Current research based on neuroendocrinology, functional magnetic resonance imaging (fMRI), and positron emission tomographic (PET) studies of brain architecture and activation under conditions with and without stress (Armony & LeDoux, 1997; Canive et al., 1997; Pitman, 1997; Shin, et al., 1997; Spiegel, 1997) have established that PTSD, rather than representing an impaired access to traumatic memories (Foa & Hearst-Ikeda, 1997, as cited in Harvey & Bryant, 1999), more likely involves disorganization in adequately creating explicit memories (Harvey & Bryant, 1999). These findings, enumerated in the following four points, are particularly important for compositionists because they point to biological mechanisms of memory involved in writing about personal trauma.

1. People with lifetime or chronic PTSD retain measurable physiologic sensitivity to environmental stimuli (hyperarousal or hyperstartle) even though they may not currently complain of current PTSD arousal or reexperiencing symptoms.

Research by Kerr and Landfield (as cited in Bear et al., 2001) supports the explanation that initially cortisol makes the brain more alert, perhaps by allowing brain cells to admit more excitatory calcium, and “better able to cope with stress” (p. 506). Bear et al. suggest that cortisol serves as well to “mobilize energy reserves and suppress the immune system” (p. 504). But chronic stress, with the chronic flow of calcium and cortisol, correlates with neuroreceptor site alteration (Southwick et al., 1997) and with destruction (from excitotoxicity)—and, at times, permanent damage in parts of the brains such as the hippocampus. Such widespread alterations can either stem from or result in abnormalities in “at least seven unique neurobiological systems” (Friedman, 1997, p. 367; Pitman, 1997; Southwick et al., 1997).