Preface

Humans are remarkably resilient in the face of crises, traumas, disabilities, attachment losses, and ongoing adversities. In fact, resilience to stress and trauma may be the norm rather than the exception. However, to date, most research in the field of traumatic stress has focused on neurobiological, psychological, and social factors associated with trauma-related psychopathology and deficits in psychosocial functioning. While much has been learned in these areas of research, particularly about post-traumatic stress disorder (PTSD), far less is known about resilience to stress and healthy adaptation to stress and trauma.

The study of resilience is enormously challenging. The first hurdle involves definition. Currently, there is no single agreed-upon definition of resilience in the clinical or scientific literature. In a review of the published literature on risk, vulnerability, resistance, and resilience, Layne and colleagues (2007) described the lack of precision and numerous terminological inconsistencies in the meanings of these concepts, and identified at least eight distinct meanings for the term “resilience.” For example, definitions of resilience have ranged from symptom-free functioning following trauma exposure (Bonanno et al., 2006) to positive adaptation despite adversity (Garmezy, 1993), and even to enhanced psychobiological regulation of stress/fear-related brain circuitry, neurotransmitters, and hormones (Charney, 2004). The American Psychological Association (2010) has defined resilience as “the process of adapting well in the face of adversity, trauma, tragedy, threats or even significant sources of threat.”

There is understandable reluctance to utilize pharmacotherapy during the immediate aftermath of exposure to a traumatic event. Although most people will be distressed during the acute post-impact phase, the great majority will recover during the following weeks. As a result, clinicians are hesitant to “pathologize” such normal reactions to traumatic stress by utilizing medications.

It is recognized that a substantial minority of survivors will not recover on their own but will go on to develop a psychiatric disorder such as post-traumatic stress disorder (PTSD), depression, another anxiety disorder, or alcohol/substance misuse. Since PTSD is the most common post-disaster adverse psychiatric consequence, and because what little empirical research that has been published on acute post-traumatic pharmacotherapy has focused on that disorder, I will only discuss early interventions for PTSD. It should be kept in mind, however, that some survivors who never develop PTSD may become symptomatic with a different psychiatric problem.

Ideally, there would be a reliable way to identify the minority of survivors who are at greatest risk of developing PTSD following disasters. Such a reliable method for psychiatric triage would support the argument for early pharmacotherapy as prophylaxis, despite the reluctance to prescribe medications, discussed previously. Several prodromal signs and symptoms have been proposed as predictors of post-disaster PTSD such as acute stress disorder (ASD), elevated heart rate, peritraumatic dissociation, or manifestation of PTSD's A2 criteria (e.g., expression of “fear, helplessness, or horror”) (Friedman et al., 2004; Friedman and Karam, in press).