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

Abstract

Chronic neck pain represents a major public health burden with rising prevalence, significant functional impact, and unfavorable projections over the coming decades. Its clinical presentation is heterogeneous and often not adequately explained by structural or imaging findings, highlighting the limitations of the traditional biomedical model. According to the International Association for the Study of Pain, nociplastic pain is defined as pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory nervous system. In chronic neck pain, nociplastic features may manifest to varying degrees through a bidirectional interaction between peripheral input and central processing, potentially involving reduced endogenous inhibition, pain hypersensitivity, attenuated exercise-induced hypoalgesia, and sensorimotor control disturbances. Classification based on the predominant pain mechanism integrates chronicity, symptom distribution, absence of adequate nociceptive or neuropathic explanation, documented hypersensitivity, and associated comorbidities. Rehabilitation is organized according to the predominant mechanism and functional status, emphasizing patient education and reconceptualization, graded exposure and load tolerance regulation, sensorimotor retraining, and functionally targeted exercise, while passive interventions maintain an adjunctive and time-limited role. Future studies incorporating mechanism-based stratification and mechanism-aligned outcomes are needed.

Key Words: Chronic neck pain; Nociplastic pain; Nociplastic features; Mechanistic pain descriptors; Predominant pain mechanism; Pain hypersensitivity; Sensorimotor training; Graded exposure; Rehabilitation

Core Tip: This review integrates the concept of nociplastic pain, a mechanistic pain descriptor recognized by the International Association for the Study of Pain, into the understanding and rehabilitation of chronic neck pain. It encompasses the pathophysiological framework of altered nociception, proposes a clinical reasoning approach based on the predominant pain mechanism, and translates these concepts into rehabilitation principles including patient education, graded exposure, sensorimotor retraining, and functionally targeted exercise. This mechanism-based framework supports individualized clinical decision-making beyond structural explanations and may reduce the risk of misdirected interventions.

INTRODUCTION

Neck pain constitutes a major public health challenge with a growing global burden. In 2020, it affected approximately 203 million people worldwide and ranked 11^th among 369 conditions in terms of years lived with disability, with projections estimating a 32.5% increase by 2050[1]. The burden is disproportionately higher in women and peaks during the most productive years of life. The principal clinical and socioeconomic impact arise not from acute, self-limiting episodes but from persistent and recurrent symptoms. Chronic neck pain (CNP) is associated with increased healthcare utilization, reduced work capacity, and prolonged functional limitation[1,2].

CNP does not represent a single clinical entity but a heterogeneous spectrum with variable course and expression[3]. Historically, its management has depended on structural explanations; however, existing evidence demonstrates that imaging findings do not consistently correlate with pain intensity, chronicity, or functional outcomes[4]. Furthermore, the clinical presentation frequently extends beyond local pain to include headache, dizziness, and disturbances in head-eye coordination, without a proportional relationship to identifiable structural pathology[5]. This discrepancy highlights the need for a clinical framework that moves beyond anatomical localization toward recognition of the predominant mechanism by which pain is transmitted and maintained over time[6,7]. The nociplastic descriptor has not been systematically applied to the assessment and rehabilitation of CNP, despite its increasing use across various chronic pain conditions. Most existing guidance continues to rely on structural or generic exercise models. The purpose of this review is to clarify nociplastic CNP as a category based on the predominant mechanism of pain transmission and maintenance, to summarize the key pathophysiological and functional characteristics associated with altered nociception, and to translate this framework into clinical reasoning and rehabilitation principles.

Terminological note

In this review, several related expressions recur. The term “nociplastic features” is the main descriptive term. It describes clinical findings that point to altered nociception without being associated to a specific diagnosis. The term is preferred because, in cases of CNP, these findings seldom exist in isolation; they often coexist with nociceptive and, at times, neuropathic inputs, and their significance can vary from patient to patient. Therefore, a categorical label would imply a level of certainty than the clinical presentation usually does not support. The extent of these features in a particular patient is referred to as “nociplastic involvement”, representing a spectrum rather than a binary assessment. Where nociplastic processing appears to be the main driving factor, the terms “predominant nociplastic mechanism” and “nociplastic CNP” are utilized. The overall objective is to situate each case within a mechanistic continuum rather than assign it a specific disease label[7,8].

