Neurobiology of Chronic Pain, Posttraumatic Stress Disorder, and Mild Traumatic Brain Injury

Abstract

Objectives: This article describes the neurobiology of psychological injuries-chronic pain, concussion/mild traumatic brain injury (MTBI), and fear/posttraumatic stress disorder (PTSD)-toward elucidating common mechanisms in central and peripheral sensitization that contribute to their onset, exacerbation, and maintenance. Central sensitization refers to central nervous system (CNS) and related processes, while peripheral sensitization is typically referred to as receptor field expansion. The three psychological injury diagnoses/conditions are accompanied by impairments in function after negligent events (such as motor vehicle accidents (MVAs)) that lead to tort court action.

Methods: The conducted literature review involved an extensive scoping review of recent neurobiological literature on chronic pain, PTSD, and MTBI. The literature review sought biological markers that distinguish them.

Results: For chronic pain, concussion/MTBI, and fear/PTSD, this article reviewed definitions and critical neurobiological research. The literature review did not find evidence of biological markers, but the role of sensitization emerged as important.

Conclusions: Common therapeutic processes, such as focusing on sensitization, might be helpful for these conditions. As for causal mechanisms related to sensitization in the causality of psychological injuries, the major ones hypothesized relate to the biopsychosocial model, psychological control, and activation-inhibition coordination.

Keywords: chronic pain; mild traumatic brain injury; neurobiology; posttraumatic stress disorder; sensitization.

Figure 1

This figure illustrates how brain/central and bodily/peripheral functions and their sensitivities/dysregulations mutually interact in the generation of symptoms and exaggerations/exacerbations of psychological symptoms that take place after negligent events at claim. These processes can apply equally to PTSD and MTBI symptoms and not only chronic pain ones. The central part of the figure depicts the interaction of central and peripheral sensitizations in the process. The right part of the figure indicates the reciprocal interactions over different sensitizations related to reception, sensation, perception, and conception, which, respectively, relate to chronic pain, MTBI/concussion, PTSD/fear, and generalized sensitivity. The left side of the figure depicts the different levels of the CNS that are involved in the psychological injuries and their own reciprocal, dynamic interactions. The literature review on the neurobiology of the psychological injuries reviewed in the first part of this article supports these dynamic models of sensitization and the CNS generally depicted in the model. That said, the arrows in the model are not meant to represent formally established pathways that have been empirically supported in the present context; they indicate pathways requiring further precision, empirical support, and connection to the conditions/diagnoses at issue. Aside from further conceptualization and testing, the model in the figure needs research on its potential practical applications, including how sensitization-informed practice can help ameliorate patient conditions, providing adjunct added value to more standard and empirically supported approaches.