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

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.