FROM THE BIOMEDICAL MODEL TO MECHANISM-BASED PAIN CLASSIFICATION

The shift from structural interpretation and anatomical localization toward understanding the mechanism by which pain is transmitted and maintained reflects a broader conceptual revision, captured in the updated International Association for the Study of Pain (IASP) definition of pain as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage”[9]. In parallel, chronic pain is now recognized as a distinct pathological condition, involving persistent changes in pain processing[6]. Because purely structural explanations fall short, newer approaches reason beyond anatomical localization and match pain characteristics to treatment. In this context, the IASP introduced three mechanistic pain descriptors, nociceptive, neuropathic, and nociplastic, as a framework for characterizing the predominant mechanism of pain transmission and maintenance[7,10].

IASP mechanistic pain descriptors and clinical framework

The term “mechanistic pain descriptor” refers to pain categories organized according to the probable underlying neurobiological mechanism[7,9]. In the present work, this framework is used to classify clinical presentation with the aim of estimating the predominant way in which the pain experience is generated and maintained. Nociceptive pain arises from actual or threatened damage to non-neural tissue through activation of peripheral nociceptors. It typically serves as a protective function, is relatively well-localized, reproducible with loading, and shows a predictable stimulus-response relationship[9-11]. Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system. It presents with a distribution consistent with the neuroanatomy of the affected structure and is accompanied by positive or negative sensory signs, such as burning or electric-type pain, paresthesias, dysesthesias, and altered sensation[6,12,13].

Nociplastic pain, as defined by the IASP, is pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory nervous system causing the pain[7,10]. Its introduction addressed the need to describe chronic conditions where the intensity and persistence of symptoms are not adequately explained by structural or neurological findings. In such presentations, the predominant mechanism is attributed to altered processing and regulation of nociceptive information by the nervous system, without a dominant nociceptive or neuropathic mechanism being documented[7,14]. This altered nociception may involve, in some cases, changes in excitability or in the function of inhibitory mechanisms, though these findings do not constitute universal or mandatory criteria[15,16]. Peripheral mechanisms may coexist without being the dominant driver of pain persistence[7,16]. Clinically, nociplastic pain tends to present with a diffuse or disproportionate pain distribution that cannot be adequately explained by tissue damage or neural involvement. Additionally, it presents features consistent with altered pain regulation, including enhanced sensitivity to stimuli, disproportionate functional burden, variable or reduced tolerance to functional load, and indications of impaired endogenous inhibitory modulation. These findings are indicative rather than mandatory and are weighed within the framework of mechanism-based classification[6,7,10]. These features are summarized in Table 1.

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.

Distinction of nociplastic pain from related concepts

Nociplastic features have been described in conditions such as fibromyalgia, complex regional pain syndrome type I, and chronic musculoskeletal or visceral disorders where symptom intensity and distribution are not adequately explained by identifiable tissue damage or neural disease[10]. However, the term is not synonymous with “pain of unknown etiology”, nor is it used simply when a structural explanation fails[7,8,17]. Of particular importance is the distinction between nociplastic pain and central sensitization. Central sensitization describes neurophysiological phenomena of increased excitability or reduced inhibitory regulation within the central nervous system, which may lead to pain hypersensitivity and amplified responses to stimuli[7,14,18]. These phenomena are not specific to nociplastic pain and can occur across all pain categories. Nociplastic pain, by contrast, represents a clinical classification based on the predominant mechanism, within which central sensitization constitutes a possible but not mandatory component[7,8,14,16]. A summary of the key distinctions between nociplastic pain and central sensitization is provided in Table 2.

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.

Clinical significance of mechanism-based pain classification

The clinical importance of descriptors lies in their ability to guide reasoning and treatment direction rather than merely labeling the patient[19]. Early identification of nociplastic features, even when the taxonomy remains uncertain, helps clinicians avoid pursuing a non-existent structural target and promotes a multimodal treatment approach[15]. Current data supports a graded rating system. In cervical radiculopathy, network and cluster analyses have identified a subgroup (approximately 25% of patients) with a complex mixed-pain profile of multisite pain, sleep disturbances, widespread sensorimotor changes, non-mechanical pain, spread along a severity continuum rather than falling into discrete categories[20]. Clinical examples of the distinction between nociplastic features and central sensitization are presented in Table 3.

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.

