Nociplastic Pain in Endometriosis

Endometriosis is an inflammatory chronic condition associated with chronic pelvic pain that is highly heterogeneous. Traditionally viewed as purely nociceptive pain—pain arising from actual tissue damage activating nociceptors—growing evidence suggests that endometriosis-related pain often involves neuropathic and nociplastic pain components as well.
What is Nociplastic Pain?
Nociplastic pain is a descriptive term for pain that cannot be exclusively defined as nociceptive or neuropathic. The International Association for the Study of Pain (IASP) defines nociplastic pain as arising from altered nociception despite no clear evidence of actual tissue damage or disease/lesion of the somatosensory system causing the pain.
The underlying mechanism in nociplastic pain is Central Sensitization (CS). CS describes the "amplification of neural signaling within the Central Nervous System (CNS) that elicits pain hypersensitivity".
Clinically, a patient may be considered to have possible nociplastic pain if they meet four criteria, including: a pain duration of at least three months, a regional pain distribution, pain not entirely explained by nociceptive or neuropathic mechanisms, and signs of pain hypersensitivity.
Why Does Pain Phenotyping Matter in Endometriosis?
Endometriosis patients with clinical indicators of Central Sensitization often experience worse pelvic pain symptoms and have a worse quality of life, independent of the type of endometriosis or prior surgery.
Importantly, patients with a significant nociplastic pain component may not respond well to hormonal suppression or surgical treatments alone, as these typically target the peripheral, nociceptive pain source. Therefore, classifying nociplastic pain is crucial for implementing personalized treatment plans.
How Is Nociplastic Pain Detected? (The Scoping Review Findings)
Currently, there are no standardized methods for characterizing nociplastic pain in endometriosis-specific populations. A recent scoping review analyzing the literature found that researchers and clinicians use a diversity of tools, grouped into three main categories, to identify CS and nociplastic pain:
1. Patient-Reported Questionnaires (Most Common): These tools act as proxies for centralized pain and include the Central Sensitization Inventory (CSI), which has a validated cut-off point (≥40/100) indicating CS symptoms in this patient population, and the Fibromyalgia Survey Score (FSS). Other questionnaires used are the PainDETECT, McGill Pain Questionnaire, and Visual Analog Scale (VAS).
2. Semi-Objective Assessments (Research Tools): These include Quantitative Sensory Testing (QST) modalities used to detect modulations in somatosensory processing. The Pressure Pain Threshold (PPT) was the most commonly referenced semi-objective assessment. While resource-intensive and often not feasible for clinical settings, QST is important for research.
3. Clinical Assessments: Clinicians use methods such as the digital exam to identify abdominopelvic myofascial trigger points or the Convergence Pelvic and Perineal (PP) criteria to assess sensitivity and pain diffusion.
Looking Forward: Treatment Strategies
Identifying nociplastic pain encourages the use of interdisciplinary care models that address central, local, and psychosocial pain contributors. These models have shown significant effects in improving patient-reported pain outcomes.
Interdisciplinary approaches often include:
• Pain Neuroscience Education: Validating pain and explaining the influence of psychological and social aspects on pain perception.
• Psychological Treatments: Including Cognitive Behavioral Therapy (CBT), mindfulness, and acceptance and commitment therapy.
• Physiotherapy: Site-specific manual physiotherapy has been shown to improve symptoms like dysmenorrhea and dyspareunia in women with endometriosis.
• Health Behavior Changes: Such as dietary modifications that target comorbidities.

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Based on the Scoping Review: "Nociplastic Pain in Endometriosis: A Scoping Review," published in J. Clin. Med. 2024.

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