Psychological trauma can result from witnessing an event that is perceived to be life-threatening or to pose the potential of serious bodily injury to self or others. Such experiences, which are often accompanied by intense fear, horror, and helplessness, can lead to the development of, and are required for the diagnosis of, post-traumatic stress disorder (PTSD).1
It was originallythought that PTSD represented a normative response, at the extreme end of a response continuum, the severity of which related primarily to trauma/stressor intensity. However, it has become clear over time that the response of an individual to trauma depends not only on stressor characteristics, but also on factors specific to the individual.2
For the vast majority of the population, the psychological trauma brought about by the experience of profound threat is limited to an acute, transient disturbance. Though transient, such reactions can be quite unpleasant and are typically characterized by phenomena that can be grouped for the most part into three primary domains: (i) reminders of the exposure (including flashbacks, intrusive thoughts, nightmares); (ii) activation (including hyperarousal, insomnia, agitation, irritability, impulsivity and anger); and (iii) deactivation (including numbing, avoidance, withdrawal, confusion, derealization, dissociation, and depression). As these reactions are self-limiting by definition, in general they provoke minimal functional impairment over time. On the other hand, for a significant minority of the population, the psychological trauma brought about by the experience of profound threat leads to a longer-term syndrome that has been defined, validated, and termed PTSD in the clinical literature. PTSD is often accompanied by devastating functional impairment.
PTSD is characterized by the presence of signs and symptoms in the three primary domains described above for a period extending beyond 1 month (such periods can in some cases occur long after the original, precipitating traumatic exposure). The signs and symptoms of PTSD, therefore, appear to reflect a persistent, abnormal adaptation of neurobiological systems to the stress of witnessed trauma. The neurobiological systems that regulate stress responses include certain endocrine and neurotransmitter pathways as well as a network of brain regions known to regulate fear behavior at both conscious and unconscious levels. Not surprisingly, much research has consequently focused on exploring these systems in more detail as well as attempting to elucidate the pathological changes that occur in patients who develop PTSD. More specifically, there have been and continue to be ongoing efforts to link neurobiological changes identified in patients who suffer from PTSD to the specific clinical features that constitute PTSD, including altered learning/extinction, heightened arousal, and intermittent dissociative behavior as examples relevant to each of the three primary domains. Efforts to identify neurobiological markers for PTSD originally presumed that abnormalities were acquired “downstream” from an exposure, as a consequence of traumatic experience. It could be, however, that certain abnormalities in the patient with PTSD simply represent pre-existing or “upstream” pathology that is functionally dormant until released by trauma exposure and detected thereafter upon investigation. Along these lines, recent interest has focused on factors that seem to modulate outcome variation in neurobiological systems following trauma exposure including genetic susceptibility factors, female gender, prior trauma, early developmental stage at the time of traumatic exposure, and physical injury (including traumatic brain injury - TBI) at the time of psychological trauma; these parameters likely contribute to vulnerability for, versus resilience against, developing PTSD.
Although the biological, psychological, and social ramifications of PTSD have been under scientific scrutiny for some time now, and treatment has improved dramatically, much remains unknown about this condition and controversy persists in both the neuroscientific as well as the clinical/treatment literature. In this text, we review the neurobiological impact of psychological trauma from the perspective that genetic, developmental, and experiential factors predispose certain individuals to the development of PTSD. More specifically, we review the current database as pertains to biological markers of PTSD and the possibility that some biological markers may not be acquired but, rather, may in fact predate trauma until functionally “unmasked” by stress. Where relevant, we also make note of similarities between PTSD and TBI, which extend beyond wellknown signs and symptoms (such as irritability and social withdrawal) to include abnormalities in the same neurobiological systems. Lastly, the article includes a short section on basic considerations for future direction. Ideas put forth in this communication are done so in the interest of developing a consistent model for conceptual purposes. It is recognized at the outset that numerous inconsistencies can be found in the literature that highlight the multifactorial and complex nature of this field.