Citation

Weis CN, Webb EK, deRoon-Cassini TA, Larson CL. Biol. Psychiatry 2021; ePub(ePub): ePub.

Copyright

(Copyright © 2021, Elsevier Publishing)

DOI

10.1016/j.biopsych.2021.07.023

PMID

unavailable

Abstract

The psychological trauma associated with events resulting in traumatic brain injury (TBI) is an important and frequently overlooked factor that may impede brain recovery and worsen mental health following a TBI. Indeed, individuals with comorbid post-traumatic stress disorder (PTSD) and TBI have significantly poorer clinical outcomes than individuals with a sole diagnosis. Emotion dysregulation is a common factor leading to poor cognitive and affective outcomes following TBI. Here we synthesize how acute post-injury molecular processes stemming either from physical or emotional trauma may adversely impact circuitry subserving emotion regulation, and ultimately yield long-term systems-level functional and structural changes that are common to TBI and PTSD. In the immediate aftermath of traumatic injury, glucocorticoids stimulate excess glutamatergic activity, particularly in prefrontal cortex-subcortical circuitry implicated in emotion regulation. In human neuroimaging work, assessing this same circuitry well after the acute injury, TBI and PTSD show similar impacts on prefrontal and subcortical connectivity and activation. These neural profiles indicate that emotion regulation may be a useful target for treatment, including for early intervention to prevent the adverse sequelae of TBI. Ultimately, the success of future TBI and PTSD early interventions depends on the fields' ability to address both the physical and emotional impact of physical injury.

Language: en

Keywords

glutamate; HPA axis; neuroimaging; postconcussion syndrome; posttraumatic stress disorder; traumatic brain injury