Controversies

The descriptor is recent and remains contested. The dispute is not about whether altered nociceptive processing occurs clinically (it does), but rather about where the term fits within the broader pain taxonomy. Clear distinctions between nociceptive, neuropathic, and nociplastic pain are not always attainable. These categories overlap, and there are no biomarkers that can differentiate them[17]. Häuser and Kosek[8] suggest that nociplastic pain should be viewed less as a discrete category and more as a component that fluctuates within mixed presentations, varying across patients and over time, which is the perspective adopted here. Conversely, Toda[21] contends that this construct should be reintegrated into the neuropathic framework instead of remaining separate. The debate is ongoing. We consider the construct clinically useful while acknowledging that its boundaries are still being defined.

NOCIPLASTIC CNP: PATHOPHYSIOLOGICAL FRAMEWORK AND FUNCTIONAL ORGANIZATION

In CNP, nociplastic pain is not a new or separate pathology but a change in how the pain transmission and processing system is functionally organized[7,10]. The central organizing principle is the bidirectional interaction between peripheral input and central processing: Persistent changes in sensory information from the cervical spine and adaptations in central regulation do not operate independently but co-determine one another, creating a self-reinforcing system that may contribute to the maintenance of altered nociception. This impaired regulation may be reflected in increased temporal summation of pain (TSP), reduced effectiveness of conditioned pain modulation (CPM), and attenuated exercise-induced hypoalgesia[7,16,22]. These adaptations should not be considered necessarily permanent or generalized and are dependent on context, functional load, and chronicity[7,16].

Central neuroplastic adaptations

In presentations where nociplastic features predominate, changes have been described in the functional organization and connectivity of brain networks involved in the sensory, cognitive, and emotional dimensions of pain, including the insula, the anterior cingulate cortex, and the amygdala, affecting how sensory information is evaluated and meaning is attributed[7,15,16]. In parallel, changes in central nervous system excitability and descending inhibitory function have been described, resulting in reduced endogenous inhibition and increased amplification of nociceptive input[7,16]. In CNP, these changes extend beyond pain intensity to affect overall sensory processing, influencing appraisal, attentional allocation, and the emotional salience attributed to bodily stimuli[15].

Sensorimotor, multisensory and peripheral adaptations

The cervical spine is the segment primarily responsible for active positioning and orientation of the head in space, depending on rich proprioceptive input from the deep cervical and suboccipital muscles, structures characterized by high muscle spindle density and a critical role in precise head control[23-25]. In CNP, persistent nociceptive input and its altered central processing are accompanied by changes in neuromuscular organization, including altered deep cervical muscle activation patterns, increased superficial muscle co-activation, and reduced proprioceptive accuracy[23,26]. Meta-analytic data confirm that individuals with neck pain demonstrate worse performance in head repositioning tests and greater postural sway, with the magnitude of the difference influenced by pain intensity and the presence of dizziness[27]. Stiffer gait strategies and performance differences under dual-task conditions have also been reported, with a potential contribution of fear of movement[28-30].

The cervical spine is also a critical junction for proprioceptive, visual, and vestibular interaction. Impaired cervical proprioceptive input in subgroups of patients with CNP may be associated with less effective multisensory integration, manifesting as increased visual dependence, difficulty under demanding functional conditions, and symptom exacerbation during simultaneous head movement and visual targeting[5,27]. In cases where nociplastic features predominate, these phenomena are not uniform across all patients and are considered within the context of the overall clinical presentation[7,8].

At the peripheral level, findings consistent with peripheral sensitization and increased local mechanosensitivity have been described, including lower pressure thresholds and proposed facilitatory mechanisms such as ion channel changes or sympatho-afferent interactions[16]. Structural and functional changes in cervical muscles, as well as altered mechanoreceptor activity in degenerative cervical discs and facet joints, may also contribute to ongoing afferent input[23,26]. These peripheral findings shape the afferent signal but cannot by themselves explain the intensity and persistence of symptoms in CNP[7,16,23,26].

CLINICAL REASONING AND CLASSIFICATION BASED ON NOCIPLASTIC FEATURES IN CNP

The assessment of nociplastic features in CNP relies on a systematic analysis of clinical data from the patient’s history, clinical examination, and functional behavior[7,8,31]. Nociplastic features in CNP are expressed clinically as a disproportionate impact of pain on function and as symptom variability that does not follow a linear relationship with mechanical or functional load[7,16]. Functional burden does not merely reflect pain intensity but the degree to which pain affects motor control, posture, load tolerance, and participation in demanding activities[6]. Clinically, performance becomes hard to sustain as functional and sensorimotor demands rise: Tolerance fluctuates, cervical function varies, and patients deteriorate disproportionately under high multisensory or cognitive load[5,30].

