Chronic pain is a widespread and debilitating health issue, characterized by pain that persists beyond normal tissue healing. Increasing evidence highlights the role of endogenous pain modulation—the body’s internal mechanisms for enhancing or inhibiting pain signals - in the development and maintenance of chronic pain.
Key neural circuits, especially descending inhibitory and facilitatory pathways involving the brainstem and spinal cord, can become dysregulated, leading to increased pain sensitivity and the phenomenon known as central sensitization. Understanding the underlying neurobiological processes and functional impairments in endogenous pain modulation is critical, as this knowledge can shed light on why some individuals develop chronic pain and do not respond to conventional treatments.
Goal
The primary goal of this Research Topic is to explore and clarify how endogenous pain modulation becomes altered in chronic pain conditions, and the implications this has for assessment and treatment. Despite significant advances in pain research, the precise mechanisms by which modulation pathways—such as conditioned pain modulation (CPM) and diffuse noxious inhibitory controls (DNIC)—are disrupted in chronic pain remain unclear. Moreover, clinically accessible methods to evaluate these pathways are underused, and therapeutic strategies to restore their function are not yet well established.
This collection seeks to address these gaps by promoting interdisciplinary research that examines the physiological, molecular, and psychological components of endogenous pain regulation in chronic pain patients. In particular, we welcome contributions that investigate psychological resilience- including coping resources, adaptive emotion regulation, and related protective factors -and how resilience may shape endogenous inhibition and facilitation, influence central sensitization, or help explain variability in symptom burden and treatment response. By bringing together original studies, reviews, and perspectives, the aim is to advance understanding and support the development of targeted assessment tools and individualized pain management strategies.
Scope and Information for Authors
This Research Topic welcomes submissions addressing the mechanisms, assessment, and therapeutic modulation of endogenous pain pathways in chronic pain populations. We encourage Original Research, Systematic Reviews, Narrative Reviews, Brief Research Reports/Brief Communications, Perspectives/Opinions, and Clinical Case Series (where appropriate). Submissions should provide clear implications for future research, clinical practice, or therapeutic innovation in chronic pain and endogenous pain modulation.
Specific themes include, but are not limited to:
Neurochemical and neuroimaging studies of endogenous pain modulation
Advances in clinical assessment tools (e.g., QST, CPM) and their clinical utility
Links between modulation dysfunction and psychological, genetic, or other individual-difference factors
Psychological resilience as a moderator/mediator of CPM/DNIC and pain outcomes
Interventions aiming to enhance endogenous inhibition or reduce facilitation (including multimodal approaches)
Article types and fees
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Brief Research Report
Case Report
Clinical Trial
Data Report
Editorial
FAIR² Data
FAIR² DATA Direct Submission
General Commentary
Hypothesis and Theory
Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.
Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.