Chronic Pain and Neuroplasticity: Mechanisms, Maladaptive Remodeling, and Clinical Implications

Chronic pain is increasingly recognized as a brain-based condition sustained by maladaptive neuroplasticity rather than persistent nociceptive input alone. This review integrates structural, functional, and connectomic evidence to examine how chronic pain reorganizes neural circuits involved in sensory processing, emotional regulation, cognitive control, and motivational learning. Findings from neuroimaging studies consistently demonstrate gray matter volume alterations, white matter microstructural changes, aberrant task-evoked activity, and disruptions in resting-state networks such as the default mode, salience, and sensorimotor systems. Predictive markers—including corticostriatal connectivity, corticolimbic anatomy, and prefrontal regulatory capacity—suggest that emotional reinforcement patterns and diminished cognitive modulation contribute to the transition from acute to chronic pain. These mechanisms highlight chronic pain as a self-reinforcing neural state shaped by interactions between sensory, cognitive, and affective processes. The review underscores the need for mechanism-based, interdisciplinary clinical approaches and emphasizes the relevance of these findings for diverse healthcare settings, particularly in Latin America. Future work should prioritize longitudinal, multimodal investigations to refine biomarker candidates and support personalized, neuroplasticity-informed interventions.