Chronicity and symptom distribution

Classifying a presentation as predominantly nociplastic requires symptom chronicity (> 3 months) and the presence of regional or disproportionately widespread musculoskeletal pain[7]. A central finding is a distribution that is not clearly localized or is disproportionately extensive, exceeding the expected boundaries of a single peripheral source or documented neural lesion[7]. In CNP, this frequently presents as symptom extension toward the shoulder, scapula, or upper limb without consistent neuroanatomical correspondence, variable localization, and discordance between symptomatology and imaging findings[3,4,32,33]. The co-occurrence of non-local symptoms, such as headache, dizziness, or a sense of unsteadiness, has been described in CNP populations, reflecting multisensory involvement of cervical proprioceptive input[5,23,24]. An extended or variable pain distribution increases the likelihood of nociplastic involvement, provided that no adequate alternative explanation is documented[7]. However, such patterns should not be presented as automatic proof of a specific pain mechanism but rather as clinical expressions of a system operating under persistent pain and dynamic alteration of nociception[8,17].

Ruling out a predominant nociceptive or neuropathic mechanism

A key step in mechanism-based classification is to assess whether a predominant nociceptive or neuropathic mechanism can adequately explain the clinical presentation[7]. Neurodynamic tests possess high sensitivity but limited specificity when evaluated in isolation[6,7,31,34]. In the absence of objective neurological deficits or documented somatosensory system lesions, positive neurodynamic findings do not establish neuropathic disease. Mechanosensitivity in this context may reflect heightened nervous system sensitivity rather than structural neural damage[7,31,34].

Documentation of pain hypersensitivity

Pain hypersensitivity to evoked stimuli is a key element supporting possible nociplastic involvement[7]. On history taking, reports of hypersensitivity in the painful region, such as sensitivity to touch, pressure, movement, or thermal stimuli, as well as disproportionate responses to low-intensity functional stimuli, prolonged worsening after mild activity, and reduced tolerance to everyday loads suggest altered nociceptive processing[7,32,33]. On clinical examination, the reproduction of disproportionate pain in response to mild mechanical or thermal stimuli constitutes a central finding. Specifically, static and dynamic mechanical allodynia, thermal allodynia, and lingering painful sensation following assessment have been described and documented in CNP populations[7,31,33,35,36].

Comorbidities and sensorimotor assessment

The co-occurrence of heightened sensitivity to sensory stimuli (such as sound, light, or odors), sleep disturbances with frequent nocturnal awakenings, fatigue, and cognitive difficulties (such as impaired concentration or memory), increases the certainty of nociplastic involvement when combined with hypersensitivity and widespread distribution[7,8]. Sensorimotor assessment provides functional indicators of reduced adaptability, which are weighed alongside pain distribution and hypersensitivity within the framework of mechanism-based clinical reasoning[5,37]. Treleaven[5] proposes a structured clinical assessment framework organized across four domains, head movement control, head-eye coordination, postural stability, and oculomotor control, with performance compared in neutral vs cervical torsion positions considered to separate a cervical from a vestibular contribution.

The head repositioning test, relocating the head to a neutral or predefined target after movement with vision occluded, serves as a practical bedside example within this framework[5]. When nociplastic features are predominant, a degraded result should be interpreted cautiously and not as a fixed proprioceptive lesion requiring mechanical correction. Cervical sensorimotor performance shows inconsistent correlation with pain intensity and duration, and it does not change predictably over time[38]. Moreover, when differences arise, their magnitude is influenced by both pain intensity and dizziness[27]. Consequently, the result is evaluated as a context-dependent indicator of reduced sensorimotor adaptability, considered alongside hypersensitivity and pain distribution, rather than viewed as a definitive structural endpoint.

Synthesis and mechanism-based classification

The final classification is based on the combined consideration of chronicity, extended or poorly localized distribution, absence of adequate explanation from predominant nociceptive or neuropathic mechanisms, and reported and/or clinically evoked hypersensitivity and comorbidities[7]. It serves to synthesize clinical data and guide treatment[8]. The reasoning process is schematically depicted in Figure 1.

Figure 1  Clinical decision algorithm for grading nociplastic pain, adapted from Kosek et al[7].

