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Thomas, Laurance, Jacobs, and Nadel (1995) summarized a neurobiologically based model of memory that 1) predicts temporary functional amnesia under traumatically stressful conditions; 2) predicts recovery of emotional memories laid down during functional amnesia; and 3) predicts that the accuracy of recovered traumatic memories varies in a systematic manner (see also Jacobs & Metcalfe, in review; Jacobs & Nadel, 1985, in press, in review; Nadel & Jacobs, in press). The model, which is based on findings from modern cognitive neuroscience, also provides a neurobiologically sound alternative to the psychodynamic concept of repression.
The model focuses on two neuroanatomically separable memory systems, each with its own properties and developmental profile: a "hot" memory system with the amygdala as its centerpiece, and a "cool" memory system with the hippocampus as its centerpiece. The amygdala-based system is critical for the conditioning and retention of emotion itself; the hippocampus-based system is critical for the conditioning and retention of spatiotemporal context (Jacobs & Metcalfe, in review; see also Davis, 1992; Davis, Rainnie, & Cassell, 1994; Kim & Fanselow, 1992; LeDoux, 1992, 1994; Nadel & O'Keefe, 1974; O'Keefe & Nadel, 1978; Phillips & LeDoux, 1992). The model assumes that psychopathology develops when there are dissociations between these (and other) memory systems (Nadel & Jacobs, in press).
At a physiological level, dissociation may occur because of increases in concentrations of glucocorticoids released during stress. Glucocorticoids differentially affect the physiology of the amygdala and hippocampus. Activity in the amygdala increases as glucocorticoid concentrations increase (LeDoux, 1993; McGaugh, 1992; McGaugh et al., 1993; Swanson & Simmons, 1989). In contrast, activity in the hippocampus initially increases but then dramatically diminishes as glucocorticoid concentrations increase (de Kloet, Oitzl, & Jo=89ls, 1993).
By the model, activity in the relevant structures is one determinant of memory encoding (including consolidation). Thus, increasing stress enhances coding of emotional memory but disrupts coding of spatiotemporal context. Under traumatic stress, emotional memories are laid down without a significant contribution from the hippocampal system. This produces a pool of stimulus-bound emotional memories that have been encoded without a coherent event-specific spatiotemporal frame to organize them. This pool is, essentially, a population of traumatic memory fragments. Upon retrieval, traumatic memories cannot be experienced as a memorial event with a beginning, end, and internal spatiotemporal structure. Instead, each emotional memory is experienced as fragmented, disorganized, and intrusive (Thomas et al., 1995).
Humans, when faced with fragmented or meaningless material, tend to blend it by effortless, innocent, and unintentional narrative confabulation (e.g., Gazzaniga, 1985). Narrative confabulation appears to be driven by internal or external schema (e.g., Bartlett, 1932; Mandler, 1985). Notice that, by the model, all true traumatic memories are recovered in the sense of being reconstructed from memory fragments. In some cases, the person will construct a narrative immediately; in others, there will be a time lag between the traumatic experience(s) and narrative construction. The model anticipates no differences in the base characteristics of immediate or "recovered" traumatic memories.
Thomas et al. (1995) suggested such narratives will vary in accuracy when encoded under traumatic circumstances, but did not specify the circumstances under which the model predicts differences in accuracy. The purpose of the present paper is to specify those circumstances.
Given current knowledge, the most parsimonious way to think of emotional memory fragments is that they belong to a pool (or population) of relatively independent elements. Each act of retrieval is a sample (N=3D1) from the elements in that pool. We expect more than one sample to be taken for any given traumatic memory, because there are rich cues available to "call up" these fragments. Although such sampling is not random (it is often driven by extant stimuli), we will use the notion of random sampling from a pool as a heuristic because it illustrates the principle driving the predictions.
A pool of emotional memories might consist of many similar fragments (little variability), many different fragments (wide variability), and may be normally distributed, skewed, or multimodal. Because emotional memories are laid down and retrieved as fragments, we might think of the retrieved material as equivalent to a limited random draw from a pool of numbers. Once drawn, we assume they will be integrated within an ongoing spatiotemporal frame of reference and stabilized, partly through narrative construction.
