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When Your Nervous System Won’t Stand Down After Endometriosis Surgery

Why does pain persist—and what might “central sensitization” mean for you ?

A woman stands in a sunlit office, hand on her abdomen clearly in pain.

If you’ve had endometriosis surgery and your pain is still here (or only partly improved), it can feel like the rug got pulled out from under you. You finally found the "right" surgeon and the surgeon excised the disease. So why does your body still act like there’s an emergency going on?


One increasingly supported explanation is that the nervous system can become overprotective and over-responsive after months or years of pain. In other words, even when surgery addresses a major pain driver, your “alarm system” may keep firing—sometimes loudly. This post pulls together findings from multiple recent studies to explain how that happens, how it’s assessed, and what it means for next steps.


Central sensitization: when the volume knob gets turned up


“Central sensitization” is a medical term for increased sensitivity of pain-processing pathways in the brain and spinal cord. A major 2023 review describes strong converging support for this concept from human pain models and modern imaging work. The key idea is simple: pain intensity doesn’t always match the amount of visible tissue injury—because pain is produced by the nervous system, not by lesions themselves.


That doesn’t mean pain is “in your head.” It means your nervous system may have learned, through repeated threat signals, to respond faster and stronger than it needs to.


How it can feel in real life


People often describe patterns like:

  • Pain that spreads beyond the original area (for example, pelvic pain plus low back pain or whole-body achiness)
  • Sensitivity to touch/pressure, flares from mild activity, or “everything sets it off”
  • Sleep disruption, fatigue, brain fog, or heightened sensitivity to sound/light


These broader features overlap with what the International Association for the Study of Pain calls nociplastic pain—a category related to altered pain processing. The same 2023 review cautions that nociplastic pain and central sensitization overlap but are not identical concepts, and the criteria used clinically can differ.


“But my surgery was successful”—why pain may continue anyway


It’s not rare for surgery to help and still not fully solve pain. In a 2023 cohort study following 239 people after endometriosis surgery, pain scores improved on average—but the range of outcomes was wide. About 55% achieved a meaningful improvement in chronic pelvic pain (defined as at least a 2-point drop on a 0–10 scale), while around 37% had little change and about 8% felt worse.


This doesn’t mean the operation was pointless. It means pain after endometriosis is often multifactorial, and removing lesions is sometimes only one part of the story.


A particularly important finding from that study: people who reported more symptoms consistent with “central sensitization” before surgery—measured by the Central Sensitization Inventory (CSI) questionnaire—were more likely to have more severe ongoing pain at follow-up, even after accounting for how much pain they had before surgery. Higher CSI scores were also linked with worse outcomes for deep pain with sex, pain with bowel movements, and back pain.


One striking detail: CSI scores changed only slightly after surgery on average. That suggests surgery may reduce peripheral drivers (like inflammation or lesion-related irritation), yet not fully “reset” a sensitized nervous system—at least not quickly, and not for everyone.


How do clinicians tell if central sensitization is part of your picture?


The 2023 review emphasizes that commonly used tools are surrogates, not definitive diagnostic tests. In practice, clinicians might look for nuanced patterns such as:

  • Pain in multiple regions (not only where endometriosis was found)
  • Hypersensitivity at distant sites (for example, pressure sensitivity in areas not directly related to the pelvis)
  • Larger pain areas on body maps
  • Symptoms captured by questionnaires like the CSI (sleep issues, fatigue, concentration problems, sensitivity symptoms)


However, the same review cautions that even when there is widespread sensitivity, it doesn’t prove the cause is purely “central.” Peripheral contributors can still exist, including ongoing inflammation, other pelvic pain generators, or even nerve/small-fiber issues. So the most helpful framing is often: central sensitization may be one contributor among several.


A very practical example: pain that worsens with orgasm


Some pain patterns point strongly toward nervous-system and muscle contributions—not just lesion location. A 2024 study in a tertiary endometriosis clinic found that about 14% of patients reported pelvic or lower abdominal pain that worsened with orgasm in the prior three months.


What this symptom correlated with is telling:

  • It was more common in people with pelvic floor muscle tenderness (pelvic floor myalgia) on exam.
  • It was also associated with higher CSI scores, and with worse deep pain with penetration, more sexual distress, and higher anxiety/depression symptom scores.


Notably, in that cohort, orgasm-worsened pain was not associated with ultrasound evidence of adenomyosis or with uterine/cervical tenderness on exam. And surgical/anatomic endometriosis findings didn’t clearly separate those with and without orgasm-related pain. Taken together, this fits a pattern patients often experience: sexual pain isn’t always explained by what is seen on imaging or even at surgery—because the pelvic floor and nervous system can amplify pain during intense muscle contractions and arousal.


If you recognize this symptom, it’s worth mentioning explicitly. Many people only report “pain with sex,” but orgasm-related pain can be a distinct clue that guides evaluation (especially toward pelvic floor and sensitization-informed care).


