The long-term costs of traumatic stress: intertwined physical and psychological consequences

One of the greatest challenges to the field of traumatic stress has been the observation that many individuals who coped at the time of their traumatic exposure became unwell at a later date. This observation was particularly challenging in the context of World War I and World War II because the prevailing psycho-pathological theories at the time did not have a clear rationale for this phenomenon and led to considerable stigmatization of disabled veterans 1. The later emergence of disability in veterans was attributed to compensation neurosis, pre-existing personality disorder, and suggestibility 2. Furthermore, with the blossoming of the general life events stress literature, this pattern of morbidity was not consistent with the prevailing views about high levels of acute distress that progressively ameliorated with time 3–4. The life events literature which reached its zenith in the 1960s and 1970s focused on notions such as brought-forward time, and emphasized that there was generally a window of approximately six months following which a life event stress could lead to the onset of disorder 5. Delayed onset post-traumatic stress disorder (PTSD) was seen as inconsistent with this conclusion about the window of effect of stressful life events 6. A primary question has been about how a model of psychopathology could account for this lingering and delayed impact of extreme adversity. Prevailing psychoanalytic constructs and later learning theory did not readily provide an answer to this question. Many significant observations in the context of the depression literature have not been readily adapted by the field of traumatic stress until recent links through the research concerning the relevance of child abuse to depression 7. This paper explores the evidence about the delayed effects of traumatic stress and their cumulative burden on psychological and physical health. An underlying psychopathological model is summarized and its potential implications for treatment are discussed. The relation between acute post-traumatic symptoms and the emergence of PTSD is an issue of considerable theoretical and clinical importance. There is now a significant body of research documenting that the majority of people who develop PTSD do not initially meet the diagnostic criteria for an acute stress disorder 8. In contrast, the majority of those who have an acute stress disorder are likely to display subsequent PTSD. A number of longitudinal studies of accident victims have demonstrated that it is only with the passage of time that the level of symptoms crosses a threshold sufficient to warrant a clinical diagnosis 9–13. A similar phenomenon was found in a study of severely injured US troops who were assessed at one month, 4 months and 7 months. This study demonstrated that 78.8% who had a disorder at 7 months did not attract a diagnosis at one month 14. Further support for the delayed emergence is the finding from the screening of military populations that symptoms increase in the first six months following deployment 15–16. Additional adversity, conflict or stress plays a role in the later emergence of psychopathology 17. Hence, in a significant number of individuals, PTSD is a disorder that is not initially manifest in the aftermath of the trauma. Rather, there is a progressive escalation of distress or a later emergence of symptoms, particularly in military and emergency service personnel. A related construct is delayed onset PTSD. Delayed/late onset PTSD is defined in the DSM-IV 18 as a disorder meeting the diagnostic criteria for PTSD which is present after a post-trauma adjustment period of at least 6 months during which diagnostic criteria were absent or sub-threshold 19. From a theoretical point of view, these are likely to be individuals who have managed to contain their individual distress by adaptive means, but subsequent stresses and/or the natural progression of neurobiology have led to the manifestation of the symptoms. A recent review emphasized the confusion which has arisen from different definitions of delayed onset PTSD 20. For example, different interpretations of the concept include an individual who has had sub-syndromal symptoms that have subsequently crossed a threshold of clinical severity as well as an individual who has been asymptomatic and then at some later point developed the disorder. The existence of this delayed form of PTSD emphasizes how a traumatic experience can apparently lie relatively dormant with an individual only to become manifest at some future point. Many unanswered questions remain about when and how this sub-clinical state is triggered into a full-blown syndrome of PTSD. However, increasingly the evidence would suggest that sub-clinical symptoms leave the individual at risk of progressive activation with further environmental stress or trauma exposure. A related construct in the depression literature is how individuals who have had partial remission following treatment for an episode of a major depressive disorder are at significantly greater risk of a further recurrence 21. This vulnerability relates to the sensitivity of individuals with residual depressive symptoms to environmental triggers. The underlying neural structures that are sensitive to activation are the same that have been identified as being relevant to the aetiology of PTSD. For example, Ramel et al 22 highlighted that amygdala reactivity is an important issue in people with a history of depression in contrast to those without such a history. These results indicated that the amygdala plays an essential role in modulating mood congruent memory, particularly during the induction of sad states of mind in individuals who are vulnerable to depression. In such individuals, the cognitive and neural processing of emotional information potentially contributes to the vulnerability for negative emotions and the onset of depressive episodes 23. Hence, there is a significant body of literature documenting that individuals who are primed in emotionally labile and sensitive states are at risk for the progressive intensification of further symptoms, particularly when these resonate with the environment. Hence, the presentation of delayed onset of PTSD is not a unique construct in mental health. Furthermore, Hedtke et al 24 demonstrated that there is a cumulative effect of exposure to interpersonal violence in terms of PTSD, depression and substance abuse problems. The cumulative risk model highlights the ongoing interaction between prior stress exposure and subsequent life events. The severity of stresses that are experienced prior to and following a traumatic exposure have a significant impact on the incidence and severity of the condition 25. Hence, delayed onset PTSD is intimately involved with the fact that individuals live in a dynamic environment in which traumatic events and other life stresses interact, with the progressive accumulation of risk. A related question is whether a longer duration of repeated exposures to trauma in defined time periods carries a greater risk of PTSD, a question relevant to the military and