Nociplastic chronic neck pain: From mechanisms to physical therapy clinical practice

Table 1 Summary of pain mechanisms based on the predominant mechanism of transmission and maintenance (International Association for the Study of Pain)

Pain mechanism	Brief description	Illustrative clinical examples1
Nociceptive	Pain arising from the activation of peripheral nociceptors due to actual or threatened tissue damage. Typically well-localized with a predictable relationship to loading	Whiplash-type injury, facet joint arthropathy
Neuropathic	Pain caused by a lesion or disease of the somatosensory nervous system. Distribution consistent with neuroanatomy, often with burning/electric character and sensory deficits	Cervical radiculopathy from disc herniation, right C5 foraminal stenosis
Nociplastic	Pain associated with altered nociception without adequate evidence of active tissue damage or neural disease. Often accompanied by widespread distribution, pain hypersensitivity, and disproportionate functional burden	Chronic neck pain with widespread hypersensitivity, neck pain with diffuse back pain and headache

¹Examples are illustrative and do not imply a “pure” mechanistic category, as mixed features frequently coexist in clinical practice.

Table 2 Comparison between nociplastic pain and central sensitization

	Nociplastic pain	Central sensitization
What it is	A pain category in which the predominant mechanism of transmission and maintenance relates to altered processing and regulation of nociceptive information by the nervous system, without adequate explanation from dominant tissue damage or documented somatosensory disease	A neurophysiological phenomenon of increased amplification or reduced inhibition of pain signals within the central nervous system, producing enhanced sensitivity to stimuli
Indicative findings (non-specific, non-diagnostic)	Altered modulation of pain; enhanced response to sensory stimuli; reduced descending inhibition; widespread or variable pain distribution; diffuse pressure hypersensitivity; attenuated exercise-induced hypoalgesia; sensorimotor disturbances. May include central sensitization phenomena but is not limited to them	Increased spinal neuron excitability; temporal summation; hyperalgesia; allodynia; expanded receptive fields; and reduced descending inhibition. May contribute to nociplastic pain but does not itself constitute a pain category
Is it a pain category?	Yes, a category based on the predominant mechanism	No, a functional phenomenon, not a diagnosis
Coexistence with other mechanisms?	Frequently coexists with nociceptive or neuropathic features	Can occur across different pain categories
Relationship between the two	May include central sensitization phenomena	Is not equivalent to the nociplastic pain category
Ref.	Treede et al[6], 2019; Kosek et al[7], 2021; Raja et al[9], 2020; Kosek et al[10], 2016

Nociplastic pain is a pain category based on the predominant mechanism of transmission and maintenance, as defined by the International Association for the Study of Pain. Central sensitization is a neurophysiological phenomenon of increased facilitation or reduced inhibitory regulation that can be observed across pain categories. The findings listed are indicative and non-specific and do not constitute diagnostic criteria.

Table 3 Examples of neck pain with predominant nociplastic features without strong evidence of central sensitization, and cervical radiculopathy with secondary central sensitization without change in pain category

Neck pain with predominant nociplastic features without strong evidence of central sensitization		Cervical radiculopathy with central sensitization without predominant nociplastic features
Patient with chronic neck pain	Diffuse pain distribution in the neck and shoulder girdle; disproportionate functional burden relative to mild or non-specific imaging findings; increased fatigue and low tolerance to functional load; limited pain reduction following exercise; and impaired head-eye coordination	Patient with C6 radiculopathy	Pain with clear neuroanatomical distribution; neurological findings consistent with radicular involvement; and imaging confirmation of nerve root compression
Pain phenotype	No marked increase in pain with repeated stimuli; endogenous pain inhibition is borderline normal; and no widespread hypersensitivity beyond the painful area	Pain phenotype	Increased pain intensity with repeated stimuli; reduced effectiveness of endogenous inhibitory mechanisms; and secondary hypersensitivity in the broader region
Interpretation	The clinical presentation is consistent with predominant nociplastic features, without clear evidence of pronounced central sensitization on available testing	Interpretation	The predominant pain mechanism remains neuropathic. Central sensitization functions as an additional amplifying mechanism without changing the pain category
Ref.	Treede et al[6], 2019; Raja et al[9], 2020; Kosek et al[10], 2016

These examples are presented for conceptual clarification of the distinction between a pain category based on the predominant mechanism and specific neurophysiological phenomena.

Table 4 Indicative rehabilitation emphasis according to the predominant pain mechanism

Intervention	Predominantly nociceptive	Predominantly neuropathic	Predominantly nociplastic
Patient education	Tissue healing timelines; load management relative to tissue tolerance; expected recovery trajectory	Nature of nerve sensitivity; neuroanatomical explanation of symptoms; realistic neural recovery expectations	Dissociation between pain and tissue damage; symptom intensity as altered processing rather than structural harm; reassessment of movement as safe
Graded exposure and load tolerance	Progressive loading matched to tissue healing stages; symptom response proportional to mechanical load	Gradual increase in activity within neural mechanosensitivity thresholds; avoidance of sustained provocative positions	Progression based on predetermined functional criteria rather than symptom intensity; qualitative load modifications (duration, complexity, cognitive demand)
Sensorimotor retraining	Restoration of local motor control and segmental stability relevant to the injured structure	Retraining of movement patterns adapted to neural mechanosensitivity; graded neurodynamic exposure	Improvement of proprioceptive accuracy, head-eye coordination, and postural control; reduction of protective overactivity
Functionally targeted exercise	Task-specific loading replicating demands of daily or occupational activities relative to tissue capacity	Functional reintegration with consideration of nerve sensitivity and fatigue management	Complex functional contexts approximating real-world participation; emphasis on consistency and tolerance under variable conditions
Passive interventions	Pain modulation and facilitation of tissue mobility to support active loading	Neural tissue mobilization; management of local inflammation and mechanosensitivity	Modulation of sensory input and threat context; short-term facilitation of tolerance to active participation
Ref.	Treleaven et al[5], 2024; Kosek et al[7], 2021; Häuser et al[8], 2026; Raja et al[9], 2020; Kosek et al[10], 2016; Smart et al[11], 2010; Treede et al[12], 2008; Colloca et al[13], 2017; Nijs et al[14], 2023; de Zoete et al[22], 2023; Hage et al[34], 2024; Thapa et al[40], 2025; Cook et al[56],2023

The table presents indicative emphases and does not imply mutually exclusive categories. Mixed mechanistic features frequently coexist, and intervention selection is based on clinical reasoning according to the predominant mechanism.

Table 5 Functional patterns of load intolerance and therapeutic exercise principles in chronic neck pain with nociplastic features

Functional expression	Clinical significance	Therapeutic exercise principle
Intolerance to sustained postures	Pain or fatigue emerges before functional demands are met	Progressive increase in duration rather than intensity, with emphasis on performance consistency
Early fatigue in low-intensity activities	High control cost for simple everyday functions	Exercise at submaximal load with emphasis on maintaining quality over time
Deterioration under cognitive or time pressure	Difficulty combining movement control and attention	Integration of cognitive or environmental demands into functional exercises
Variable performance from day to day	Unstable functional tolerance	Progression based on a tolerable performance range rather than a single “good” session
Avoidance or hesitation in daily activities	Participation restriction, independent of strength or range of motion	Task-oriented practice directed at the execution of functional activities
Ref.	Treleaven et al[5], 2024; de Zoete et al[22], 2023; Camerota et al[52], 2024

Functional patterns are illustrative and do not constitute diagnostic criteria. Therapeutic targeting is determined by the overall clinical presentation and the predominant pain mechanism.