The full integrated experience of such retrieval and stabilization might be characterized as a mean of that draw, which is biased by the constructed narrative. Thus, we can represent the veracity of the integrated memory by the relation between the mean and the individual numbers in the pool. Assuming the draw is not unduly biased, the model predicts various patterns of veracity as a function of previous experience. We will first generate predictions in the abstract and then apply them to specific examples.
If the numbers in the pool are relatively homogeneous, the sample mean represents each number fairly well. There is some "slippage" between the sample mean and any given number in the pool, but the mean is an adequate characterization of most of the numbers (a "theme" of the numbers). Although the mean misrepresents each number, it represents an overall structure of the numbers adequately. If the numbers in the pool vary widely, or if the distribution is skewed or multimodal, then the mean misrepresents the majority of the numbers in the pool: it is a poor characterization of the theme(s) of the numbers. Finally, if the draw is biased in some way, then the mean may misrepresent or more accurately represent most of the numbers in the pool, dependent on the direction of the bias but independent of the variability or distribution of those numbers.
For example, suppose a person has experienced one massive traumatic event, for example an intense, long-lasting firefight in combat. Under these conditions, a homogeneous pool might be created. Given the limited sampling opportunities, a recovered memory should be relatively accurate both for theme and event because there is only one event to represent. We would have some confidence in memories for events and for themes recovered under these circumstances.
Suppose a person has been repeatedly sexually assaulted in one place, at one time of night, by one perpetrator, with one act. Under these conditions, a homogeneous pool of traumatic fragments with the same theme might be created. Although a memory recovered from this pool may not adequately represent any individual assault, it should adequately capture the "theme" of the assaults. We would have some confidence in memory recovered under these circumstances.
Suppose a client has experienced many related, but different, traumatic events; for example, physical assault by several different perpetrators, numerous war experiences, and multiple automobile accidents. Under these conditions, a nonhomogeneous pool might be created. A recovered memory could misrepresent both individual traumatic events and the theme of any one of the groups of traumatic experiences. We would have little confidence in memory for events recovered under these circumstances, and we would expect that this memory would be thematically inaccurate.
Finally, suppose a client's experience has produced a pool of emotional memories with reasonable variance and two distinct themes. Also suppose that draws from the pool are not random, but are guided by another person with an agenda; perhaps the guide is committed to a particular model of psychopathology, or has been shaped by experience to interpret memories for trauma in a particular way, or has access to a factual account of the traumatic event. Only fragments of certain types would be retrieved while fragments of other types would not. Under guidance, a recovered memory could reflect combinations of the client's schema, the guide's schema, and the statistical characteristics of the pool. Thus, we expect an imposed schema to have a small effect given minor variability in the pool (e.g., repeated stereotypical assault, a single massively traumatic experience), but large effects given great variability or polymodality in the pool (e.g., a number of distinct traumatic experiences). In the latter case, the impact of the guide's schema on the veracity of recovered memory will be determined by the (unknown) relation between the imposed schema and the "target" traumatic event. Unless the guide has access to a factual account of this event, it seems best to remain suspicious of memory for events and themes recovered under these circumstances.
Thus, the model predicts different patterns of veracity given different types of traumatic experience. We might test these predictions using a variation of Strong Inference (Platt, 1964): First, we should keep a theory constrained by data from the fields immediately below it (in this case, anatomy/physiology) and by data from the fields immediately above it (in this case, clinical psychology).
Second, we should examine predictions from the theory using both field and laboratory work. Naturalistic and clinical observations set the questions, experiments sharpen the observations, and the results of the experiments provide means for making new observations. Disconfirmation of a given prediction might happen either in the field or in the laboratory.
Applying the principles developed above, the model predicts relative patterns among the correlations. In naturalistic studies, for example, the model predicts high correlations between the content of a traumatic memory and a single catastrophic experience. It predicts somewhat lower correlations between the content of a traumatic memory and events that were part of a series of related traumatic experiences. It predicts relatively low correlations between the content of a traumatic memory and any event that occurred over a lifetime of wide-ranging physical, mental, sexual, and legal assaults. In short, the model predicts patterns of relationships that should be observed in the clinic and under naturalistic conditions.
