Reexperiencing/Hyperaroused and Dissociative States in Posttraumatic Stress Disorder

In support of this model, there is significant evidence for medial prefrontal involvement in both the monitoring and the modulation of emotions.^24,25 Furthermore, several studies suggest that the prefrontal cortex has inhibitory influences on the emotional limbic system, including PET studies that showed a negative correlation between blood flow in the left prefrontal cortex and the amygdala.^26,27

The activations we found in the superior and middle temporal cortices during dissociative states in PTSD are consistent with the temporal lobe hypothesis of dissociation. The epilepsy literature has described dissociative symptoms with seizures of various foci, including both right and left hemispheres.^28,29 Penfield and Rasmussen³⁰ have also reported depersonalizationlike symptoms in response to stimulation of the superior and middle temporal cortices during neurosurgery.

Moreover, Teicher and colleagues³¹ have explored the relationship between early abuse and limbic system dysfunction as measured by the Limbic System Checklist-33.³¹ This checklist includes symptoms that are often experienced by persons with temporal lobe epilepsy and may explain why some patients with PTSD who have more extreme dissociative pathology exhibit pseudopsychotic symptoms that can mimic a psychotic disorder and result in misdiagnosis.³² Limbic System Checklist-33 scores have been found to correlate strongly with Dissociative Experiences Scale scores.^31,33 Thus, altered activation of the superior and middle temporal cortex may contribute to the dissociative experiences that patients have while recalling their traumas.

Importantly, individual differences in responses to trauma reminders can be conceptualized categorically, as qualitatively different response subtypes, as well as dimensionally, as involving different symptom severities and associated neural activation patterns within each response subtype. In addition, even patients who have PTSD without major dissociative pathology may have dissociative responses when traumatic memories are triggered. Thus, in a subsequent study, we used fMRI to examine correlations between severities of reexperiencing and dissociative responses to trauma scripts and activity in regions associated with awareness and regulation of arousal and emotions.¹⁶ The study included 27 patients with PTSD that had resulted primarily from traumatic motor vehicle accidents; these patients had differing degrees of dissociative pathology but relatively mild dissociative symptoms overall. Subjective experiences of state reexperiencing and dissociative symptom responses to trauma scripts in the fMRI were assessed with the Response to Script-Driven Imagery Scale.¹⁸

As hypothesized, state reexperiencing severity was positively correlated with right anterior insula activation and was negatively correlated with activation of rostral ACC, while dissociative response severity was negatively correlated with right anterior insula activation and positively correlated with activation of medial prefrontal cortex and dorsal ACC. In addition, dissociation severity correlated positively with left medial prefrontal cortex and right superior temporal cortex activation and correlated negatively with left superior temporal cortex activation.

The dissociation findings are consistent with those in our study using the categorical approach to compare severely dissociative patients who have PTSD with trauma-exposed controls. They are particularly noteworthy because the present participants had relatively low trait dissociation levels on average, which was similar to our previous participants with PTSD who displayed predominantly hyperaroused reexperiencing responses¹¹—levels of dissociation that characterize many patients with PTSD who are encountered in clinical practice—and much lower trait and state dissociation than the “dissociative” script responders in our other prior study. Finally, these findings provide support for a model of such dissociative reactivity as a form of emotion dysregulation that involves extreme underengagement mediated by midline prefrontal inhibition of limbic activity. Figure 3 summarizes these findings while visually presenting a broader emotion dysregulation account of reactivity to trauma-related stimuli in PTSD.