TBI, PTSD, and Depression


Interesting article in yesterday’s New England Journal of Medicine about new research into PTSD, depression, and physical health problems in U.S. troops who have suffered “mild” traumatic brain injuries. (“Mild traumatic brain injury” sounds benign, but MTBIs are “mild” only in comparison with more severe brain injuries.)

In this study, mild traumatic brain injury was significantly associated with psychiatric symptoms, notably PTSD, and the association remained significant after combat experiences had been controlled for. More than 40% of soldiers with injuries associated with loss of consciousness met the criteria for PTSD. The data indicate that a history of mild traumatic brain injury in the combat environment, particularly when associated with loss of consciousness, reflects exposure to a very intense traumatic event that threatens loss of life and significantly increases the risk of PTSD.

This is apparently the first such epidemiological study of TBI in soldiers.

MTBI is defined as a head injury resulting in loss of consciousness or in altered mental status — “being dazed, confused, or `seeing stars,’ or not remembering the injury”.

The authors do not venture to suggest a single mechanism for the greater risk of PTSD in soldiers who have suffered MTBIs:

The mechanisms of these relationships are complex. Studies have not confirmed any direct link between PTSD and injury to brain tissue from the concussion itself, although this is an important area of research that makes use of new technology, such as diffusion tensor imaging. There is evidence that implicit processing of traumatic memories and fear conditioning, both mechanisms for the development of PTSD, occur even in persons with severe traumatic brain injury who are amnesic for the traumatic event. Mechanisms that are likely to underlie both the onset of PTSD after traumatic brain injury and the physical symptoms related to PTSD and depression include biologic processes associated with exposure to extreme stress, activation of the hypothalamic–pituitary–adrenal axis, autonomic reactivity, reactive cell–mediated immune responses, disturbed sleep physiology, and altered perception of symptoms.

In an editorial, Richard A. Bryant, Ph.D. discusses the possible mechanism in more depth:

The finding that mild traumatic brain injury is associated with an increased incidence of PTSD raises interesting possibilities about how mild traumatic brain injury may compound PTSD. Biologic models posit that a fundamental mechanism underpinning PTSD involves an exaggerated response of the amygdala, resulting in impaired regulation by the medial prefrontal cortex. The amygdala is central to the development and expression of conditioned fear reactions, and studies in humans and animals have shown that learning to inhibit these fear reactions involves inhibition by the medial prefrontal cortex. Consistent with this model, patients with PTSD have diminished activation of the medial prefrontal cortex during the processing of fear. Mild traumatic brain injury often involves damage to the prefrontal cortex due to shearing forces of the frontal regions against the skull. It is possible that a person’s capacity to regulate the fear reaction may be impaired after mild traumatic brain injury because the neural networks involved in the regulation of anxiety may be damaged as a result of the mild traumatic brain injury.

Cognitive models propose that PTSD is maintained when trauma survivors have inadequate cognitive resources to manage their trauma memories and to engage adaptive cognitive strategies to manage the traumatic experience (e.g., they are unable to appraise a distressing state as temporary and, therefore, have heightened anxiety). Mild traumatic brain injury can impair cognitive resources and may compromise the capacity to engage in cognitive strategies to manage the aftermath of a psychological trauma. There is overwhelming evidence that maladaptive cognitive strategies (e.g., ruminating that one will never recover from the traumatic experience) after trauma are a major predictor of PTSD. Therefore, it is possible that people with mild traumatic brain injury have insufficient cognitive resources to engage appropriate cognitive strategies, which results in a greater incidence of PTSD.

In lay terms, the bruised brain has difficulty dealing with fear and memories of trauma, and either sort of difficulty may increase the chance of PTSD.

One lesson for criminal-defense lawyers is to always be aware of the possibility of TBI and PTSD. Lots of people suffer minor traumatic brain injuries — I’ve received a couple myself — and nobody knows which ones cause permanent impairment. Another lesson is to look for TBI when PTSD presents itself, and look for PTSD when TBI presents itself.

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