-Caveat Lector- Hi ! Below please find an article dealing with traumatic memory. Sincerely, Neil Brick Excerpts from : http://rdz.stjohns.edu/trauma/art3v2i2.html On the Veracity and Variability of Traumatic Memory Jacobs, W. J., Laurance, H. E., Thomas, K. G. F., Luzcak, S. E. & Nadel, L. (1996). University of Southern California, Seeley G. Mudd Building, #501, Department of Psychology, Los Angeles, CA 90089-1061. Traumatology, [On-Line] 2,2. Available: http://rdz.stjohns.edu/trauma/art3v2i2.html 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). ... 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. 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 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. 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. DECLARATION & DISCLAIMER ========== CTRL is a discussion and informational exchange list. Proselyzting propagandic screeds are not allowed. Substance�not soapboxing! These are sordid matters and 'conspiracy theory', with its many half-truths, misdirections and outright frauds is used politically by different groups with major and minor effects spread throughout the spectrum of time and thought. That being said, CTRL gives no endorsement to the validity of posts, and always suggests to readers; be wary of what you read. CTRL gives no credeence to Holocaust denial and nazi's need not apply. Let us please be civil and as always, Caveat Lector. ======================================================================== Archives Available at: http://home.ease.lsoft.com/archives/CTRL.html http:[EMAIL PROTECTED]/ ======================================================================== To subscribe to Conspiracy Theory Research List[CTRL] send email: SUBSCRIBE CTRL [to:] [EMAIL PROTECTED] To UNsubscribe to Conspiracy Theory Research List[CTRL] send email: SIGNOFF CTRL [to:] [EMAIL PROTECTED] Om
