The Nature of Trauma Memory

The memory recalled by PTSD survivors (PTSD memory) shares many features with implicit memory. Like implicit memory, it is characterized by limited accessibility due to declared memory gaps and is characterized by deficits in intentional recalling of important peripheral sensory and self-meaningful details about the trauma (Herlihy, Scragg, & Turner, 2002; Tuval-Mashiach, Freedman, Bargai, Boker, Hadar, & Shalev, 2004). PTSD memory reports are often distinguished from the memory of asymptomatic trauma survivors by their confusion about the traumatic event’s temporal order and incoherence (Foa, Molnar & Cashman, 1995; Hembree & Foa, 2000). They are also characterized by having perceptually driven flashbulb or hotspot qualities, as intrusive trauma perceptions are often reexperienced involuntarily and unintentionally with a good deal of arousal and distress in isolation of their traumatic context (Ehlers, Hackmann, & Michael, 2004; Berntsen & Rubin, 2006). Abreactions as such according to neuroimaging findings are enhanced by hippocampal activations suggesting its role during intermediate consolidation processes (Osuch, Benson, Geraci, Podell, Herscovitch, McCann et al., 2001). PTSD traumatic memory is behaviorally inferred in its reported symptoms of avoidance, arousal, dissociation, and in its “unintended” reliving of sensory emotional fragments of the trauma (van der Kolk & Fisler, 1995). This also suggests a supportive role for the hippocampus, for as noted in the triple dissociation studies earlier, lesioning the striatum allows expression of hippocampal tendencies for the unintentional retrieving of previously learned behavioral sequences (DeCoteau & Kessner, 2000; Packard & McGaugh, 1996). Traumatic manifestations are also behaviorally inferred. Unbeknownst to the PTSD survivor traumatic memory can be represented in harmful aggressive behaviors to self and others, in the cyclical revictimizing of oneself or others (Marx, Heidt, & Gold, 2005; van der Kolk, 1989) and in producing persistent victim identification with aspects of the trauma, e.g. compulsion for dressing and identifying with one’s prior military experience two decades later (McNally, Lasko, Macklin & Pitman, 1995; Berntsen & Rubin, 2006). PTSD memory is also modality specific and data driven. A fragment of a single perceptual experience such as a trigger can elicit a portion of the traumatic memory, much in the way that priming-induced fragments can elicit perceptual recognition for pattern completion (Michael, Ehlers, & Halligan, 2005) or presentation of the CS can elicit an association with an aversive US.

In contrast to fear conditioning, implicit responses to traumatic stress are fast learning; a single session of traumatic stress can overwhelm and reverberate thought processes despite attempts at traumatic thought avoidance. As noted above this is probably due to fast-learning hippocampal mediated intermediate consolidation involvement. Like fear conditioning PTSD perceptual memory is also multi-modal

PTSD symptom expression is often slowly acquired, necessitating as much as three months for assuring chronic symptom establishment and memory impairment (American Psychiatric Association (APA), 1994; Bryant & Harvey, 2002). Furthermore thought suppression and traumatic forgetting processes supporting avoidance symptom expression, are probably implicit processes as well, as memory and intentionality of their intial use is not recallable and consciously accessible. Their use however is behaviorally inferred and evidenced in later peripheral and contextual memory deficits with regards to the trauma. Previous discussion can be summarized below.

ImplicitExplicit

1. PTSD memory has limited accessibility, necessitating perceptual triggers reminiscent of the trauma. When present the traumatic trigger can elicit a representative portion of the traumatic memory f acilitating perceptual recognition and traumatic pattern completion.In contrast to fear conditioning traumatic and PTSD memories are fast learning. A single traumatic session overwhelms the brain and central nervous system and probably interferes in consolidation processes.

2. PTSD memory is characterized by deficits in intentional recollection, trauma narrative coherence, and temporal order. In contrast to fear conditioning paradigms, which employ healthy subjects, research studies monitoring PTSD reactions use healthy controls, asymptomatic and PTSD symptomatic subjects.

3. Trauma memories are reexperienced as perceptions having sensory flashbulb or hotspot qualities. The involuntary reliving and retrieval of trauma-related sensory memory is likely mediated by a functionally intact hippocampus (in accordance with the findings from triple dissociation studies noted earlier). The process of reliving is an explicit process; however in PTSD this reliving is often involuntary (i.e. during abreactions or during nightmares reminiscent of the trauma) and therefore reflective of implicit processes.

4. PTSD symptoms are behaviorally inferred in symptoms of avoidance, arousal, dissociation, and unintended reliving of sensory emotional traumatic fragments.

