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Posttraumatic stress disorder (PTSD) is a pervasive and highly debilitating condition that affects approximately 8% of the general population in the US and 15% to 30% in specific high-risk groups, such as survivors of war, torture, or rape (1,2). It is defined in the DSM-IV-TR (3) as an anxiety disorder comprising 4 major criteria: 1) exposure to or witnessing of an event that is threatening to one’s well-being; 2) symptoms of reexperiencing, such as intrusive memories, nightmares, a sense of reliving the trauma, or psychological and physiological distress when reminded of the trauma; 3) avoidance of thoughts, feelings, or reminders of the trauma, and inability to recall parts of the trauma, withdrawal, and emotional numbing; and 4) arousal, as manifested in sleep disturbance, irritability, difficulty concentrating, hypervigilence, or heightened startle response. These symptoms must cause marked impairment in functioning and persist for at least 1 month posttrauma. PTSD is unique in having a specific etiology and time of onset subsequent to exposure to a traumatic event. Nevertheless, it is well known that the experience of a traumatic event in itself is not sufficient to evoke PTSD. While most trauma survivors develop a range of PTSD reactions in the initial weeks after a traumatic event, most also adapt effectively within approximately 3 months. This appears to be a critical phase during which, for most individuals, the stress response subsides (4). Those who fail to recover after approximately 3 months are at risk for developing a long-lasting chronic disorder (5). A smaller subpopulation fails to recover, even after many years of psychiatric treatment (2). It is evident from both the phenomenology and the etiology of PTSD that the abnormal nature of the traumatic memory is a central feature of the disorder manifested by symptoms of reexperiencing, such as intrusive thoughts, nightmares, flashbacks, and physiological or psychological reactivity (6). At the same time, memory impairment in the form of amnesia and delayed recall is also a known phenomenon in traumatized individuals (7); it has been documented in response to such diverse traumatic events as natural disasters, war, torture, and physical or sexual abuse. The complexity of traumatic memories attracted the attention of early scholars, including Pierre Janet (during the 1880s, in his scientific examination of the memory process), Charcot, Breuer, and Freud (in 1893). It has since been accepted that memory is a dynamic organization of past experiences: it is often distorted and influenced by the person’s emotional state at the time of recall and by the significance of the experience itself. Emotional memories, especially of traumatic events, seem to be fragmented and incomplete (8), inflexible and unchanged by other life experiences (9), and primarily sensory, emotional, and nonverbal (10). As a result, traumatic memories tend to intrude upon the individual’s consciousness at any given time. Indeed, laboratory studies of individuals with PTSD have shown that they process trauma-relevant material selectively, demonstrate enhanced memory for trauma-related material, and exhibit difficulty forgetting trauma words during directed forgetting (11). They also experience problems retrieving specific autobiographical memories in response to cue words, recalling “overgeneral” memories instead (8). Heightened emotion and arousal are considered to be key features of the trauma response. Studies examining the effect of heightened emotion and arousal on the accuracy of memory have found that, for nonviolent content, participants’ confidence in their own testimony and accuracy of memory are related (12). However, this relation between confidence and accuracy was not found in response to violent content, implying that memory encoded under emotionally charged situations is potentially distorted. Other studies suggest that attention to details immediately relevant to the arousing situation is actually heightened, possibly at the expense of attention to general details. These findings may support the observation that memories of trauma are fragmented, displaying hyperawareness of some details and an apparent disregard of others (13). These recurring observations have given rise to the perception that memories of traumatic events are inherently unique and probably encoded and processed differently than are nontraumatic events (14,15). The intricate system of memory is commonly thought of as comprising 2 primary pathways. The first is regular memory, called explicit or declarative memory. This refers to conscious awareness of facts (17) and requires focal attention for processing; it is probably mediated by the medial temporal lobe system that includes the hippocampal formation and related structures that enable verbal representation (18,19). Conversely, the second pathway, called implicit or nondeclarative memory, refers to memories