Nociplastic pain is not central sensitisation, and the difference is not pedantry

"Central sensitisation" and "nociplastic pain" are used interchangeably in a great deal of writing about chronic pain, including by clinicians. The people who defined the second term say the two are not synonyms, that nociplastic pain is not the same thing as chronic primary pain either, and that it is not a new label for pain of unknown origin [s2]. There is no diagnostic test for it. The published criteria work substantially by exclusion, and that design is itself contested by some of the same experts [s2].

What the category is for

Pain medicine has long distinguished two mechanisms. Nociceptive pain arises from tissue injury. Neuropathic pain arises from nerve injury. A Lancet review of chronic pain describes the third category, nociplastic pain, as arising from a sensitised nervous system — and notes that all three affect work-up and treatment decisions at every level, while in practice there is considerable overlap between mechanisms within and between patients, such that many experts regard pain classification as a continuum rather than a set of boxes [s3].

The clinical need is real. A patient with widespread pain, hypersensitivity to pressure and touch, poor sleep and no imaging finding that explains any of it does not fit either older category, and has historically been managed as though the absence of a lesion meant the absence of a mechanism. The International Association for the Study of Pain formally recognised the nociplastic descriptor in 2017 [s6], and in 2021 a group of pain researchers published clinical criteria and a grading system for chronic nociplastic pain affecting the musculoskeletal system in the journal Pain [s1]. Since that recognition the descriptor has drawn both endorsement and critique, and a team registering a systematic review of expert commentary describes the current state as one of misinterpretation, conceptual confusion, clinical challenges and ongoing debate [s6].

The objections, from inside the field

A 2026 paper in the European Journal of Pain, extending a main session on nociplastic pain held at the European Pain Federation conference in Lyon on 26 April 2025, sets out both the settled points and the live disputes [s2].

The settled points are mostly warnings against conflation. Nociplastic pain is defined as pain that arises from altered nociception and is not fully explained by nociceptive or neuropathic mechanisms [s2]. It is not synonymous with chronic primary pain. It is not synonymous with central sensitisation. It is not a new term for pain of unknown origin [s2].

The disputes are more interesting. The authors record that "nociplastic" may not be the best term; that other specialties, such as internal medicine, use different terms and concepts for the clinical conditions pain medicine calls nociplastic; that fibromyalgia syndrome — usually presented as the prototype — is not always a purely nociplastic condition; and that nociplasticity may be a continuous component of pain rather than a separate type, which is why the requirement to exclude nociceptive and neuropathic pain before diagnosing it has been questioned [s2].

That last objection is the structurally important one. If altered nociception is a dimension present to some degree in many pain conditions, then a category defined by ruling the other categories out will systematically misclassify the majority of patients, who have some of each.

Is it testable?

This is where the concept is most vulnerable to the charge of being unfalsifiable, and where the empirical work is currently concentrated. Quantitative sensory testing — measuring pressure pain thresholds, temporal summation and conditioned pain modulation — is the main candidate for an objective marker.

A cross-sectional study of 225 patients with active rheumatoid arthritis tested whether routinely collected clinical measures could stand in for those laboratory tests [s4]. It used three measures of discordance between what patients report and what examiners find: the tender-minus-swollen joint count difference (mean 5.4, SD ±8.2), the proportion of the Disease Activity Score in 28 joints made up of subjective components (mean 49.7%, SD ±13.3%), and patient global assessment minus evaluator global assessment (mean 0.7, SD ±2.2) [s4].

Two of the three tracked the sensory measures. Higher tender-swollen joint count difference was associated with lower trapezius pressure pain threshold (β = −0.05; 95% CI −0.08 to −0.02) and higher temporal summation (β = 0.29; 0.05 to 0.53) [s4]. Higher DAS28-P was likewise associated with lower pressure pain threshold (β = −0.05; −0.07 to −0.04) and higher temporal summation (β = 0.21; 0.06 to 0.35) [s4]. Patient-minus-evaluator global assessment was associated with none of the sensory measures [s4]. The authors describe the associations as modest and read them as evidence that discordance between patient-reported and physician-assessed disease activity may reflect an element of nociplastic pain [s4].

"Modest" is doing real work in that sentence. These are correlations between two imperfect instruments in one disease. They are a long way from a test that could tell a clinician whether a given patient's pain is nociplastic.

The methodological argument about whether quantitative sensory testing can bear this weight at all is unresolved and public: the discussion in Pain has run through editorial, correspondence and published responses into 2026 [s5].

Useful idea or untestable one?

The fairest answer available from the current literature is: useful, provisional, and not yet operationalised.

It is useful because it names something clinicians see and previously had no mechanism for, and because it implies different treatment. It is provisional because its own authors list field testing and eventual modification of the criteria as an outstanding task, alongside developing pharmacological and psychological treatment guidelines organised around the three pain types and working out the pathophysiology driving altered nociception [s2].

It is not yet operationalised because there is no test. A diagnosis reached by excluding two other categories, in a field where its own proponents suspect the categories overlap continuously, is a clinical judgement wearing the clothes of a mechanism [s2] [s3].

None of that makes the pain less real, and the Lancet review is explicit that the associations between chronic pain, psychological distress and sleep disturbance run in both directions — a point frequently lost when a patient is told there is nothing wrong because nothing showed up [s3].

What to watch

Whether the criteria get revised in response to the exclusion objection, and whether any objective marker — sensory testing or otherwise — reaches the point of being able to classify an individual patient rather than separate groups on average.

This article is informational and is not medical advice.

Sources

• Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system — Pain, 2021-05-11
• Nociplastic Pain: Facts, Controversies and Future Tasks — European Journal of Pain, 2025-11-26
• Chronic pain: an update on burden, best practices, and new advances — The Lancet, 2021-05-29
• Association Between Discordance of Disease Activity Indices and Quantitative Sensory Testing Measures of Nociplastic Pain in Patients With Rheumatoid Arthritis — Arthritis Care & Research, 2025-10-16
• Discussion on the value of quantitative sensory testing in nociplastic pain continues: response to 2 letters — Pain, 2026-06-01
• Expert perspectives on the nociplastic pain descriptor: a systematic review of textual evidence protocol — JBI Evidence Synthesis, 2026-07-09