We mentioned earlier that behavior had to be considered in context to be properly understood. At that point "context" meant considering the behavior in terms of the patient's history and the antecedents and consequences of his or her behavior. Context actually entails even more. At a psychological level, a patient is changed by every new experience that contributes to his or her history. Treatment itself can be thought of as adding to the person's history to change the impact of the traumatic event. Behavior theory long ago rejected any implied dualism between body and behavior. Behavior exists in a biological milieu. Behavior and biology cannot be separated and still retain sensible meaning. Therefore, one other source of behavioral variance to consider is how neurophysiological changes associated with traumatic experiences can alter the patient's interactions with the world. It is well beyond the scope of this chapter to try to resolve all of the interesting, though often conflicting, neurophysiological and neuroanatomical changes that are sometimes attributable to traumatic experiences, especially when experienced by the young. However, many functional and sometimes structural changes have been noted that may involve memory impairment: changes in the hippocampus that could affect declarative memory, possible frontal lobe changes, and even changes in amygdaloid regions. Because of a variety of methodological and measurement problems, it is not known the extent to which these changes are due to PTSD alone or in combination with comor-bid conditions, are transient, or even reach clinical significance (cf. Brandes et al., 2002; Bustamante, Mellman, David, & Fins, 2001; Danckwerts & Leathem, 2003; Neylan et al., 2004). However, some of the clinical changes observed in PTSD could be influenced by a biologically changed person who interacts differently with his or her environment, thereby adding to the sense of loss of control and estrangement. These findings are still speculative as to their duration, cause, and significance. Yet a complete functional analysis of target behaviors to be addressed during an intervention requires a consideration of these emerging data as additional changes that might contribute to altered relationships between the patient and his or her environment. There is convincing evidence that these changes, if substantiated, could be the target of therapy to restore pretrauma levels of functioning, at least in adults.
Once again, the issue that would remain important to assess is not just the topography of the trauma response but the stimulus functions the patient presents to others. Whether or not memory disturbances are related to trauma or other comorbid conditions, memory or emotion regulation functions that are altered from what significant people in the environment are used to expecting, can produce distressing interactions that exacerbate symptoms or change the way in which people respond to the patient.
Certainly the immediate reactions of a patient to a traumatic event are appropriately the focus of evidence-based treatments. What we have described thus far is the notion that there are social consequences to these reactions that are far reaching and can lead to problems of their own (e.g., Soloman, 1989). We have further suggested that these reactions can produce or exacerbate some of the symptoms that are the basis for making the PTSD diagnosis.
Was this article helpful?