Another explanation for trauma-related autobiographical memory problems is that they reflect more general memory deficits caused by the harmful physiologic effects of chronic or traumatic stress on the structure and function of the brain. Much of the research relevant to this hypothesis has focused on cortisol-related damage to the hippocampus, an area of the brain thought to be involved in the consolidation of memory traces into cohesive, context-rich episodic memories (Nelson, 2000; Nelson & Carver, 1998). This work suggests that under conditions of high stress, the hypothalamic-pituitary-adrenal (HPA) axis stimulates the release of excessive levels of the stress hormone cortisol (Stansbury & Gunnar, 1994), which then floods the hippocampus (Bremner, 1999; Nelson & Carver, 1998; Sapolsky, 1996, 2000; Squire, 1992). These elevated levels of cortisol impair the mechanisms that are thought to be involved in memory consolidation in the hippocampus (Fillipini, Gijsbers, Birmingham, & Dubrovsky, 1991; Gould, Tanapat, McEwen, Flugge, & Fuchs, 1998), presumably leading to the formation of highly fragmented memories (Nadel & Jacobs, 1998). Further, prolonged exposure to high levels of stress hormones may lead to a reduction in the volume of the hippocampus and more chronic memory dysfunctions (Bremner, 2005; Bremner & Narayan, 1998; Kitayama, Vaccarino, Kutner, Weiss, & Bremner, 2005; for a recent review of this literature, see Chapter 1 in this volume).
Consistent with these claims, manipulations that involve both direct application of cortisol to the brain and inductions of highly stressful events have been shown to result in hippocampal atrophy and learning impairments in nonhuman animals (Gould et al., 1998; Sapolsky & McEwen, 1986). However, empirical support for the argument that trauma itself impairs hippocampal functioning in humans is less conclusive. On the one hand, there is some evidence that exposure to child physical or sexual abuse is related to reduced hippocampal volume in adults (Bremner et al., 1997; Stein, Koverola, Hanna, Torchia, et al., 1997; Vythilingam et al., 2002). For instance, Vythilingam et al. (2002) found bilateral decreases in hippocampal volume in depressed women who reported childhood abuse histories, relative to both depressed nonabused women and healthy, nonabused controls. On the other hand, there is also evidence to suggest that hippocampal atrophy in adults with a history of trauma is more specifically associated with trauma-related psychological disorders such as PTSD (Bremner, 2001; Bremner et al., 1997; Bremner et al., 2003; Kitayama et al., 2005) and depression (Bremner et al., 2000; Sheline, Sanghavi, Mintun, & Gado, 1999), rather than the trauma itself. Bremner et al. (2003), for example, found that women with childhood sexual abuse (CSA) histories and PTSD had significantly smaller hip-pocampal volume than women with CSA histories without PTSD diagnoses or nonabused control subjects. Some researchers, moreover, have posited that smaller hippocampal volume is not a consequence of trauma or psychopathology but rather is a preexisting risk factor for the development of psychopathology following exposure to trauma (Gilbertson et al., 2002; Sapolsky, 1996; Stein et al., 1997). In addition, it is unclear how early in development trauma-related alterations in brain structure and function might occur, as most of this research has focused on adult populations and there has been little corroborative research on this issue with children. A study by DeBellis, Hall, Boring, Frustaci, and Moritz (2001) found no neuroanatomical differences between children who had developed PTSD in response to maltreatment and healthy, nonmaltreated children when the children were tested either pre- or post-pubescently. Nevertheless, the finding that high levels of glucocorticoids used to treat child asthma patients are associated with memory problems suggests that cortisol elevation could lead to deficits in memory function during childhood (Annett & Bender, 1994). Thus, even if trauma-related hippocampal volume deficits are not observed during childhood, it is possible that trauma-induced stress hormone dysregulation could lead to memory problems during childhood and eventual cell death in the hip-pocampal structure in adulthood.
If hippocampal dysfunction is in fact one of the mechanisms involved in the autobiographical memory impairments that typify abuse victims, it seems likely that these autobiographical memory problems would be accompanied by a broad range of memory deficits. The hippocampus is thought to be central in the consolidation of verbal declarative memory traces (Bremner et al., 2003; Bremner, Vythilingam, Vermetten, Vaccarino, & Charney, 2004; Elzinga, Bakker, & Bremner, 2005; Squire, 1992), and it has also been implicated in the retrieval of declarative memories (de Quervain, Roozendaal, & McGaugh, 1998), implicit memory processes (Chun & Phelph, 1999), and spatial memory (Maguire, Frackowiak, & Frith, 1997). Thus individuals with trauma-related autobiographical memory problems should also be expected to show deficits in nonautobiographical memory, and they should show evidence of impaired encoding and storage processes as well as retrieval processes. Surprisingly few studies of trauma-related autobiographical memory disturbances have actually addressed these possibilities. One exception is the study by de Decker et al. (2003) that illustrated that immediate and delayed story recall were unrelated to trauma-associated memory problems in their sample of adolescent psychiatric inpatients. Although more research is needed in this area, there is currently a dearth of empirical evidence to confirm that stress-related hippocampal damage accounts for the autobiographical memory problems observed in traumatized individuals.
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