5. Survivors with PTSD symptoms can unknowingly and unintentionally reexperience implicit behavioral perceptual-motor-emotional aspects of the trauma by inadvertently victimizing others or seeking out masochistic relationships that victimize the self.

6. PTSD symptom expression is often slowly acquired, necessitating at least three months for assuring chronic symptom establishment.

7. Thought suppression mediating traumatic avoidance behaviors are likely implicit processes, as their initial cognitive-behavioral strategy, selection, and use are not easily recallable.

According to this analysis one can conclude that PTSD traumatic memory and symptom expression shares many features with implicit memory. Its fast learning quality is probably mediated by hippocampal processes, which as noted earlier enhance implicit learning processes, and are likely reflective of mid-consolidation process effects.

According to the multiple memory systems model, the striatal behavioral and amygdaloid motivational stimulus-response systems and cortical perceptual system (singly and in interaction) are probably biased expression in PTSD. Hippocampal mediated reactivations in these regions can account for PTSD memory’s implicit features of involuntary perceptual reexperiencing of traumatic sensory fragments and traumatic emotion like fear as well as behavioral reliving and identifying with traumatic material. Impairments or disruptions in traumatic memory’s ability for intentional and declarative recall and retrieval of a cohesive trauma narrative suggest contextual deficits in hippocampal functional integrity.

It would be important to emphasize that the hippocampal region supports implicit learning and memory in certain situations, e.g. initial novelty processing, the learning and later recall of confusing cues, and implicit cognitive demands needing relational processing. Furthermore a functionally viable hippocampus seems to be needed to declaratively transform implicit fear conditioning memory explicit making it later recallable and retrievable. This process is noted below. It is a modification of Squire (2004). It depicts emotional conditioning’s place in implicit learning and memory. When fear conditioning is not linked with hippocampal processes, this memory’s post-training ability for declarative recall is impaired. As indicated earlier hippocampal linkage and viability modulates conditioning memory to make it declarative and retrievable.

References

American Psychiatric Association (APA) (1994). Diagnosis and Statistical Manual of Mental Disorders of Mood Disorders, 4th Ed. Washington, D.C.: American Psychiatric Association.

Berntsen, D. & Rubin, D.C. (2006). Flashbulb memories and posttraumatic stress reactions across the life span: age-related effects of the German occupation of Denmark during World War II. Psychology and Aging, 21(1), 127-139.

Bryant, R.A., & Harvey, A.G. (2002). Delayed-onset posttraumatic stress disorder: a prospective evaluation. Australian New Zealand Journal of Psychiatry, 36(2), 205-209.

DeCoteau, W.E., & Kesner, R.P. (2000). A double dissociation between the rat hippocampus and medial caudoputamen in processing two forms of knowledge. Behavioral Neuroscience, 114(6), 1096-1108.

Ehlers, A., Hackmann, A., & Michael, T. (2004). Intrusive re-experiencing in post-traumatic stress disorder: phenomenology, theory, and therapy. Memory, 12(4), 403-415.

Foa, E.B., Molnar, C., & Cashman, L. (1995). Change in rape narratives during exposure therapy for posttraumatic stress disorder. Journal of Traumatic Stress, 8(4), 675-690.

Hembree, E.A., & Foa, E.B. (2000). Posttraumatic stress disorder: Psychological factors and psychosocial interventions. Journal of Clinical Psychiatry, 61 Supplement 7, 33-39.

Herlihy, J., Scragg, P., & Turner, S. (2002). Discrepancies in autobiographical memories-implications for the assessment of asylum seekers: repeated interviews study. BMJ, 324(7333), 324-7.

Marx, B.P., Heidt, J.M., & Gold, S.D. (2005). Perceived uncontrollability and unpredictability, self-regulation, and sexual revictimization. Review of General Psychology, 9(1), 67-90.

McNally, R.J., Lasko, N.B., Macklin, M.L., & Pitman, R.K. (1995). Autobiographical memory disturbance in combat-related posttraumatic stress disorder. Behaviour Research and Therapy, 33(6), 619-630.

Michael, T., Ehlers, A., & Halligan, S.L. (2005). Enhanced priming for trauma-related material in posttraumatic stress disorder. Emotion, 103-112.

Osuch, E.A., Benson, B., Geraci, M., Podell, D., Herscovitch, P., McCann, U.D., & Post, R.M. (2001). Regional cerebral blood flow correlated with flashback intensity in patients with posttraumatic stress disorder. Biological Psychiatry, 50(4), 246-253.

Packard, M.G., & McGaugh, J.L. (1996). Inactivation of hippocampus or caudate nucleus with lidocaine differentially affects expression of place and response learning. Neurobiology of Learning and Memory, 65(1), 65-72.

