On March 13, 1996, a gunman shot and killed sixteen kindergartners and one adult at a primary school in Dunblane, Scotland. Other children who witnessed the massacre experienced post-traumatic stress disorder (PTSD), an anxiety disorder that persists for months or even years after a traumatic event or series of events. Likewise, many children who survived events such as 9/11 bereavement or the Indian Ocean tsunami also developed the symptoms of PTSD. Yet a significant subset did not. Some research even suggests that resilience is less a rare exception than an “especially effective form of normal adaptation” – what one researcher termed “ordinary magic” (1, 2, 3). What protective factors – environmental, cognitive, and neurophysiological – serve to enhance such resilience? And what implications does such a multifactorial analysis have for resilience-promoting interventions and treatment?
What is PTSD?
Post-traumatic stress disorder (PTSD) is classified as an anxiety disorder, but unlike other anxiety disorders, does not have an element of irrationality. It occurs after a traumatic event, which the DSM-IV-TR defines as involving “actual or threatened death, serious injury or the threat to self or others” (APA, 2000) (Appendix 1). These traumas can be acute – one-off, unique and un-anticipated events such as 9/11, the Virginia Tech school shooting, or house fires. Or they can be chronic – involving continued exposure to horrific events such as chronic child abuse. In children, reactions to trauma include intense fear, helplessness, horror, agitation or disorganised behaviour; they may re-enact the traumatic event or have nightmares about it, for example.
PTSD has three symptom clusters: re-experiencing, avoidance and increased arousal (4). Children may re-experience the event by participating in repetitive play that revisits aspects of the trauma; they may have intrusive, distressing recollections of the event that are triggered by traumatic reminders – for instance, a child who survived the Indian Ocean tsunami may see a film about the sea and shriek in terror. Young children might also have nightmares as a result of the traumatic event without any recognisable trauma content.
In addition, children may avoid stimuli associated with the traumatic event, choosing not to talk about it. Avoidance may also be expressed as numbing – for example, the child who has lived through a serious car accident may feel detached from her friends and cease to enjoy playing with them. Finally, the third symptom cluster involves heightened physical and emotional arousal. The PTSD sufferer may be unable to sleep, have difficulty concentrating on his schoolwork, or be unusually angry or irritable. Thus PTSD in children must be distinguished from other anxiety or mood disorders, and clinicians should note that PTSD symptoms may manifest differently depending on a child’s age and developmental stage.
Vulnerabilities, Risks and Protective Factors in PTSD
According to the diathesis-stress model of psychopathology, individuals with certain genetic vulnerabilities are more susceptible to developing psychopathology when they are exposed to environmental stresses. Some biological vulnerabilities, such as an overactive hypothalamic-pituitary-adrenal (HPA) axis, translate into cognitive or behavioural vulnerabilities like hypervigilance or a tendency to dissociate – to ‘split off’ emotionally – when faced with trauma. However, no single factor, whether biological, psychological or environmental, is necessary and sufficient for an individual to develop PTSD (2, 5, 6).
In addition, it may be worthwhile to include protective factors (that increase resilience) in a model of psychopathology. Hoge et al. (5) believe that resilience-enhancing factors are more than the inverse of vulnerabilities – for example, a small hippocampus may be a vulnerability to PTSD, but it does not logically follow that having a normal-sized hippocampus is protection from the disorder. Rather, resilience-enhancing factors are processes and mechanisms that offer protection (5). The effects of such protective factors are often tangible only when they interact with other stresses – for instance, an inner-city child of divorced parents who has an adaptive coping strategy may excel in school and stand out amongst her peers. This section of the paper will examine vulnerabilities, risks and protective factors from three standpoints: biological, psychological and environmental.
One symptom of PTSD is the tendency to re-experience the trauma in flashbacks or nightmares. In order for re-experiencing to occur, the trauma must be coded into an individual’s emotional memory. Researchers thus suggested that people with higher levels of chemicals such as cortisol that modulated memory formation would be more prone to PTSD (5). Conversely, those with higher levels of DHEAS (dehydroepiandrosterone), which has an antagonistic relationship with cortisol, are less susceptible to stress (5).
