Dissociation—a common feature of posttraumatic stress disorder (PTSD)1,2—involves disruptions in the usually integrated functions of consciousness, memory, identity, and perception of the self and the environment.3 Acute dissociative responses to psychological trauma have been found to predict the development of chronic PTSD.4-9 Moreover, a chronic pattern of dissociation in response to reminders of the original trauma and minor stressors has been found to develop in persons who experience acute dissociative responses to psychological trauma.9
Bremner and associates10 hypothesized that there may be 2 subtypes of acute trauma response that represent unique pathways to chronic stress-related psychopathology: one is primarily dissociative and the other is predominantly intrusive and hyperaroused. Using data from our own neuroimaging studies,11-16 we will show that these 2 subtypes of response can persist in persons with chronic PTSD17 and that they are associated with distinct patterns of neural activation upon exposure to reminders of traumatic events.
The term “dissociation” has denoted a wide variety of phenomena in the literature encompassing both states and traits. Here the focus is on dissociative symptomatic responses to trauma-related stimuli in PTSD—particularly states of depersonalization and derealization. We have operationalized this definition with 4 questions from the Responses to Script-Driven Imagery Scale, which is a validated measure of evoked symptoms that we developed to advance psychobiological and treatment outcome research in PTSD.18
• Did what you were experiencing seem unreal to you, like you were in a dream or watching a movie or play?
• Did you feel like you were a spectator watching what was happening to you, like an observer or outsider?
• Did you feel disconnected from your body?
• Did you feel like you were in a fog?
For most clinicians, these are familiar descriptions of some of their PTSD patients’ responses to trauma-related stimuli and situations, and such states are witnessed firsthand in their offices.
Functional brain imaging studies
Over the past 15 years, the application of functional neuroimaging research on PTSD has resulted in an explosion of new data that have begun to reveal the brain circuits that are involved in the pathophysiology of this disorder. Studies that use positron emission tomography (PET) and blood oxygenation level–dependent functional MRI (BOLD fMRI) have examined neural responses to a variety of stimuli, including fearful, happy, and neutral faces; trauma-related images and sounds; and “script-driven imagery” of traumatic experiences. A recent review and meta-analysis found that persons with PTSD tend to exhibit greater brain activation in the amygdala and insula than persons without PTSD; these structures are involved in fear conditioning and the perception of bodily states (among other functions), respectively.19 Moreover, the dorsal anterior cingulate cortex (ACC), rostral ACC and ventromedial prefrontal cortex, which are involved in the experience and regulation of emotion, have repeatedly been observed to be less activated in patients with PTSD than in controls who have a history of trauma but not PTSD.19
Our research has shown that in patients with PTSD, psychobiological responses to recalling traumatic experiences can differ significantly, and a sizable proportion do not fit the conventionally studied “reexperiencing/hyperaroused” response.20,21 For example, in our initial brain imaging studies, approximately 70% of patients relived their traumatic experience and showed an increase in heart rate while recalling the traumatic memory,11,13 while the other 30% had a dissociative response with no concomitant increase in heart rate.14,15
We have investigated the neuronal circuitry that underlies reexperiencing/hyperaroused and dissociative responses in PTSD using BOLD fMRI and script-driven imagery. In this paradigm, patients construct a narrative of their traumatic experience that is later read to them while they are in the scanner. They are instructed to recall the traumatic memory as vividly as possible during “trauma scripts” and immediately afterward while the MRI scanner measures oxygen use in different brain areas.
Our first study involved 9 patients with sexual abuse– or motor vehicle accident–related PTSD and 9 controls who had a history of sexual abuse or motor vehicle accidents but in whom PTSD never developed. Figure 1 demonstrates that compared with controls, patients who relived their traumatic experience and had a hyperaroused response to the traumatic script exhibited significantly less activation in the rostral ACC and medial prefrontal cortex as well as in the thalamus and occipital cortices.11 Lower levels of ACC activation and medial prefrontal activation are consistent with previous PET studies of sexual abuse and combat-related PTSD.10,17,22 These brain activation patterns differ strikingly from those observed in a second study of 7 patients who dissociated in response to the traumatic script and of 10 trauma-exposed controls.12 Figure 2 shows that these dissociative patients had higher levels of brain activation in the rostral ACC and dorsal ACC, medial prefrontal cortex, and areas in the superior and middle temporal cortices.
The most remarkable findings in these 2 studies are the opposite patterns of brain activation. The more typical reexperiencing/hyperaroused group exhibited abnormally low activation in the medial anterior brain regions that are implicated in arousal modulation and emotion regulation more generally (ACC and medial prefrontal cortex), while the dissociative group exhibited abnormally high activation in these regions.
These findings are entirely consistent with the phenomenology and clinical presentations of patients with PTSD who need help to overcome pathological overengagement or underengagement with traumatic memories and the associated emotions and bodily experiences. Low activation in these regions is consistent with failed inhibition of limbic reactivity associated with hyperaroused overengagement. High activation is consistent with hyperinhibition of those same limbic regions in states of pathological underengagement with trauma-related emotions.
More specifically, the findings are compatible with the corticolimbic model of depersonalization. That model postulates that depersonalization involves a corticolimbic disconnection in which left medial prefrontal activation with reciprocal amygdala inhibition results in hypoemotionality and decreased arousal, while right dorsolateral prefrontal cortex activation with reciprocal ACC inhibition leads to an emptiness of mental content.23 In this model, after a threshold of anxiety is reached, the medial prefrontal cortex inhibits emotional processing in limbic structures (eg, the amygdala) that, in turn, leads to a dampening of sympathetic output and reduced emotional experience.