When findings conflict or are incomplete, they do not carry equal weight. Evoked pain hypersensitivity in the affected region is the crucial feature; without it, the criteria for even a potential nociplastic classification are not met, regardless of significant functional disproportionality[7]. When hypersensitivity is present, a history of it, combined with relevant comorbidities, shifts the classification from possible to probable. Therefore, the typical case of regional pain with severe functional impact but no observable hypersensitivity does not support a nociplastic rating. It is more appropriately viewed as provisional, with a predominantly nociceptive or mixed presentation needing to be reconsidered first, followed by a reassessment of the patient over time.

REHABILITATION BASED ON THE PREDOMINANT PAIN MECHANISM

Principles and clinical reasoning

Rehabilitation in CNP with nociplastic features is grounded in matching the predominant pain mechanism with the patient’s clinical presentation, rather than relying on diagnostic labels or structural findings[8]. The clinical approach shifts from pursuing a presumed pain “source” toward understanding how pain shapes functional behavior, sensorimotor organization, and load tolerance[7,14]. The broader management of nociplastic pain also encompasses pharmacological agents targeting central pain processing, psychological interventions such as cognitive-behavioral therapy, and lifestyle modifications within a biopsychosocial framework[15,39,40].

Mechanism-based rehabilitation constitutes a set of techniques embedded and originating from a staged clinical reasoning framework. Classification based on pain characteristics is incorporated as a dynamic process of clinical interpretation, continuously reassessed according to changes in symptomatology, functional behavior, and response to intervention[6,7]. A central principle is the recognition that the clinical presentation often arises from the coexistence of nociceptive, neuropathic, and nociplastic features with variable relative predominance[7,20]. Direct analgesia is not the primary goal; symptom reduction may emerge secondarily through improved functional regulation[8,40].

Intervention selection is based on the estimated predominance of nociplastic involvement, the patient’s clinical presentation, and tolerance to therapeutic stimuli, not on diagnosis or pain intensity as standalone criteria[8,15]. Contemporary mechanism-based approaches combine interventions that reduce perceived threat, gradually restore load tolerance, and functionally re-regulate the pain system[7,40]. An overview of rehabilitation emphasis according to the predominant pain mechanism is presented in Table 4.

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.

Patient education and reconceptualization

Patient education aims to reduce the threatening interpretation of symptoms, shape realistic expectations, and support active engagement in rehabilitation[15,40]. As a targeted, mechanism-based process, it focuses on the differentiation between pain and tissue damage, the understanding that symptom intensity may reflect altered central processing, and the reassessment of movement safety, enabling gradual reintegration into functional activity even in the presence of mild expected symptoms[7,8,15,40]. It is critical to avoid oversimplified or purely psychological interpretations of pain. Education must remain consistent with the mechanism, creating the conditions for safe graded exposure and sensorimotor retraining[7,14].

Graded exposure and load tolerance regulation

Graded exposure gradually restores load tolerance and dampens disproportionate pain-system responses to functional stimuli[7,40,41]. In CNP with nociplastic features, symptom intensity and persistence do not bear a proportional relationship to mechanical load but reflect altered central processing and reduced tolerance to routine functional demands[7,14,16]. In practice, this involves controlled and progressive re-exposure to postures and movements that provoke disproportionate responses, such as gradually increasing the duration of sustained upright cervical posture or the range of cervical rotation during exercise, initially under clinical supervision[22,40].

Progression follows predetermined functional criteria, initial tolerable activity dose, consistent application, and reassessment against overall functional response, rather than on momentary symptom intensity. Progression is achieved through qualitative load modifications, duration, complexity, sensorimotor or cognitive demand, rather than necessarily through intensity increases. For example, progressively increasing the duration of a cervical stabilization exercise or the number of movement directions performed in a single session before modifying resistance or load parameters[22,40]. Low-to-moderate symptom fluctuations are considered expected, provided they are not accompanied by prolonged worsening or substantial limitation of functional participation. Their interpretation as a normal adaptive response, rather than as an indication of tissue damage, constitutes a key element of managing patients with increased nociplastic involvement[7,15].

Sensorimotor retraining

Sensorimotor retraining targets how the nervous system controls and perceives movement. In CNP, sensorimotor dysfunction manifests as reduced proprioceptive accuracy, altered head-neck control, and increased muscular co-activation[5,7]. Improved sensorimotor accuracy is associated with more economical motor patterns and reduced protective overactivity, even when pain intensity has not fully resolved[42,43].

