves a biologically meaningful function. Chronic pain operates differently. After some time, it ceases to be solely a signal of damage and becomes a clinical problem in its own right, with its own maintenance mechanisms, independent of the original cause.

Endometriosis begins as a source of acute pain, driven by inflammation, cramping, and bleeding of endometrial tissue outside the uterus. However, with prolonged disease and repeated episodes of severe pain, the nervous system undergoes changes that can cause the pain to take on a life of its own, regardless of what's happening in the pelvis.

Central Sensitization: When the Nervous System Becomes Hypersensitive

Central sensitization is a phenomenon that underlies many of the changes in pain observed in women with endometriosis. It is a state of persistent lowering of the pain threshold in the central nervous system that develops in response to prolonged or intense painful stimuli.

Simply put, the spinal cord and brain, which have been processing pain signals from the pelvis for years, become increasingly sensitive. Neurons in the dorsal horns of the spinal cord, responsible for transmitting pain information to higher levels of the nervous system, increase their excitability. Several things begin to happen simultaneously.

First, stimuli that were previously not perceived as painful begin to trigger pain. Sitting for an hour, a full bladder, or slight pressure in the lower abdomen become sources of discomfort or pain. This phenomenon is called allodynia. Second, stimuli that were previously mildly painful now cause disproportionately intense pain. This phenomenon is called hyperalgesia. Third, the area from which the pain is felt expands beyond the original source. Pain from the pelvis begins to be felt in the back, hips, thighs, and perineum. Fourth, the pain begins to appear spontaneously, without a perceptible external stimulus.

Central sensitization is well documented in endometriosis and explains many observations that women describe as a "game-changer" in the disease. Importantly, its presence does not mean that the endometriosis is progressing or that the surgery has failed. It indicates that the nervous system itself requires attention, regardless of the status of the pelvic lesions.

Neuropathic Pain: When Nerves Become the Source of Pain

In addition to central sensitization, neuropathic pain can develop in endometriosis. Neuropathic pain occurs when damaged or sensitized nerves begin to generate pain signals on their own, without an external stimulus.

In endometriosis, nerves can be damaged directly by disease foci, particularly in the deeply infiltrating form, where lesions penetrate the richly innervated retroperitoneal space. They can also be compressed by adhesions or infiltrates. Over time, even after lesions are removed, these modified nerves can persist in pain regardless of the presence of active endometrial tissue.

Neuropathic pain has characteristic descriptions: burning, tingling, shooting, electric shock, and numbness. It often radiates along the nerve, explaining why endometriosis pain can radiate down the leg, appear in the buttock, or radiate to the groin. It is also often asymmetric, which can be confusing and leads women to seek an explanation for the pain in the spine, hips, or neurological syndromes unrelated to endometriosis.

Neuropathic pain responds less to traditional painkillers, another observation many women describe with frustration: ibuprofen, which used to help, now makes no difference.

Adhesions and mechanical sources of altered pain

Not all changes in the nature of pain in endometriosis are due to changes in the nervous system. Some have mechanical causes, related to adhesions that develop during the course of the disease or as a complication of surgery.

Adhesions are bands of connective tissue that hold together abdominal organs and structures that should normally move freely. An ovary adhered to the pelvic wall, a bowel adhered to the uterus, or a bladder attached to the anterior uterine wall by adhesions—each of these situations alters the biomechanics of organs and can cause pain with previously painless movements. Sitting, standing, stretching, or filling the bowel or bladder become painful not because a new endometriosis lesion has developed, but because movement tightens the structures attached by adhesions.

Adhesion pain is often described as a dull, aching pain associated with specific body position or activity. It appears in areas where there was no pain before surgery, which can be a source of considerable anxiety. It's important to know that postoperative adhesions are a common occurrence after any abdominal surgery and that their presence does not indicate a surgical error or recurrence of endometriosis.

Visceral pain and its peculiarities

Endometriosis, especially when it affects the intestines, bladder or retroperitoneal space, can generate visceral pain, which is governed by different rules than somatic pain from muscles or skin.

