Pain shows up in almost every pelvic health plan of care, but a lot of providers were never actually trained to teach pain in a way that changes outcomes. We learn how to assess tissues, strength, tone, and pathology, but pain is not a simple “damage meter.” It’s a protective output of the nervous system, shaped by context, perceived threat, inflammation, prior experiences, hormones, and learned responses. When we skip pain science education (or keep it vague), patients often stay fearful, hypervigilant, and stuck, especially when imaging is normal or symptoms don’t “match” what we see.
Endometriosis, among other pelvic pain conditions, is one of the clearest examples of why this matters. Endometriosis is characterized by lesions containing endometrium-like epithelium and stroma that develop outside the uterus and are biologically distinct from normal uterine endometrium. Endo is a real inflammatory disease with lesions that can be found on the bowel, bladder, ureters, abdominal wall, and peritoneum commonly. And yet pain severity doesn’t reliably correlate with lesion size, number, or location. Some patients with extensive disease report minimal pain, while others with smaller disease experience life-altering symptoms. Pain science helps us explain that gap: the nervous system can become sensitized over time, turning up the volume on danger signals even when tissues are stable or after the primary driver has been addressed.
Clinically, one of the most important skills is being able to distinguish peripheral pain generators from sensitization. Peripheral drivers include things like active lesions/inflammation, adhesions, pelvic floor overactivity, tissue irritation, and organ-specific contributors. Sensitization shows up when pain persists beyond expected healing, spreads, becomes disproportionate to findings, or is paired with hypervigilance, fear-avoidance, and strong symptom reactivity to stress, sleep disruption, and attention. In pelvic health, cross-talk between organs adds another layer, bladder, bowel, uterus, and pelvic floor can share neural pathways, so symptoms don’t always point neatly to the true source.
This is where pain science education becomes a part of treatment. For endometriosis, an example of pain science education starting point could be: “Endo can absolutely create pain through inflammation and lesion activity, but pain isn’t always a direct reflection of how much disease is present. Over time, your nervous system can become extra protective, like an alarm system that’s gotten too sensitive. That doesn’t mean the pain is in your head. It means your pain IS real, and your nervous system is amplifying signals. The good news is the system can be retrained through the right combination of medical care, pelvic rehab, graded exposure, and nervous system regulation.”
When providers can explain pain clearly, patients stop interpreting every symptom spike as damage. They become more confident with movement, more consistent with rehab, and more resilient during flares. And that’s why pain science education is so important, because endometriosis, IC/PBS, prostatitis, IBS, vaginismus/dyspareunia, and primary dysmenorrhea, your hands matters, but what you do with your words can be the turning point.
If you’re treating endometriosis, or any chronic pelvic pain condition, and you’re not sure whether you’re addressing the “spark” (peripheral drivers) versus the “fuel” (sensitization), this Pain Science class is designed to make that clinical reasoning practical, teachable, and immediately usable in your sessions.
Dr. Tara Sullivan, PT, DPT, PRPC, WCS, IF