To the Editor: I thank Dr. Pope for addressing the issues of the script-driven imagery symptom provocation paradigm as a means of examining memory recall and the influence of comorbid conditions on the results of our functional connectivity study with PTSD patients.

The script-driven imagery symptom provocation paradigm has been a standard and well-established symptom provocation paradigm in the PTSD literature (1). In our laboratory, PTSD subjects consistently report that listening to the 30-second trauma script serves as a "trigger" for an intense, vivid remembrance or flashback that begins during the script but continues well afterward. Of importance, the period to which the connectivity analyses pertain is the 30 seconds after the script reading has ended and subjects are engaged in recall of their traumatic memory. Thus, while the script may be a particular type of trigger, or eliciting stimulus, PTSD subjects consistently report that the traumatic script elicits an intrusive memory of the traumatic event that is quite typical for them, and it was the neural correlates of such typical memories that we assessed. Furthermore, our approach is consistent with the autobiographical memory literature, in which the recall of autobiographical memory is often examined by using specific techniques to elicit recall of past memories (2–4).

In terms of comorbid conditions, flashbacks and reliving symptoms associated with past traumatic events, the focus of the present article, are not part of the diagnostic criteria of any of the comorbid conditions exhibited by some of the PTSD subjects, including major depression, dysthymia, panic disorder, and substance use disorder. It is therefore unlikely that comorbid conditions such as depression or nicotine abuse that characterize some of the PTSD subjects are responsible for the brain activation changes observed.

The brain areas that showed significantly different brain activation patterns in the PTSD group included the occipital cortex, the parietal lobe, and the posterior cingulate gyrus. These are not brain areas that have traditionally been associated with changes in emotional arousal (5). Rather, as noted in our article, these areas have been shown to predominate in retrieval of nonverbal episodic memories (3, 4). It is therefore not likely that differences in emotional arousal alone could explain the observed differences in brain activation patterns between PTSD and comparison subjects.

In summary, the script-driven imagery symptom provocation paradigm serves as a trigger for intense, vivid memories of traumatic experiences. Flashback and reliving symptoms of past traumatic experiences are not part of the diagnostic criteria of any of the comorbid conditions exhibited by some of the PTSD subjects in the present study. Finally, the overall pattern of brain activation in the PTSD subjects reporting typical traumatic memories with intense emotions and sensations, as compared to comparison subjects reporting normal autobiographical memories, includes regions associated not with emotional arousal but with nonverbal episodic memory retrieval.