Besides such biochemical vulnerabilities and protective factors, genetics also plays a part in susceptibility to PTSD. In one study, maltreated boys with a long version of the gene encoding monoamine oxidase A (MAOA) were less likely to commit violent crimes and score high on tests of aggression, while those with a short version of the gene were much more likely to do so (7). And in twin studies, monozygotic twins of subjects with anxiety disorders were more likely to have symptoms of anxiety (8). Such findings about the biochemical and genetic factors in PTSD have important implications about the type and timing of drug therapy for the disorder.
Finally, neurophysiology can increase or decrease susceptibility to PTSD. Brain areas such as the anterior cingulate, which is concerned with emotion processing and working memory, and the dorsolateral prefrontal area, which modulates cognitive control and helps inhibit emotional arousal, can influence the cognitive and behavioural components of a child’s response to stress (6). Similarly, a smaller-than-average hippocampus and an overactivated HPA axis may be vulnerabilities to PTSD (9) as the hippocampus is involved in the formation of conditioned fears, and a smaller hippocampus may lead to poorer regulation of the HPA axis (10).
However, this research faces some limitations. Something that looks like a vulnerability may in fact be a consequence of PTSD or vice versa, depending on the perspective from which the study is conducted. For example, a smaller-than-average hippocampus has been implicated as a potential vulnerability to PTSD and other anxiety disorders (4, 10), but also as a consequence of trauma (11). Ultimately, research on the relationship between PTSD and hippocampal size was inconclusive (12, 13). Likewise with the child’s intelligence quotient (IQ) – it is commonly believed that low IQ is another potential vulnerability to PTSD, but at the same time, the expression of PTSD symptoms may have an adverse effect on IQ test scores. (In any case, IQ is only a reflection of a child’s cognitive potential in areas such as executive function.) In sum, there is a chicken-and-egg problem – causality is difficult to determine for many biological and psychological aspects of PTSD.
Young children with PTSD may be susceptible to cognitive distortions that heighten their distress, such as believing they could have prevented the trauma. Similarly, a lower IQ may be a cognitive vulnerability, as children with a lower IQ may be more prone to such cognitive distortions and misattributions. (However, Wenar and Kerig (4) also indicate that “in order for an event to be traumatic, it must be perceived as such”; one might expect greater cognitive ability – the capacity to grasp the enormity of trauma – to be maladaptive in this case.) Likewise, poorer emotional adjustment – children who are unable to self-soothe and tend to blame themselves are more likely to have severe post-traumatic reactions (4). In addition, dissociation during trauma may also predict later PTSD symptoms (Berg et al., 2005, cited in 5).
More research has been done on the psychosocial aspects of resilience than the biological ones. Some psychological resiliency factors are associated with temperament – that is, children with a sunny disposition and secure attachment to their caregivers may be less likely to develop PTSD to begin with. (Securely-attached toddlers are willing to explore and engage with strangers in the presence of their caregivers, become distressed when caregivers leave and are soothed when caregivers return.) Alternatively, children with these characteristics can attract and take better advantage of social support networks, drawing empathy from family and community members.
Perhaps the protective psychological factors most relevant to PTSD intervention are the affective, cognitive and behavioural ones. A high level of executive function is important for inhibiting emotional arousal and regulating behaviour, which may mitigate the child’s response to trauma (6). During or after trauma, a child with a sense of hopefulness (the notion that “things will get better”) and a tendency for positive self-talk is likely to function better than a child without such characteristics (14, 15), as these cognitions may mitigate the perceived severity of trauma. Finally, a child who has a locus of self-control (the belief that one can shape one’s life) and who is competent in various tasks (arts, sports etc.) is less likely to succumb to “learned helplessness” and is more able to cope with stress (5). All these protective factors have implications for cognitive-behavioural therapy.
Arguably, environmental risk factors are the most significant predictors of PTSD. In one longitudinal study, children in high-risk environments had much higher rates of psychopathology than children in low-risk environments, even when individual resilience factors such as social-emotional competence and intelligence were taken into account – that is, low-resilience children in low-risk environments did better later in life than high-resilience children in high-risk environments (16). Consequently, even though social support networks can be enhanced or mitigated by individual characteristics (5), parental and social support is the most significant risk factor and perhaps the most important in PTSD interventions. Environmental risk factors besides parental support include a high incidence of traumatic events, chronic rather than acute trauma, and trauma that could conceivably be repeated, rather than a fluke event such as a car crash (9).