This gives rise to the question: What have we observed in the clinic and naturalistically? First, there are many reported cases of trauma-induced amnesia (e.g., Kaszniak, Nussbaum, Berren, & Santiago, 1988; Williams, 1994, 1995). Second, there are reported cases of recovered memory of events that occurred during trauma-induced amnesia (e.g., Grinker & Spiegel, 1945; Kaszniak et al., 1988; Williams, 1994, 1995). Third, there are cases in which the veracity of such memory has been determined (e.g., Williams, 1994). Fourth, there are reported cases of recovered memory that are completely (but innocently) confabulated, and cases that are surprisingly accurate descriptions of traumatic events (Dalenberg, in press; Hedges, 1994; Venn, 1986). We can use such data to test the current model by gathering as accurate as possible an account of the traumatic event (e.g., by taking a complete history from the client and family, by examining police reports), estimating the variability in the "traumatic pool," and examining correlations between the recovered memory and any "objective" facts that may exist.
Finally, it is possible to predict variation in the microstructure of memories laid down under stress in laboratory studies. For example, the model predicts that well-designed experiments will detect temporal and spatial distortions, and selective "amnesia" for specified aspects of the events experienced under stress (e.g., Burke, Heuer, & Reisberg, 1992). It predicts administering a drug such as propranolol before the stressor will alleviate "hyperencoding" of emotional memory (e.g., Cahill Prins, Weber, & McGaugh, 1994). It also predicts that long-term glucocorticoid treatment will produce "hypoencoding" of autobiographical memory (e.g., Keenan, Jacobson, Soleymani, & Newcomer, 1995). In addition, it predicts double dissociations between spatiotemporal memory and emotional memory when an individual is under the influence of therapeutic doses of glucocorticoids (Jacobs & Metcalfe, in review; Jacobs & Nadel, in review). Under this condition, learning and remembering spatiotemporal (and related) tasks should decline dramatically while emotional learning and memory should markedly improve. In short, the model predicts patterns of relationships that should be observed in the clinic and under experimental conditions.
Thus far, the model integrates results from a substantial literature on stress and memory. It also provides a rubric for classifying traumatic memory and provides guidance for continued empirical investigations of traumatic memory. We have tried to present these ideas in ways that might be challenged on logical grounds or disproven on empirical grounds. Through such a process, rapid progress might be made in the clinical sciences.
We thank our colleagues and friends for their many suggestions. We, of course, hold full responsibility for the content. This research was supported by a grant from the James H. Zumberge Faculty Research and Innovation Fund to the first author. Address correspondence to jakej@rcf.usc.edu; kevint@rcf.usc.edu; laurance@scf.usc.edu; luczak@rcf.usc.edu, or nadel@ccit.arizona.edu. References
Bartlett, F. C. (1932). Remembering. London: Cambridge University Press.
Burke, A., Heuer, F., & Reisberg, D. (1992). Remembering emotional events. Memory & Cognition, 20, 277-290.
Cahill, L., Prins, B., Weber, M., & McGaugh, J. L. (1994). Beta-adrenergic activation and memory for emotional events. Nature, 371, 702-704.
Dalenberg, C. (in press). Making and Finding Memories: A Commentary on the "Repressed Memory" Controversy. Journal of Child Sexual Abuse.
Davis, M. (1992). The role of the amygdala in fear and anxiety. Behavior Research and Therapy, 24, 461-470.
Davis, M., Rainnie, D., & Cassell, M. (1994). Neurotransmission in the rat amygdala related to fear and anxiety. Trends in Neurosciences, 17, 208-214.
de Kloet, E. R., Oitzl, M. S., & Jo=89ls, M. (1993). Functional implications of brain corticosteroid receptor diversity. Cellular and Molecular Neurobiology, 13, 433-455.
Gazzaniga, M. S. (1985). The social brain: Discovering the networks of the mind. New York: Basic Books.
Grinker, R. R., & Spiegel, J. P. (1945). Men under stress. London: J. & A. Churchill.
