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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.
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Kapernaros et al. (2026) studied this question.
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