Conversely, while it is clear that environmental factors such as family cohesion, socioeconomic status and lower levels of life stress can be protective, some researchers believe it is “individuals’ contribution to these factors that confers their status as characteristics of resilience” (5). Still, the presence of positive environmental factors like family cohesion and support networks can help moderate PTSD in survivors. For instance, Hyman et al. (17) found that different levels (and perceptions) of social support had different effects on PTSD outcomes in survivors of childhood sexual abuse. Four types of social support were examined: appraisal support (advice in coping with problems), self-esteem support (increasing the individual’s self-percept), tangible support (availability of material resources) and belonging support (being part of a social group). Self-esteem support and appraisal support were ultimately most effective in reducing PTSD symptoms.
Implications for intervention
Given what we know about resilience factors in PTSD, how can we use this understanding to treat children with the disorder or to develop preventive interventions? Biochemical vulnerabilities and protective factors are useful for pharmaceutical research on drugs to treat PTSD, or to be administered as soon as possible after trauma and before the onset of PTSD. For instance, glucocorticoids administered after trauma may interfere with the retrieval of traumatic memories, while emotional arousal can be blocked with a beta-blocking (beta-adrenergic receptor antagonist) drug known as propanolol (Roozendaal, 2003 and Cahill et al., 1994, cited in 5). In addition, there may be critical sensitive periods during which drugs can affect processes of neural plasticity (such as the formation of traumatic memories), and more research should be done on this.
Cognitive-behavioural therapy is perhaps one of the most commonly used forms of treatment for PTSD, and such therapy should be tailored to a child’s developmental stage. Also, some types of therapy may be indicated for different symptoms of PTSD – Mancini & Bonanno (15) suggest that adult grief therapy focusing on insight, for example, may be most recommended for problems of internalisation such as self-blame, hopelessness and sadness, and skill-focused interventions are more suitable for externalising problems. This may extrapolate well to child PTSD, but again, more research needs to be done.
Stallard (18) did a review of CBT interventions in children with sexual-abuse-related PTSD. These interventions focused on various aspects of PTSD: decreasing sexualised (re-enacting) behaviour, helping children communicate about their abuse (decreasing avoidance), and revising abuse-related cognitions like self-blame, stigmatisation and powerlessness. While each intervention was itself effective, the relative effectiveness of each type of CBT intervention still needs to be assessed.
Post-trauma therapies seem successful in treating children, but pre-emptive interventions can help improve the resilience of children at risk for PTSD. One form of resilience-enhancing intervention involves developing competencies and empowering children. Researchers conducted a study of structured activities in Palestinian children living in war-torn areas of Gaza and the West Bank. These included activities like sports and arts, and were aimed at developing skills and competencies to help children feel successful. It was found that the intervention improved children’s internalising and externalising problem scores, but did not increase children’s hopefulness (though hopefulness scores did not decline – still a positive sign in an environment where war was ongoing) (14).
Another type of resilience-promoting intervention focuses on improving executive function (EF) in school-aged children (6), based on the premise that executive function is important for appraising a traumatic event and its emotional meaning, regulating emotions to solve problems and gather more information, and responding behaviourally to a traumatic event. The intervention improved children’s inhibitory control and verbal fluency in comparison to a control group and decreased children’s internalising and externalising problems. However, the impact of improved EF on PTSD may be difficult to measure without a corresponding traumatic event or a high-risk environment. One might expect such resilience-enhancing pre-emptive interventions to also be of use in treating childhood PTSD. Finally, given that environment and social support networks may be the most important factors in preventing or alleviating PTSD, one should consider family therapy in the treatment of PTSD, establishing therapeutic alliances where possible. Forms of social and family support should focus on improving individuals’ self-percepts, helping people ‘belong’ within the family or community, and offering guidance in coping with problems.