Tuval-Mashiach, R., Freedman, S., Bargai, N., Boker, R., Hadar, H., & Shalev, A.Y. (2004). Coping with trauma: narrative and cognitive perspectives. Psychiatry, 67(3), 280-293.

Van der Kolk, B.A. (1989). The compulsion to repeat trauma. Psychiatric Clinics of North America, 12(2), 389-411.

Van der Kolk, B.A., & Fisler, R. (1995). Dissociation and the fragmentary nature of traumatic memories: overview and exploratory study. Journal of Traumatic Stress, 8(4), 505-525.

Clinical Implications

When I was providing treatment to foster children in the 1990’s, most clinicians in current relied on on psychopharmacological and talking therapies that sought to neurobiologically stabilize and enhance ongoing problem solving skills, respectively. Because little attempt was made to help each child reexamine previously experienced trauma in a safe environment to promote psychological healing, breaches in drug adherence often yielded profound unfortunate suffering after discharge from foster placement.

During clinical practice with foster children with histories of early severe physical and sexual abuse, children present profound memory gaps for previously experienced traumatic events from their early childhood. Many of these children have experienced profound and sustained traumas during a time of rapid brain and central nervous system development. Loss of memory is also associated with compulsive preoccupation of aspects reminiscent of traumas (e.g. guns, fighting, (perpetrator related) monsters, etc.) (clinical observations), vivid hyperarousal in reexperiencing, avoidance, and, identification with trauma related material (Rothbaum, Foa, Murdock, Riggs, & Walsh, 1992; Berntsen & Rubin, 2006) and aggression, and sensitivity to aggressive responses to ongoing benign triggers (clinical observations). Apparently, the earlier the traumatic insult, the greater the likelihood for later recall deficits into adulthood (Terr, 1988).

Alterations in the ability for recalling early childhood traumatic experience are more common than one would expect. A prospective longitudinal study documented that as many as over 1/3 of a sample of 129 women at initial inquiry had amnesia “at some time” in adult life for previous hospital recorded childhood sexual abuse (Williams, 1994). Moreover with subsequent inquiry sixteen percent of 75 and seventeen percent 142 sampled adults, respectively, cited a time when they lacked total or partial memory for childhood sexual abuse, despite previously reported hospital and/or legal documentation or prosecutorial involvement (Goodman, Ghetti, Quas, Edelstein, Alexander, Redlich, et al., 2003; Williams, 1995). The tenuous nature of traumatic recall has been further supported by another study of twelve women who noted with initial inquiry “that there were time periods during which they had not recalled their abuse.” Interestingly with further inquiry into prior sexual abuse these same women noted that “they had never forgotten their (early childhood sexual abuse) experiences” (Fivush & Edwards, 2004, p. 6). The transient nature of memory from one moment to the next can explain these apparent contradictions. In contrast traumatized adults without memory deficits tend to report increased opportunity for sharing their trauma narratives with others on or around the trauma. Those without this opportunity present later recall deficits (Mechanic, Resick, & Griffin, 1998).

The following sections will examine the neurobiological nature of such deficits by examining lesioning effects of certain brain regions in both the human and the rodent and neuroimaging studies on asymptomatic and symptomatic trauma victims. Findings suggest a role for expressing traumatic emotion in mediating resilience to trauma’s effects.

References

Fivush, R., & Edwards, V.J. (2004). Remembering and forgetting childhood sexual abuse. Journal of Child Sexual Abuse, 13(2), 1-19.

Goodman, G.S., Ghetti, S., Quas, J.A., Edelstein, R.S., Alexander, K.W., Redlich, A.D., Cordon, I.M., & Jones, D.P. (2003). A prospective study of memory for child sexual abuse: new findings relevant to the repressed-memory controversy. Psychological Science, 14(2), 113-118.

Mechanic, M.B., Resick, P.A., & Griffin, M.G. (1998). A comparison of normal forgetting, psychopathology, and information-processing models of reported amnesia for recent sexual trauma. Journal of Consulting and Clinical Psychology, 66(6), 948-957.

Rothbaum, B.O., Foa, E.B., Murdock, T., Riggs, D., & Walsh, W. (1992). A prospective examination of post-traumatic stress disorder in rape victims. Journal of Traumatic Stress, 5, 455-475.

Terr, L. (1988). What happens to early memories of trauma? A study of twenty children under age five at the time of documented traumatic events. Journal of American Academy of Child and Adolescent Psychiatry, 27 (1), 96-104.

Williams, L.M. (1994). Recall of childhood trauma: a prospective study of women’s memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62(6), 1167-1176.

Williams, L.M. (1995). Recovered memories of abuse in women with documented child sexual victimization histories. Journal of Traumatic Stress, 8(4), 649-673.