Conditioned pain modulation, cortical imbalance, and arthrogenic muscle inhibition: an integrative model with implications for exercise in chronic pain.

OBJECTIVE: Conditioned Pain Modulation (CPM), cortical excitability, psychosocial factors, and arthrogenic muscle inhibition (AMI, defined as reflex inhibition of musculature surrounding a damaged joint), proposing a framework linking these domains in chronic pain. METHODS: A narrative literature search was conducted in databases, focusing on studies addressing endogenous pain modulation, cortical mechanisms, psychosocial influences, and motor dysfunction in chronic musculoskeletal conditions. RESULTS: Evidence suggests that impaired CPM is associated with altered cortical function, including compromised prefrontal top-down control and maladaptive motor cortex excitability. In this context, AMI reflects peripheral joint-driven adaptations and centrally mediated alterations in motor output. We propose that CPM and AMI interact through a shared cortical-motor axis, where the dorsolateral prefrontal cortex acts as an executive top-down regulator of brainstem nociceptive pathways, while the primary motor cortex serves as a crucial neurophysiological intersection actively engaged during CPM paradigm, collectively contributing to persistent AMI. DISCUSSION: Chronic pain involves complex interactions among pain modulation, cortical mechanisms, and motor control. Consequently, baseline CPM efficiency may help predict AMI severity, offering a novel perspective for early patient identification and stratified, timely multimodal rehabilitation; however, further empirical research is required.