Hedges, L. E. (1994). Remembering, repeating, and working through childhood trauma: the psychodynamics of recovered memories, multiple personality, ritual abuse, incest, molest, and abduction. Northvale, N.J.: J. Aronson.
Jacobs, W. J., & Metcalfe, J. (in review). The effects of stress on 'cool' and 'hot' memory systems. Behavioral and Brain Sciences.
Jacobs, W. J., & Nadel, L. (1985). Stress-induced recovery of fears and phobias. Psychological Review, 92, 512-531.
Jacobs, W. J., & Nadel, L. (in press). The neurobiology of the first panic attack. In R. Klein & J. Fentress (Eds.), A Memorial Volume to D. O. Hebb.
Jacobs, W. J., & Nadel, L. (in review). Intrusive memory. Psychological Review.
Kaszniak, A. W., Nussbaum, P. D., Berren, M. R., & Santiago, J. (1988). Amnesia as a consequence of male rape: A case report. Journal of Abnormal Psychology, 97, 100-104.
Keenan, P. A., Jacobson, M. W., Soleymani, R. M., & Newcomer, J. W. (1995). Commonly used therapeutic doses of glucocorticoids impair explicit memory. Annals of the New York Academy of Sciences, 761, 400-402.
Kim, J.J., & Fanselow, M.S. (1992). Modality specific retrograde amnesia of fear. Science, 256, 675-677.
LeDoux, J.E. (1992). Brain mechanisms of emotion and emotional learning. Current Opinion in Neurobiology, 2, 191-198.
LeDoux, J.E. (1993). Emotional memory systems in the brain. Behavioural Brain Research, 58, 69-79.
LeDoux, J.E. (1994). Emotion, memory and the brain. Scientific American, 270, 50-57.
Mandler, G. (1982). Mind and emotion. Malabar, FL: R.E. Krieger.
McGaugh, J.L. (1992). Neuromodulatory regulation of memory - role of the amygdaloid complex. International Journal of Psychology, 27, 403.
McGaugh, J.L., Introini-Collison, I.B., Cahill, L.F., Castillano, C.D., Parent, M.B., & Williams, C.L. (1993). Neuromodulatory systems and memory storage: Role of the amygdala. Behavioural Brain Research, 58, 81-90.
Nadel, L., & Jacobs, W. J. (in press). The role of the hippocampus in PTSD, panic, and phobia. Hippocampus: Functions and clinical relevance. Amsterdam: Elsevier Science B.V.
Nadel, L., & O'Keefe, J. (1974). The hippocampus in pieces and patches: An essay on modes of explanation in physiological psychology. In R. Bellairs & E.G. Gray (Eds.), Essays on the nervous system: A Festschrift for J.Z. Young. Oxford: The Clarendon Press.
O'Keefe, J., & Nadel, L. (1978). The hippocampus as a cognitive map. Oxford: Oxford University Press.
Ofshe, R., & Watters, E. (1994). Making monsters : false memories, psychotherapy, and sexual hysteria. New York: Charles Scribner's.
Phillips, R.G., & LeDoux, J.E. (1992). Differential contribution of amygdala and hippocampus to cued and contextual fear conditioning. Behavioral Neuroscience, 106, 274-285.
Platt, J.R. (1964). Strong inference. Science, 146, 347-353.
Swanson, L.W., & Simmons, D.M. (1989). Differential steroid hormone and neural influences on peptide m-RNA levels in CRH cells of the paraventricular nucleus: A hybridization histochemical study in the rat. Journal of Comparative Neurology, 285, 413-435.
Thomas, K. G. F., Laurance, H.E., Jacobs, W. J. & Nadel, L. (1995). Memory for traumatic events: Formulating hypotheses and critical experiments. Traumatology, 1:2, http://www.shef.ac.uk/uni/projects/gpp/traumai.html.
Venn, J. (1986). Hypnosis and the reincarnation hypothesis: A critical review and intensive case study. Journal of the American Society for Psychical Research, 80, 409-425.
Williams, L. M. (1994). Recall of childhood trauma - a prospective-study of womens memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167-1176.
Williams, L. M. (1995). Recovered memories of abuse in women with documented child sexual victimization histories. Journal of Traumatic Stress, 8, 649-673.
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