Visceral pain is poorly localized, diffuse, and difficult to pinpoint. It often radiates to distant sites because visceral organs share nerve pathways with distant areas of the body. Pain from the intestines can be felt in the back. Pain from the uterus can radiate to the thighs. Pain from the retroperitoneal space can mimic sciatica. This explains why the description of endometriosis pain can be so varied and why women consult orthopedists, neurologists, and gastroenterologists before anyone connects the symptoms with endometriosis.

The visceral nature of pain also has other implications. Internal organs are innervated by the autonomic nervous system, which responds to stress, anxiety, and emotional states. Therefore, the severity of visceral pain in endometriosis often correlates with stress levels, sleep deprivation, and psychological state. This does not mean that the pain is "psychosomatic" or contrived. It does mean that the autonomic nervous system is an integral part of the pain mechanism and that psychological factors have a real, biological impact on pain perception.

Does a change in pain mean the disease is progressing?

This is a question many women ask themselves, and it requires an honest answer: not always.

A change in the nature of pain may result from the progression of endometriosis and the appearance of new lesions or infiltrates, especially if it is accompanied by other new symptoms, such as bladder or intestinal bleeding, worsening fertility problems, or significant cyst enlargement. In such cases, diagnostic imaging and specialist consultation are necessary.

However, pain changes can also result from central sensitization, neuropathic pain, postoperative adhesions, or a shift in the balance between various pain mechanisms, without any progression of the endometriosis itself. Removing the disease foci during surgery does not automatically reset the changes that have occurred in the nervous system over the years. Therefore, pain may persist or change in nature even after technically successful surgery.

Distinguishing between these scenarios is of practical importance, as treating neuropathic pain and central sensitization requires different tools than treating active endometriosis lesions. An approach focused solely on further surgery, without considering the neuropathic component, may not provide the desired relief.

When and where to seek help

Some general directions for women whose pain has changed character and has stopped responding to previous treatment.

Discussing the change in pain with your gynecologist is always the first step. It's important to describe the change as specifically as possible: when the pain changed, what it looks like now, where it radiates, what makes it worse and what relieves it, and how it responds to current medications. This information helps plan further diagnostics.

A pain management specialist or pain clinic is a worthwhile option for chronic pain that doesn't respond to standard treatments. Treating neuropathic pain and central sensitization requires a multimodal approach that incorporates pharmacology, physical therapy, and psychological support simultaneously.

Urogynecological physiotherapy has documented applications in the treatment of chronic pelvic pain, pelvic floor hypersensitivity, and adhesion mobilization. It is an often overlooked yet highly valuable component of comprehensive care.

Psychological support in the context of chronic pain is not an admission that pain is fabricated. It is a recognition that chronic pain has a psychoneurological component that responds to psychological interventions regardless of the underlying organic cause.

Your pain has a history and a mechanism

The changing nature of endometriosis pain is one of the most disorienting experiences for women with this disease. It requires reinterpreting what's happening in the body and often confronting the fact that medicine doesn't always have simple answers.

But behind every change lies a mechanism that can be named and treated. Central sensitization, neuropathic pain, adhesions, and visceral pain are not vague labels but specific biological phenomena with documented pathways. Knowing about them is the first step to seeking help in the right place.

Źródła:

• Słomka J, Pilewska-Kozak AB. Central sensitization as a mechanism of chronic pain in women with endometriosis, a systematic review of the literature. Medical Studies, Studia Medyczne, 2026.
• Dolci C, Jean Dit Gautier E, Lannez L, Lebuffe G, Wattier JM, Rubod C. Neuropathic-like pain affects pain perception in patients with deep endometriosis: an observational study. Archives of Gynecology and Obstetrics, 2025.
• Taylor HS, Kotlyar AM, Flores VA. Endometriosis: new insights and opportunities for relief of symptoms. PMC, PubMed Central, 2025.
• EAU Guidelines on Chronic Pelvic Pain. European Association of Urology Guidelines, 2025.
• International Consensus Guidelines on Neuropelveology. Joint Guidelines of the International Society of Neuropelveology, 2026.