The hippocampus plays a significant role in the capacity to consciously recall a previous life event, that is, in declarative memory. Its role in emotion and affective style has only recently started to be explored. The hippocampus plays a significant role in context-dependent memory (O'Keefe and Nadel; Fanselow, 2000). When an animal is exposed to a cue-conditioning procedure, where a discrete cue is paired with an aversive outcome, the animal also learns to associate the context in which the learning occurs with the aversive outcome. Lesions to the hippocampus abolish this context-dependent form of memory but have no effect on learning cue-punishment contingencies (Davidson, 2001). The high density of glucocorticoid receptors in this structure supports the idea that the hippocampus may play an important role in emotion regulation. Glucocorti-coids have been shown to have a powerful impact on hippocampal neurons (Cahill and McGaugh, 1998; McEwen, 1998). Exogenous administration of large doses of hydrocortisone to humans impairs explicit memory, while more moderate amounts of cortisol may facilitate memory (e.g., Kirschbaum et al., 1996).
A number of PTSD studies have reported significantly decreased hippocampal volume in patients with PTSD (e.g., Bremner 1997, 1999; Gurvits et al., 1998) and depression. For example, Bremner et al. (1997) compared hippocampal volume in adult survivors of childhood abuse to matched controls. PTSD patients had a 12 percent smaller left hippocampal volume relative to the matched controls (p < .05), without smaller volumes of comparison regions (amygdala, caudate, and temporal lobe), while Gurvits and her colleagues found both significantly smaller left and right hippocampi in combat veterans with PTSD compared to combat controls without PTSD and normal controls. However, several well-controlled studies have failed to replicate these findings (e.g., DeBellis et al., 1999; Bonne et al., 2001). In the studies in which hippocampal atrophy has been found, investigators have proposed that excessively high levels of cortisol caused hippocampal cell death, resulting in hippocampal atrophy.
At this time it appears that smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 months of expressing the disorder. However, it is likely that subjects with long-standing PTSD and particularly those with histories of severe childhood trauma may have smaller hippocampi. These subjects also exhibit neuropsychological abnormalities that can be associated with impaired hippocampal functioning, such as difficulty learning from negative experiences, despite extreme emotional and biological reactivity to reminders of their traumas.
Davidson et al. (2000) have proposed that the impact of hippocampal involvement in psychopathology may be most apparent in the processing of emotional information and that, in individuals with compromised hippocampal function, the normal context-regulatory role of this brain region would be impaired. Consequently, individuals with hippocampal damage would be prone to display emotional behavior in inappropriate contexts. Indeed, PTSD does not involve the display of abnormal emotions per se, but the presentation of normal emotions in inappropriate contexts. Patients with PTSD behave in ways that are reminiscent of animals with hippocampal lesions, in being unable to modulate emotional responses in a context-appropriate manner.
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