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.
1. van der Kolk BA, Pelcovitz D, Roth S, et al. Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma. Am J Psychiatry. 1996;153(7 suppl):83-93. Review.
2. Stovall-McClough KC, Cloitre M. Unresolved attachment, PTSD, and dissociation in women with childhood abuse histories. J Consult Clin Psychol. 2006;74:219-228.
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders Revised, Fourth Edition. Washington, DC: American Psychiatric Association; 2000:519-533.
4. Bryant RA. Acute stress reactions: can biological responses predict posttraumatic stress disorder? CNS Spectr. 2003;8:668-674.
5. Bremner JD, Southwick S, Brett E, et al. Dissociation and posttraumatic stress disorder in Vietnam combat veterans. Am J Psychiatry. 1992;149:328-332.
6. Marmar CR, Weiss DS, Schlenger WE, et al. Peritraumatic dissociation and posttraumatic stress in male Vietnam theater veterans. Am J Psychiatry. 1994;151:902-907.
7. Koopman C, Classen C, Spiegel D. Predictors of posttraumatic stress symptoms among survivors of the Oakland/Berkeley, California, firestorm. Am J Psychiatry. 1994;151:888-894.
8. Shalev AY, Peri T, Canetti L, Schreiber S. Predictors of PTSD in injured trauma survivors: a prospective study. Am J Psychiatry. 1996;153:219-225.
9. Bremner JD, Innis RB, Ng CK, et al. Positron emission tomography measurement of cerebral metabolic correlates of yohimbine administration in combat-related posttraumatic stress disorder. Arch Gen Psychiatry. 1997;54:246-254.
10. Bremner JD, Staib LH, Kaloupek D, et al. Neural correlates of exposure to traumatic pictures and sound in Vietnam combat veterans with and without posttraumatic stress disorder: a positron emission tomography study. Biol Psychiatry. 1999;45:806-816.
11. Lanius RA, Williamson PC, Densmore M, et al. Neural correlates of traumatic memories in posttraumatic stress disorder: a functional MRI investigation. Am J Psychiatry. 2001;158:1920-1922.
12. Lanius RA, Williamson PC, Boksman K, et al. Brain activation during script-driven imagery induced dissociative responses in PTSD: a functional MRI investigation. Biol Psychiatry. 2002;52:305-311.
13. Lanius RA, Williamson PC, Densmore M, et al. The nature of traumatic memories: a 4-T fMRI functional connectivity analysis. Am J Psychiatry. 2004;161:36-44.
14. Lanius RA, Williamson PC, Bluhm RL, et al. Functional connectivity of dissociative responses in posttraumatic stress disorder: a functional magnetic resonance imaging investigation. Biol Psychiatry. 2005;57:873-884.
15. Lanius RA, Bluhm R, Lanius U, Pain C. A review of neuroimaging studies in PTSD: heterogeneity of response to symptom provocation. J Psychiatr Res. 2006;40:709-729.
16. Hopper JW, Frewen PA, van der Kolk BA, Lanius RA. Neural correlates of reexperiencing, avoidance, and dissociation in PTSD: symptom dimensions and emotion dysregulation in responses to script-driven trauma imagery. J Trauma Stress. 2007;20:713-725.
17. Bremner JD, Narayan M, Staib LH, et al. Neural correlates of memories of childhood sexual abuse in women with and without posttraumatic stress disorder. Am J Psychiatry. 1999;156:1787-1795.
18. Hopper JW, Frewen PA, Sack M, et al. The responses to script-driven imagery scale (RSDI): assessment of state posttraumatic symptoms for psychobiological and treatment research. J Psychopathol Behav Assess. 2007;29:249-268.
19. Etkin A, Wager TD. Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. Am J Psychiatry. 2007;164:1476-1488.
20. Keane TM. Guest editorial. Posttraumatic stress disorder. Future directions in science and practice. J Rehabil Res Dev. 2008;45:vii-x.
21. Orr SP, Roth WT. Psychophysiological assessment: clinical applications for PTSD. J Affect Disord. 2000;61:225-240.
22. Shin LM, McNally RJ, Kosslyn SM, et al. Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: a PET investigation. Am J Psychiatry. 1999;156:575-584.
