An adverse mental health outcome following a single-event trauma is not limited to PTSD. Clearly PTSD is of central importance, however, researchers have long noted other postdisaster anxiety and depressive states. Current data consistent with greater disaster-related fear of death and event exposure being more likely to have a PTSD/anxiety outcome, while greater loss and grief predisposes to a depression outcome. However, PTSD-depression symptom concordance is great and comorbid presentations are common.
The post-single-event trauma burden of mental illness is not restricted to new mental health presentations. Many individuals with preexisting mental illness will experience a postevent symptoms relapse. Reasons may be pragmatic, such as difficulty obtaining medications or access to therapy in the postdisaster environment. Systemic issues such as an increased likelihood of parent distress and/or depression may be significant. Psychopathology may be related to event phase; immediately postevent individuals and service providers are appropriately focused on physical safety, water, food, and shelter needs. Mental health presentations and service provision generally begin in the weeks following the disaster. It is often the case that mental health issues come to dominate in the months and years postdisaster. An example is major depression some months following a disaster, yet with clear temporal links to disaster-related events.
Estimates of the prevalence of post-single-event PTSD vary greatly. Uniform PTSD rates would be unexpected given every disaster or traumatic event is unique. PTSD estimate variability is also due to disparity in research design. Published research varies in the elapsed time since the disaster, developmental stage of participants, whether the child or parent was the primary informant, and instruments used to measure psychopathology; the last mentioned range from qualitative accounts, self-report questionnaires to structured diagnostic interviews. Some early studies included data obtained from mental health professionals working for either the plaintiff or defense in lawsuits after a disaster. Design factors include bias due to selective mortality, recall and interview bias and use of convenience samples. Significant “unpackaging” of the event, both of event-related variables and the personal meaning of the event is required for a more meaningful between-event comparison.
Examples of prevalence variability include PTSD rates between 90% and 100% of children who were kidnapped and endured harrowing hours in captivity and children trapped in a school playground by sniper fire, intermediate rates of 40–60% in children who experienced major transport disasters and lower rates of 5–15% of children screened after natural disasters. Occasional studies report no children meeting diagnostic criteria for PTSD. Even in these examples limited symptom PTSD and other anxiety disorder presentations are usually reported.
Single-event trauma research is often population-based initiatives following natural disasters. Significant research initiatives have followed the devastation of Hurricanes Hugo (1989), Andrew (1992), Iniki (1992), and Katrina (2005). Research findings include female gender, younger age, high-trait anxiety, and emotional reactivity during hurricanes independently predicted PTSD symptoms more strongly than self-report hurricane exposure. Australian wildfire disasters have been subjected to similar scrutiny and surprisingly similar rates of child and adolescent PTSD have been reported, as well as high-trait anxiety as a PTSD-predictive factor and high rates of comorbid depression. Natural disasters potentially involve large numbers of individuals and/or a large proportion of a given population. An epidemiological perspective is informative and a public health approach to service provision justified. For example, a sophisticated postdisaster-intervention strategy would include screening for PTSD, the latter consistent with the National Institute for Clinical Excellence (NICE) guidelines, followed by universal and targeted responses to identified children, adolescents, and families.
A potentially confusing range of causal theories have been advocated for PTSD presentations in childhood. Such theories are often extrapolated from adult research and include psychodynamic, behavioral, cognitive, and biological explanatory models. Given variations in a potential victim's integration of biological, emotional, and behavioral systems and age-appropriate differences in individual–context, individual–peer, and individual–family interactions, stressful events may affect individuals in different ways across the life span. Etiology can be divided into research findings, often from epidemiological designs, that identify risk, vulnerability, and resilience factors. PTSD is also informed at a more fundamental level by cognitive theory and neurobiological research. The area is not without complexity; seemingly simple associations such as gender, age, and PTSD have proven difficult to clarify. Published findings include no effect of age on PTSD prevalence, higher rates in older children and adolescents, and higher rates in younger children. McDermott and Palmer (2002) studied 2379 grade 4–12 students after a wildfire disaster and reported a peak prevalence of PTSD in the middle school years.