police. The recent UK study of Rona et al 26 provides the first reliable data from the military addressing this question and suggests that the risk of PTSD is greater in those units that have had longer durations of deployment with less time to recuperate between deployments. This study highlights that PTSD is an emerging disorder where multiple traumatic events progressively increase the risk of occurrence. The repeated recollection of traumatic memories is a central component of the phenomenological response to traumatic events. Freud highlighted the importance of traumatic memories in his first lecture with Breuer, suggesting that these were the “agent still at work” playing a central role in symptom onset and maintenance 27. Subsequently, modelling in epidemiological samples has highlighted how traumatic memories account for the relationship between exposure to traumatic events and the symptoms of hyperarousal and avoidance 28. The triggering of these memories is also a consequence of fear conditioning mechanisms 29, and these serve to sustain and kindle the increased arousal that is central to the symptoms of PTSD 30. The disorder arises because some individuals are unable to progressively shut off the acute stress response, which is ubiquitous at times of exposure to such events. From a learning theory perspective, this process is seen as a failure of extinction or new learning in the aftermath of the fear conditioning. Rather, there is a progressive augmentation of the amplitude of the response to reminders. A primary component of the symptomatology of PTSD is the reexperiencing or reliving of the traumatic memory, that has both elements of psychophysiological reactivation and psychological distress. A unique part of this condition is the repeated reactivation of the traumatic memory and the associated stress response with the attendant risk of the progressive augmentation of the reactivity of the individual 31. In fact, the suggestion has been made that in PTSD there is a failure of the retention and extinction of conditioned fear and that this is an acquired deficit in the condition 32. On reviewing the available evidence, Rauch et al 33 have suggested that in PTSD there is an exaggerated amygdala response which underpins the excessive acquisition of fear associations and the expression of fear responses. A corresponding deficit of frontal cortical functioning plays a central role in mediating extinction. There is also a deficit in the appreciation of the context of safety, which is related to hippocampal function. The central mechanism is the process of sensitization to the subtle reminders of traumatic memories as well as exposure to prior and future traumatic events. This process of reactivity to minor cues, which very frequently goes unrecognized, serves to progressively increase and exacerbate the reactivity of the dysfunctional individual 7. This leads to an interaction between the individual's distress, psychophysiological reactivity, and the neurohormonal response at the time of the traumatic event. In discussing this question, it is important to recognize that some traumas in combat and policing are not the equivalent of a single traumatic event such as being in a motor vehicle accident. Combat and emergency service work involves repeated activations of the fear and stress systems that are then prone to present as future dysregulation over time. Individuals who develop PTSD have been found to have a progressive evolution of dysfunction as described above 30. Progressively, they react to the presence of potential threat with greater amplitude or intensity and ultimately develop a generalized overreactivity to a range of stimuli in their civilian and military environments that remind them of the traumatic event. This cycle of increasing reactivity to a widening range of cues in their environment serves to further reinforce the distress response. This pattern is not unique to PTSD and has been highlighted in depression as having a critical role in early episodes 35. Elzinga and Bremner 36 have further characterized the role of the noradrenergic system in the enhanced encoding of the emotional memories and fearconditioning in individuals who develop PTSD. The failure of the normal neurotransmitter inhibitory mechanisms that quell the stress response appears to be important in the progression of the individual's distress into a full blown post-event or post-traumatic stress disorder. According to Miller 37, childhood trauma increases the risk of adult psychopathology because of the same process of sensitization 7. Shalev 38 has highlighted that this process is also intimately integrated into the person's social and cultural setting. He states that traumatic events are followed by “a critical period of increased brain plasticity, during which irreversible neuronal changes may occur in those who develop PTSD”. He also emphasizes the importance of group cohesion, marital discord, and leadership skills as mediating factors. Fear conditioning, kindling, and sensitization contribute to the manner in which repeated activation of the fear memories, in PTSD, leads to the emergence of spontaneous intrusive memories 39. In depression, a similar process predisposes an individual to negative affective appraisal and increasingly depressed mood. There is an emerging medical scientific literature indicating that pharmacological agents may be able to modify these responses 40. The measurement of the startle response can objectively characterize the sensitization that occurs in the fear and alarm response in PTSD. Increased heart rate in response to sudden loud tones is an abnormality that emerges following traumatic exposure 41–42. This increased reactivity suggests the role of fear conditioning and the impact of the environment following the event. The acquisition of an increased startle response was not related to the severity of the event or the initial intensity of the symptoms. These observations are consistent with the model of progressive neuronal sensitization and increasing heart rate reactivity over the subsequent six months to trauma exposure. This pattern of increased reactivity is also observed in relation to innocuous and aversive stimuli in a conditioning experiment where increased autonomic reactivity was demonstrated to both types of stimuli 43. Once conditioned, those with PTSD had reduced extinction to conditioned responses. PTSD is only one of the outcomes that have been associated with trauma exposure. The emergence of multiple physical symptoms also has a strong association, and the consensus opinion is that these syndromes are indicative of a general reflection of distress. The underlying mechanisms of these disorders have been related to similar mechanisms of sensitization noted in those with PTSD 44. In parallel, multiple traumas have an accumulative effect on physical health which appears to be independent of the development of PTSD 45. There is longstanding interest in the effects of stress on health, due to the strain that it places on the adaptive capacity of individuals, which thereby leads to an increased risk of disease. 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