Emotional Traumatic Brain Injury

Abstract

The definition of traumatic brain injury (TBI) has expanded to include mild TBI and postconcussive syndrome. This evolution has resulted in difficulty disentangling the physical trauma of mild TBI from the emotional trauma of posttraumatic stress disorder (PTSD). Advances in stress neurobiology and knowledge of brain injury at the macroscopic, microscopic, biochemical, and molecular levels call for a redefinition of TBI that encompasses both physical and emotional TBI. Conceptualizing a spectrum of TBI with both physical and emotional causation resolves the irreconcilable tangle between diagnostic categories and acknowledges overlapping forms of brain injury and shared systemic effects due to hormonal and inflammatory mediators. Recognizing emotional TBI shifts the interpretation of emotional trauma from a confound to a comorbid, related cause of brain injury. The mechanism of emotional TBI includes the intricate actions of stress hormones on diverse brain functions due to changes in synaptic plasticity, where chronically elevated hormone levels reduce neurogenesis, resulting in dendritic atrophy and impaired cognition. The overlapping effects of physical and emotional trauma are seen in neuropathology (ie, reduction of hippocampal volume in TBI and PTSD); fMRI (similar regional activations in physical and emotional pain); and systemic sequelae, including changes in proinflammatory cytokine levels and immune cell function. Accumulating evidence favors a change in the definition of TBI to encompass emotional TBI. The definition of TBI will be strengthened by the inclusion of both physical and emotional trauma that result in diverse and overlapping forms of brain injury with sequelae for physical and mental health.

Inflammation in Posttraumatic Stress Disorder: Dysregulation or Recalibration?

“…Similarly, increasing evidence from preclinical models of environmental and psychosocial stress indicates that stress-induced activation of resident microglia in the central nervous system (CNS) leads to mild or modest pro-inflammatory responses that are reminiscent of parainflammation rather than bona fide , pathogenic neuroinflammation [ 36 - 39 ]. Cellular and molecular signals associated with stress-induced CNS microdamage [ 40 , 41 ] are proposed to trigger in this setting a “sterile” microglia response which contributes to a recalibration of behavior in favor of neurorepair, but may nevertheless be prone to premature suppression [ 42 , 43 ] or low-grade chronicity [ 38 , 41 ]. On this account, an essentially adaptive CNS response to stressful conditions may be inadequate from the outset or ultimately amount to an unfavorable net effect in some individuals.…”

Anxiety and Mood Disruption in Collegiate Athletes Acutely Following Mild Traumatic Brain Injury

“…Anxiety and mood disruption occur acutely following mild traumatic brain injury (mTBI) and are often misidentified, not adequately assessed, and not discussed with patients [ 1 , 2 , 3 ]. MTBI is a disruption in the normal functioning of the brain following head injury and is associated with five common phenotypic profiles or subtypes: anxiety and mood disruption, vestibular impairment, cognitive impairment, headache or migraine, and oculomotor impairment [ 4 , 5 , 6 ].…”