Unlike graded exposure, sensorimotor training is characterized by clearly defined dosage parameters and specific quality criteria. The goal is to enhance sensorimotor organization through regulated low-to-moderate load stimuli that impose significant demands on precision, coordination, and neuromuscular control[5,44]. Interventions include exercises targeting head position control, cervico-ocular coordination, balance, and movement accuracy, with the goal of reducing sensorimotor dysfunction and restoring confidence in movement[43,45].

The same tasks used to evaluate sensorimotor control, such as head repositioning, gaze stability, and controlled head-eye coordination, can also serve as a low-threat entry point into movement[5]. For individuals who experience kinesiophobia or avoid movement, these tasks provide a graded, non-threatening approach to re-engage the cervical spine in activity. This allows for assessment and early sensorimotor retraining to occur along a continuum rather than as distinct stages[41,43].

A recent study achieving ≥ 80% expert consensus established a practical clinical framework for sensorimotor training in neck pain: A training cycle of 4 weeks to 12 weeks, with a frequency of 3 sessions to 21 sessions per week, session duration of 10 minutes to 20 minutes, and 2-6 targeted exercises per session[44]. Each exercise is organized in 2 sets to 5 sets of 7 repetitions to 15 repetitions or 20 seconds to 60 seconds’ duration, with 20 seconds to 40 seconds’ rest intervals. Dosage is modified based on clinical criteria such as compensatory movements, execution quality, and motor control adequacy.

Motor imagery (MI) and action observation (AO) have been proposed as complementary neurocognitive strategies targeting cortical reorganization in chronic pain. Implicit MI performance appears impaired in CNP[46]. MI and AO of cervical therapeutic exercises seem to induce immediate local hypoalgesia, with AO additionally producing remote pain modulation[47,48], while a systematic review reported superior pain relief and range of motion improvement when MI is added to standard rehabilitation in chronic musculoskeletal conditions, albeit with limited certainty of evidence[49]. A recent randomized controlled trial demonstrated that MI training combined with motor control exercises was superior to exercises alone in improving pain sensitivity, functional status, and neck awareness in women with CNP, with effects maintained at 12-week follow-up[50]. However, the evidence remains limited by small samples, heterogeneous protocols, absence of standardized MI procedures for the cervical spine, and predominance of immediate rather than sustained outcomes. The role of these approaches in CNP with documented nociplastic features has not yet been investigated. Interestingly, tactile localization training has been found to be as effective as manual therapy (MT) in pain reduction, suggesting that the “localization” and discriminative touch inherent in manual contact, rather than purely mechanical force, may drive the therapeutic reorganization of somatosensory representations[51].

Functionally targeted exercise

Functionally targeted exercise aims to restore the patient’s capacity to perform demanding daily activities with adequate control, tolerance, and consistency, not merely to execute isolated movements or exercises[22,52]. Unlike sensorimotor retraining, which primarily targets accuracy and reliability of specific motor control tasks, functionally targeted exercise incorporates complex motor and environmental contexts that approximate real-world participation demands[22,52]. Examples of functional patterns of load intolerance and corresponding therapeutic exercise principles are outlined in Table 5.

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.

Exercise is organized around functional activities requiring combined head and neck movement, stabilization, attention, and endurance over time. Exercise selection is based on the functional profile and participation limitations of the patient rather than on generalized exercise protocols[22,52]. Progression is determined by the maintenance of qualitative control and tolerable symptomatology in increasingly demanding functional contexts[40,52]. Cognitive functional therapy represents an integrated behavioral framework that combines the reconceptualization principles described above with graded functional exposure and lifestyle modification[53,54]. This emerging framework has shown promising but preliminary results in patients with CNP and requires further research before firm recommendations can be made.

Passive interventions

Passive interventions, such as MT interventions that seem to exert their clinical effect by normalizing endogenous pain inhibitory pathways[55], are incorporated with an adjunctive and time-limited role, aimed at facilitating active participation rather than serving as autonomous or corrective treatments[15,56]. Notably, while MT can shift CPM and TSP in CNP patients toward values observed in pain-free individuals, the correlation between these neurophysiological changes and clinical improvement is weak. Therefore, a measurable shift in CPM or TSP does not consistently lead to symptom relief[57].