23. Sierra M, Berrios GE. Depersonalization: neurobiological perspectives. Biol Psychiatry. 1998;44:898-908.
24. Reiman EM, Lane RD, Ahern GL, et al. Neuroanatomical correlates of externally and internally generated human emotion. Am J Psychiatry. 1997;154:918-925.
25. Damasio AR. Descartes’ Error: Emotion, Reason, and the Human Brain. New York: G.P. Putnam’s Sons; 1994.
26. Drevets WC, Videen TO, Price JL, et al. A functional anatomical study of unipolar depression. J Neurosci. 1992;12:3628-3641.
27. Davidson RJ, Sutton SK. Affective neuroscience: the emergence of a discipline. Curr Opin Neurobiol. 1995;5:217-224.
28. Kenna JC, Sedman G. Depersonalization in temporal lobe epilepsy and the organic psychoses. Br J Psychiatry. 1965;111:293-299.
29. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology. 1989;39:835-840.
30. Penfield W, Rasmussen T. The Cerebral Cortex of Man: A Clinical Study of Localization of Function. New York: Macmillan; 1950:157-181.
31. Teicher MH, Glod CA, Surrey J, Swett C Jr. Early childhood abuse and limbic system ratings in adult psychiatric outpatients. J Neuropsychiatry Clin Neurosci. 1993;5:301-306.
32. Kluft RP. First-rank symptoms as a diagnostic clue to multiple personality disorder. Am J Psychiatry. 1987;144:293-298.
33. Teicher MH, Ito Y, Glod CA, et al. Preliminary evidence for abnormal cortical development in physically and sexually abused children using EEG coherence and MRI. In: Yehuda R, McFarlane AC, eds. Psychobiology of Posttraumatic Stress Disorder. Vol 821. New York: New York Academy of Sciences; 1997:160-175.
34. Prins A, Kaloupek DG, Keane TM. Psychophysiological evidence for autonomic arousal and startle in traumatized adult populations. In: Friedman MJ, Charney DS, Deutch AY, eds. Neurobiological and Clinical Consequences of Stress: From Normal Adaptation to PTSD. Philadelphia: Lippincott-Raven; 1995:291-314.
35. Ginzburg K, Koopman C, Butler LD, et al. Evidence for a dissociative subtype of post-traumatic stress disorder among help-seeking childhood sexual abuse survivors. J Trauma Dissociation. 2006;7:7-27.
36. Foa EB, Keane TM, Friedman MJ. Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies. 2nd ed. New York: Guildford Press; 2008.
37. Foa EB, Kozak MJ. Emotional processing of fear: exposure to corrective information. Psychol Bull. 1986;99:20-35.
38. Foa EB, Cahill SP, Boscarino JA, et al. Social, psychological, and psychiatric interventions following terrorist attacks: recommendations for practice and research. Neuropsychopharmacology. 2005;30:1806-1817.
39. Jaycox LH, Foa EB, Morral AR. Influence of emotional engagement and habituation on exposure therapy for PTSD. J Consult Clin Psychol. 1998;66:185-192.
40. Jaycox LH, Zoellner L, Foa EB. Cognitive-behavior therapy for PTSD in rape survivors. J Clin Psychol. 2002;58:891-906.
41. Cloitre M, Koenen KC, Cohen LR, Han H. Skills training in affective and interpersonal regulation followed by exposure: a phase-based treatment for PTSD related to childhood abuse. J Consult Clin Psychol. 2002;70:1067-1074.
42. Cloitre M, Cohen LR, Koenen KC. Treating Survivors of Childhood Abuse: Psychotherapy for the Interrupted Life. New York: Guilford Press; 2006.
43. Ogden P, Mintun K, Pain C. Trauma and the Body: A Sensorimotor Approach to Psychotherapy. New York: W.W. Norton; 2006.
44. Vermilyea EG. Growing Beyond Survival: A Self-Help Toolkit for Managing Traumatic Stress. Baltimore: Sidran Press; 2007.
45. Spinazzola J, Blaustein M, van der Kolk BA. Posttraumatic stress disorder treatment outcome research: the study of unrepresentative samples? J Trauma Stress. 2005;18:425-436.
46. Herman J. Craft and science in the treatment of traumatized people. J Trauma Dissoc. 2008;9:293-300.
47. Herman JL. Trauma and Recovery. 2nd ed. New York: Basic Books; 1997.