Biomarkers in Chronic Pain Disorders: From Molecular Diagnosis to Molecular-Guided Therapy

Dear Colleagues,

Clinical tools establishing the chronic pain diagnosis and the severity of different pain origins have been accepted and widely employed in clinical pain practice such as the dichotomization and transition of acute and chronic pain, the definition of a refractory status of chronic pain conditions, and the characteristics of pain therapy responders and non-responders.

However, such clinical tools have been increasingly criticized, and alternatively, an objective quantification of outcome measures like molecular phenotyping of inflammatory mediators has been propagated as a potential useful methodology to differentiate the inter- and intra-individual variability and to define the cluster of chronic patients more likely to respond to pain therapy. Accumulating neuroscientific evidence—both preclinical and clinical data—supports the notion that a disrupted central and peripheral brain–immune system communication (neuroinflammation) is involved in the development and maintenance of chronic pain. This holds true for pharmacological, behavioral, and neuromodulation treatment approaches. The implementation of an individualized treatment regimen in chronic pain patients represents a complex and daunting task, mainly due to the complexity and dynamic character of chronic pain disorders and the pathophysiology of the underlying brain circuits. Such acquisition of different molecular quantitative outcome measures undoubtedly results in large amounts of data necessitating databank-based, automated, and deep-learning pattern recognition systems in order to characterize the biotypes of pain patients that are more and less likely to respond to a particular therapy. Hence, it appears to be imperative to better understand the mechanisms of action (MOAs) of inflammatory circuits mediating pain, as well as the potential of molecular phenotyping as a monitoring tool for pain diagnosis and therapy.

In this Special Issue of Diagnostics, we seek contributions that may be related to molecular-biology-based assays of neuroinflammation; assays of cerebrospinal fluid, saliva, and blood; validation of pain diagnostics and therapy using enzyme-linked immunoassays; mass spectrometry; as well as epigenetic and genetic analysis.

Prof. Dr. Thomas M. Kinfe
Dr. Shafqat Rasul Chaudhry
Guest Editors

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• central and peripheral neuroinflammation
• acute and chronic pain
• biomarker and prediction
• molecular phenotyping