In the context of nociplastic features, passive techniques may be interpreted as interventions that modulate sensory input and the threat context, rather than as means of direct mechanical or structural effect[14,56]. This framing plays a significant role in patient education. By presenting hands-on treatment as a method to enhance the perception of safety in movement, rather than as a means of repairing damage, it aligns with the broader educational message. This approach shifts the patient’s expectation from being fixed to actively engaging in movement again. When applied in this manner, a passive technique serves as a temporary bridge to active participation: It reduces the immediate barriers to movement, while the benefits are consolidated through graded exposure and sensorimotor retraining, rather than through the technique itself[15,56]. Used selectively and briefly, they can reduce short-term discomfort and improve movement tolerance, helping patients begin or continue active interventions such as graded exposure and sensorimotor retraining[5,22,43].

Current clinical practice guidelines for non-specific neck pain do not recommend the use of electrotherapy, ultrasound, or low-level laser, due to the lack of documented additional benefit over placebo or other active interventions[58]. When applied in isolation or presented as the primary treatment, passive interventions may reinforce passive care models and expectations of external correction, limiting active patient engagement in rehabilitation[8]. Their value is judged by their contribution to the overall rehabilitation process rather than by their analgesic effect alone[7,40].

LIMITATIONS

Conceptual limitations

Nociplastic pain is a relatively recent mechanistic descriptor, still maturing both conceptually and clinically[6-8]. The proposed criteria are based primarily on consensus processes and clinical documentation, without an independent biological marker for validation, which limits the objective confirmation of grading[7,8]. Furthermore, it has been argued that the current grading criteria may be incomplete, as they require sensory hypersensitivity exclusively, potentially excluding individuals with chronic primary pain who present with nondermatomal sensory deficits rather than sensory gains, a presentation documented in 20% to 40% of chronic primary pain populations[59]. These criteria were developed as a general mechanistic framework applicable across different pain systems, which may limit their specificity in particular clinical contexts such as CNP. Applying mechanism-based classification in CNP calls for interpretive caution and the avoidance of rigid, sharply drawn categories.

Methodological limitations of the available literature

Most studies in CNP include heterogeneous populations without explicit stratification by predominant pain mechanism, a recognized central methodological limitation that hampers the comparability and generalizability of findings[6,7,22]. Interventions targeting sensorimotor or functional parameters are frequently evaluated primarily through pain intensity and disability outcomes, while the systematic recording of mechanism-aligned indicators, such as sensorimotor control, remains less consistent and less standardized[14,43]. This mismatch between intervention targets and assessment outcomes limits the interpretation of results in relation to the proposed mechanism of action. Furthermore, long-term follow-up data remain limited, and substantial variability in dosage, duration, and mode of application across studies restricts the comparability of findings[43,52,60]. The recent establishment of consensus-driven dosage recommendations via Delphi[44] methodologies exemplifies the necessity for enhanced standardization. To date, no clinical trials have explicitly evaluated rehabilitation of patients with documented nociplastic features in neck pain as a distinct mechanism-based category[6,7,22].

Limitations of the present review

The present work constitutes a conceptual and narrative review rather than a systematic review with meta-analysis. The synthesis of evidence is based on critical interpretation of the available literature rather than standardized quantitative synthesis, which may affect the degree of generalizability and strength of the conclusions.

CONCLUSION

Rehabilitation in CNP with nociplastic features requires alignment of the intervention with the predominant pain mechanism and its functional expression, rather than exclusively with diagnostic labels or structural findings[6,7]. This framework shifts the emphasis from structural causality toward the regulation of functional behavior within the pain system, without negating the biological dimension of the pain experience. Rehabilitation does not guarantee linear analgesia. In fact, symptom change may be variable and non-linear, and effectiveness depends on the predominant mechanisms, their functional expression, and dynamic adaptation of the therapeutic plan to the clinical course[7,40].

No single intervention constitutes a universal solution; effectiveness depends on clinical reasoning based on the predominant mechanism and consistent matching of intervention to clinical presentation[7,14,20]. Future studies are called upon to incorporate mechanism-based classification at the design stage, to employ outcomes aligned with the therapeutic target, and to investigate response indicators to sensorimotor and functional interventions. The integration of nociplastic involvement into physiotherapy reasoning does not replace clinical judgment but organizes it within a more coherent framework, a necessary condition for targeted and sustainable rehabilitation strategies in CNP[7,8].