acquired during skill learning, habit formation, and simple, classic conditioning. It also refers to other knowledge expressed through performance rather than recollection (18). These memories are believed to be not easily accessible to consciousness (14). Traumatic memories that subjects can recall are thus part of explicit memory. The notion that memory of the traumatic event is essential for the development and definition of PTSD raises the question whether it is possible for individuals who have no recollection of trauma to develop a posttraumatic response. It has been illustrated in case reports that individuals with no conscious memory of the traumatic event are still able to reenact their experiences; however, the commonly held view is that lack of memory precludes the development of PTSD (20). The controversy regarding trauma and memory cannot be empirically resolved by experimental studies in humans, owing to practical and ethical limitations in the simulation of naturally occurring trauma and in manipulation of memory (7). As a compromise, many studies have focused on the occurrence of traumatic brain injury (TBI) (21–23). This traumatic event is often associated with loss of consciousness and impaired memory, and TBI can therefore serve as a naturalistic model for the study of memory and its role in the development of PTSD. Findings, however, are inconclusive. Studies have provided differing and sometimes conflicting results. The following sections review these findings and discuss future directions for the study of PTSD and memory, together with implications for treatment. Evidence Supporting Reduced Prevalence of PTSD After TBIIn the US alone, the estimated annual rate for TBI is 220 cases per 100 000 people (24). It is often accompanied by posttraumatic amnesia regarding events that occurred both after the injury (anterograde amnesia) and immediately prior to it (retrograde amnesia). Some researchers have argued that limited awareness at the time of the trauma makes it less likely that traumatic memories can be encoded and that, as a result, these memories remain unavailable for the mediation of reexperiencing symptoms (20,25). Without the latter, PTSD or acute stress disorder (ASD), introduced in the DSM-IV to describe acute trauma reactions within the first month posttrauma, cannot be diagnosed. For example, in a study of 47 patients with moderately severe TBI, none fully met the criteria for PTSD: despite reporting partial PTSD symptoms—particularly, symptoms of avoidance and arousal—none endorsed symptoms of reexperiencing (26). Similarly, in a study comparing the acute stress reactions of road-accident victims both with and without head injury, the two groups reported high rates of anxiety, but the group with head injury reported fewer intrusive symptoms (27). Based on these findings, it was suggested that amnesia regarding the traumatic event minimizes the possibility that any cognitive representations of the trauma will be established (28). In another study of accidental head injury, PTSD was diagnosed in only 1 out of 107 injured patients, although other psychiatric problems were found in 22% of this group (29). Further, although some have suggested that TBI is a risk factor for PTSD (30), other research indicates that this is not the case and that PTSD is in fact rare among road-accident survivors with TBI, compared with road-accident survivors without TBI (31). A less extreme view suggests that, although PTSD is unlikely to occur following TBI, it can develop following mild TBI (32). However, 1 study reports that, while patients with PTSD provided emotionally charged accounts of their traumatic experience (including nightmares, flashbacks, and intrusive imagery), such symptomatology was absent in a comparison group with mild TBI, who did not even report symptoms of emotional arousal when describing their traumatic event (20). An additional study involving 188 road-accident victims who sustained loss of consciousness reports that none exhibited symptoms of PTSD (30). Posttraumatic amnesia (PTA) is considered a marker for the degree of TBI severity and a sensitive predictor of outcome (33). To assess the extent to which PTA influences PTSD symptom development and prevalence, particularly reexperiencing of the traumatic event, 282 TBI patients were examined within a few months after injury. The sample was stratified into 4 groups according to their degree of PTA and severity of brain injury (34). All 4 groups reported intrusive and avoidant symptoms relating to the trauma, but these symptoms diminished significantly when PTA exceeded 1 hour. In some subjects, however, PTSD symptoms were present even when PTA exceeded 1 week. The nature of the intrusive phenomenology did not vary by length of PTA. This is one of few studies that tried to account for the degree of memory disruption following TBI and its relation to subsequent development of PTSD.
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