An ounce of prevention is worth a pound of cure; naturally, it is preferable to conduct pre-emptive interventions to increase the resilience of children in high-risk populations. These interventions can be informed by our increasing knowledge about the physiological and psychological factors that improve resilience in children. At the same time, it should be kept in mind that resilience does not equal invulnerability to trauma – that no matter how resilient a child is, environmental risks still play a significant part in his or her development. However, our knowledge of resilience, coupled with an understanding of developmental psychology, can and should also inform the treatment of children with PTSD – such as child survivors caught in the Indian Ocean tsunami in 2004, which was a severe and horrifying fluke event with no known risk factors to predict it.
Appendix 1: DSM-IV-TR diagnostic criteria for 309.81 Posttraumatic Stress Disorder
A. The person has been exposed to a traumatic event in which both of the following were present:
(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others
(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by disorganized or agitated behavior
B. The traumatic event is persistently reexperienced in one (or more) of the following ways:
(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young children, repetitive play may occur in which themes or aspects of the trauma are expressed.
(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable content.
(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In young children, trauma-specific reenactment may occur.
(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following:
(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma
(2) efforts to avoid activities, places, or people that arouse recollections of the trauma
(3) inability to recall an important aspect of the trauma
(4) markedly diminished interest or participation in significant activities
(5) feeling of detachment or estrangement from others
(6) restricted range of affect (e.g., unable to have loving feelings)
(7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
(1) difficulty falling or staying asleep
(2) irritability or outbursts of anger
(3) difficulty concentrating
(5) exaggerated startle response
E. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than 1 month.
F. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Acute: if duration of symptoms is less than 3 months
Chronic: if duration of symptoms is 3 months or more
With Delayed Onset: if onset of symptoms is at least 6 months after the stressor
(DSM-IV-TR, American Psychiatric Association 2000)
1. A.S. Masten, Am. Psychol. 56: 227 (2001).
2. “Resilience.” Harvard Mental Health Letter [Cambridge, MA]. (December 2006).
3. W.E. Copeland, G. Keeler, A. Angold, and E.J. Costello, Arch Gen Psychiatry 64, 577 (2007).
4. C. Wenar and P. Kerig, Developmental Psychopathology (5th Edition), McGraw-Hill: Boston, 2006.
5. E.A. Hoge, E.D. Austin, and M.H. Pollack, Depression and Anxiety 24, 139 (2006).
6. M.T. Greenberg, Ann. N.Y Acad. Sci. 1094, 139 (2006).
7. D. Cicchetti and J.A. Blender, Ann. N.Y. Acad. Sci. 1094, 248 (2006).
8. S. Taylor, D.S. Thordarson, K.L. Jang, and G.J.G Asmundson, World Psychiatry 5(1), 47 (2006).
9. J. Scheiner, in-class lecture: Psychology 52.2, Dartmouth College, May 9 2007
10. M.W. Gilbertson, M.E. Shenton, A. Ciszewski, K. Kasai, N.B. Lasko, S.P. Orr, and R.K. Pitman, Nature Neuroscience 5, 1242 (2002).
11. L.M Shin, S.L. Rauch, and R.K. Pitman, Annals of the New York Academy of Sciences 1071, 67 (2006).
12. C.L Pederson, S.H. Maurer, P.L. Kaminski, K.A. Zander, C.M Peters, L.A. Stokes-Crowe, and R.E. Osborn, Journal of Traumatic Stress 17(1), 37 (2004).
13. L.A. Tupler and M.D. De Bellis, Biological Psychiatry 59(5), 523 (2005).
14. M. Loughry, A. Ager, E. Flouri, V. Khamis, A.H. Afana, and S. Qouta, Journal of Child Psychology and Psychiatry 47(12), 1211 (2006).
15. A.D. Mancini and G.A. Bonanno, Journal of Clinical Psychology 62(8), 971 (2006).
16. A.J. Sameroff and K.L. Rosenblum, Annals of the New York Academy of Sciences 1094(1), 116 (2006).
17. S.M. Hyman, S.N. Gold, and M.A. Cott, Journal of Family Violence 18(5), 295 (2003).
18. P. Stallard, Clinical Psychology Review, 26(7), 895 (2006).
Diagrams for this article were created in-house by Tim Shen ’08.