If this is you, what actually helps?


The research base is still evolving. The 2023 review notes that many treatments proposed to dampen central sensitization have limited evidence and modest average effects, and responses vary—some people even flare with certain approaches if they start too intensely.


That said, the combined evidence supports a broader, nervous-system-inclusive plan, especially if you have widespread symptoms or a high CSI pattern before or after surgery.


In real-world care, that plan often includes:


1) Pain education is a treatment

Understanding that pain can be amplified by the nervous system can reduce the constant pressure to “find the one missed lesion” as the only explanation. Education isn’t about dismissal—it’s about expanding your options and reducing fear-driven cycles that can keep the alarm system on.


2) Rehabilitation that calms, not challenges, the system

With sensitization, the goal is often graded, paced movement and symptom-guided progress rather than “push through.” If sex-related pain is prominent, pelvic floor evaluation can matter—because the orgasm-related pain study found a meaningful association with pelvic floor myalgia.


3) Mental health support as part of pain care

In the orgasm-related pain study, anxiety and depression symptoms were higher in those with orgasm-worsened pain. That doesn’t mean mood “causes” pelvic pain; it often means the nervous system is under sustained strain. Treating sleep, stress physiology, and mood can reduce overall threat signaling and improve coping and function.


4) Medications and other modalities—selectively

Some centrally acting medications may help certain people, but the 2023 review emphasizes that evidence is often low and effect sizes modest across pain conditions. This is where individualized trial-and-error (with a clear stop/continue plan) is more realistic than expecting a single medication to “fix” sensitization.


Timeline expectations: why progress can feel slow


One reason sensitization is so frustrating is that it doesn’t always respond quickly to a single intervention. The surgery study shows that while pain can improve after surgery, sensitization-related symptom patterns may remain relatively high—especially in people with multiple overlapping pain conditions.


Many patients do best with a “two-track” mindset:

  • Track 1: address peripheral drivers (residual endometriosis, adhesions, adenomyosis, bladder/bowel contributors, hormonal factors)
  • Track 2: calm the nervous system (sleep, pacing, pelvic floor work, targeted meds when appropriate, psychological skills, trauma-informed care when relevant)


You don’t have to choose one track. For many people, lasting improvement requires both.


Practical takeaways


Use your next visit to move from “Why am I still hurting?” to “Which drivers are most likely happening in me?” Here are a few high-yield questions to bring:

  • Could we screen for central sensitization/nociplastic features (for example, with the CSI) to help set expectations and guide a plan?
  • Do my symptoms suggest pelvic floor myalgia—and can I be assessed by a pelvic floor–trained clinician? (N.B. It is far better to initiate pelvic floor therapy before surgery)
  • If I have pain with sex, do we differentiate deep dyspareunia vs orgasm-related pain? (They may point to different contributors.)
  • What is our stepwise plan for persistent pain after surgery—what do we try first, how will we measure benefit, and when do we pivot?


What we still don’t know


Even with growing evidence, there are important limits:


Central sensitization is supported by multiple lines of research, but clinical measures are imperfect. Questionnaires and bedside sensitivity findings can suggest altered pain processing, yet they don’t neatly separate “central” from “peripheral” causes—many people have both. The 2023 review stresses caution here, especially when interpreting widespread tenderness as proof of a purely central mechanism.


We also don’t yet have strong, surgery-specific clinical trials proving that treating sensitization in a particular way will reliably eliminate post-op pain in endometriosis. What we do have—especially from the surgery outcomes data—is a consistent signal that people with higher sensitization-type symptom burdens are at higher risk of persistent pain, and may benefit from earlier, more comprehensive support rather than “wait and see.” This is a very valuable takeaway if you have not had surgery yet and trying to figure out why some people do not get relief or if you are facing a repeat surgery. Engage a pain specialist who is conversant and skilled in offering options for central nervous system de-sensitization. These folks are harder to find than good excision surgeons!


In the next post in this series, we’ll zoom in on a closely related (and very treatable) contributor that often keeps the alarm system turned on: pelvic floor and myofascial pain—the muscles that won’t let go.

References

  1. Curatolo. Central Sensitization and Pain: Pathophysiologic and Clinical Insights. Current Neuropharmacology. 2023. PMID: 36237158 PMCID: PMC10716881

  2. Ding, Noga, Bouchard et al.. Pain with orgasm in endometriosis: potential etiologic factors and clinical correlates. The Journal of Sexual Medicine. 2024. PMID: 39039031 PMCID: PMC11372072

  3. Orr, Huang, Liu et al.. Association of Central Sensitization Inventory Scores With Pain Outcomes After Endometriosis Surgery. JAMA Network Open. 2023. PMID: 36848090 PMCID: PMC9972194

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Dr. Steven Vasilev delivers best-in-class endometriosis guidance and a personalized treatment plan—built on evidence and your unique biology.


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