An overarching principle is whether the functioning of the individual with PTSD has diminished. If significant, this diminution will have rendered the individual's functioning below the normal trajectory for age. A second principle is that the impaired functioning is due to a combination of event-related, proximal factors and distal factors inherent to the individual and present before the trauma. The event-related factor with the greatest empirical evidence of association with subsequent PTSD symptoms is increased traumatic event exposure. The event-exposure–PTSD association has been demonstrated in children residing in cities subject to more earthquake damage, witnessing more hurricane damage, closer proximity to gunfire, and being closer to actual wildfire flames. Note that high exposure, while a useful summary variable, is itself a multifactorial construct that includes the perception of threat of death, concern about possible loss and bereavement, witnessing a range of disaster-related phenomena including death or serious injury, perceptual experiences such as smoke from fires, and witnessing the coping or lack of coping of parents, caregivers, and other adults. Dislocation in the immediate aftermath of a disaster has been argued as a positive factor by decreasing disaster exposure and a negative factor given the lack of continuity with family and community and removing the opportunity to constructively engage in postdisaster restorative activities. In a case-controlled study of Armenian child earthquake survivors, at 30 months postdisaster, there was no difference in PTSD and depression symptoms in a group of children removed from the disaster and those who remained, distal factors significantly associated with higher PTSD symptoms in children include high-trait anxiety, a past history of emotional problems, children with a subjective sense of low self-efficacy and low social support, children employing poor coping strategies and an internal causal attribution.
Cognitive information-processing theory postulates that there is the potential of being overwhelmed by the everyday volume of information requiring processing. To counter this, information is encoded and recalled in specific ways. Cognitive schemata are developed as a primary organizing heuristic. The schema incoming information interaction influences subsequent memory encoding and retrieval. It is postulated that trauma-related information is also encoded with relation to existing schema. Dissonance with existing schema leads to conflict and the disruption of the usual memory encoding and comprehension and memory retrieval sequence. The greater the dissonance, the greater is the likelihood of trauma symptoms and impairment.
One postulate is that there are very specific schemata, which, if violated, are more likely to precipitate trauma symptoms. Fundamental beliefs such as “good things happen to good people” may be radically undermined after a traumatic event such as the experience of being raped. Possible psychological responses to information dissonant to existing schema include assimilation, altering information to fit preconceptions and accommodation, changing existing schemata to account for, and accept the new information. The last mentioned may facilitate recovery. Unfortunately accommodation may create a secondary impairment if, for instance, new schema are punitive, self-deprecatory, undermine adaptive beliefs about safety or intimacy, and make the tasks of daily living more difficult. Child and adolescent trauma complications can be more complex given the added possibility of altered parent schema about their child's safety. An example is the double jeopardy of the child who experienced a paroxysmal, unitary (type I) sexual trauma. Such an event may lead to PTSD psychopathology. If, for a protracted period thereafter, altered parent–child safety schema leads to the child not being allowed to visit friends, go on school outings, “sleep-overs,” and other events without direct parent monitoring, the normal process of child–adolescent individuation–separation may be retarded generating a secondary impairment. Further, accommodation in young children may manifest as self-blame for the event, heightened by a child's tendency to regress to a more egocentric worldview. Or by developing schema that predicts future disastrous events and ongoing extreme danger, either to themselves, friends, or family. Other changed schema may be that the event will reoccur, the event will become greater with a larger number of affected people and parents and other adults cannot protect children from traumatic events.
Neurobiological research including neuroimaging studies has been less active with child and adolescent participants. Studies that have been conducted are more likely to be with maltreated children than children who experienced a single-event trauma. Extrapolation from research with adults and maltreated children suggests possible decreased intracranial and cerebral volume in children who experience a single-event trauma. However, it may be that multiple insults during critical periods are needed for altered brain morphology. Neuroendocrine investigations suggest that dysregulation of the hypothalamus–pituitary stress system is likely following traumatic events. More definitive conclusions await further research.
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