Cognitive (Prolonged Exposure) Therapy & Extinction

According to the previous analysis a traumatic event may be considered to be an overwhelming aversive sensory condition that evokes intense negative emotion (e.g. fear, helplessness, and horror), autonomic arousal (e.g. increases in heart rate, blood pressure, and skin conductance), and sensation of perceived pain. With time and developing consolidation processes an internal representation of the trauma in the brain emerges. When undeclared in a coherent narrative, this internal representation may become trapped in consolidation processes. When PTSD trauma memory is internalized in this way, it embodies the external and internal cues that had been present and associated with the traumatic event. Evoked intense autonomic arousal, visceral sensation, negative emotion and negative implicit appraisals of self in interaction and associated emotion may get trapped into brain and central nervous system, when it is not verbally declared into a coherent trauma narrative embedded with personal meaning.

Since the 1990s cognitive-behavioral therapies like Edna Foa’s Prolonged Exposure (PE) have been successfully treating PTSD. The Prolonged Exposure (PE) method directly encourages expression of trauma-related experience. Due to its empirical testing, transparency and documented ability at modulating trauma-related amnesia this section will focus and elaborate on its methods and findings and how it links with extinction.

The PE method is an in vivo exposure method that was adapted from cognitive-behavioral therapy’s (CBT) flooding and desensitization. Traditional CBT’s exposure therapy encourages the phobic client to confront, relive, desensitize, and reduce anxiety to an innocuous fear-producing object, condition, or situation (Foa & Kozak, 1986). Repetitive reexposure to the CS-CR as such, promotes symptom relief through extinction-mediated habituation. PE also helps clients to confront and face distressing responses to overwhelming traumatic events reminiscent of initial responses to life threatening experiences, nonsexual and sexual assaults, combat and/or torture and natural disasters, etc. (Foa, Cashman, Jaycox, & Perry, 1997; Meadows & Foa, 1998). As noted earlier initially experienced traumas and responses to those traumas can become internally represented in consolidation processes and trapped. Cognitive therapy for PTSD with PE may help to release this memory in the following manner.

During PE the client is instructed to internally generate and recall sensory details of an assault “as if it were happening now.” This helps to temporarily pair the internal representation of the trauma with the existing phase of consolidation. Attending to traumatic material (CS) in this way helps to generate personally meaningful emotions (CR), like those linked with emotions of fear, anxiety, helplessness, and loss of sense of trust in oneself and others (Foa, Ehlers, Clark, Tolin, & Orsillo, 1999a; Foa, Riggs, Massie, & Yarczower, 1995a). As the inner representations (CS) of and generated response (CR) to this memory are retrieved and declared (by MTL structures) in PE therapy, this (CS) memory can be unpaired and released from fear-related consolidation neural structures. Examining the relationship between the CR and CS as such may well involve “learning about the relationships between internal affective states and external stimuli…” functions suggesting hippocampal-amygdala involvement and interactions (White & McDonald, 2002, p. 138). Relational analysis of assigning personal meaning to traumatic events may allow for the later expression of medial prefrontal structures that are involved in declared emotion and extinction. This may also allow expression of significant symptom reduction treatment effects of decreases in patient-rated indices for overall depressed mood, anxiety, and trauma related distress, e.g. numbing, dissociation, avoidance, intrusive reexperiencing of emotionally laden trauma memory, etc. (Foa, Molnar, & Cashman, 1995b; Jaycox, Foa, & Morral, 1998). The patient is also better able to develop, retrieve and declare a personally meaningful, temporally organized, and chronologically sequenced, complete trauma script, which is not only reflective of what, where and how the traumatic event happened, but also able to reference the impact of the traumatic event on the psychological and personal self (Foa et al., 1995a; van Minnen, Wessel, Dijkstra, & Roelofs, 2002). This may suggest greater mPFC involvement (Macrae, Moran, Heatherton, Banfield, & Kelley, 2004; Vogt, Berger, & Derbyshire, 2003). The client is better able to resolve feelings of self-blame (Foa & Rauch, 2004) and, with the help of cognitive restructuring’s problem solving analysis, the emotion of guilt (Resick, Nishith, Weaver, Astin, & Feuer, 2002). Finally declared traumatic memory also reduces the implicit need for sustained compensatory behavioral adaptations for active thought suppression and behavioral and cognitive avoidance of trauma reminders (Foa, Dancu, Hembree, Jaycox, Meadows, & Street, 1997; Bryant, Sackville, Dany, Moulds, & Gutherie, 1999). PE reductions in state anxiety and depression are sustained at three, six, twelve, and forty-eight month follow-up periods (Foa et al., 1999b; Bryant, Moulds, & Nixon, 2003). In fact a trend for PE’s treatment effects of reduced symptom severity, avoidance of traumatic subject matter, unwanted intrusion of troubling sensory images and distressing emotions, and arousal continues into a three-month follow-up period (Foa, Rothbaum, Riggs, & Murdock, 1991). This suggests continued post-treatment CS-unpairing and associated consolidation activity well after therapy was concluded.

References

Bryant, R.A., Moulds, M.L., & Nixon, R.V. (2003). Cognitive behaviour therapy of acute stress disorder: A four-year follow-up. Behaviour Research and Therapy, 41(4), 489-94.

Bryant, R.A., Sackville, T., Dany, S.T., Moulds, M., & Gutherie, R. (1999). Treating acute stress disorder: an evaluation of cognitive behavior therapy and supportive counseling techniques. American Journal of Psychiatry, 156(11), 1889-1891.

Foa, E.B., Cashman, L., Jaycox, L., & Perry, K. (1997). The validation of a self-report measure of PTSD: the posttraumatic diagnostic scale TM (PDSTM). Psychological Assessment, 9(4), 445-451.

Foa, E.B., Dancu, C.V., Hembree, E.A., Jaycox, L.H., Meadows, E.A., & Street, G.P. (1999b). A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. Journal of Consulting and Clinical Psychology, 67(2), 194-200.

Foa, E.B., Ehlers, A., Clark, D.M., Tolin, D.F., & Orsillo, S.M. (1999a). The post-traumatic cognition inventory (PTCI): Development and validation. Psychological Assessment, 11, 303-314.

Foa, E.B., & Kozak, M.J. (1986). Emotional processing of fear: exposure to corrective information. Psychological Bulletin, 99(1), 20-35.

Foa, E.B., Molnar, C., & Cashman, L. (1995b). Change in rape narratives during exposure therapy for posttraumatic stress disorder. Journal of Traumatic Stress, 8(4), 675-690.

Foa, E.B., & Rauch, S.A. (2004). Cognitive changes during prolonged exposure versus prolonged exposure plus cognitive restructuring in female assault survivors with posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 72(5), 978-884.

Foa, E.B., Riggs, D.S., Massie, E.D. & Yarczower, M. (1995a). The impact of fear activation and anger on the efficacy of exposure treatment for posttraumatic stress disorder. Behavior Therapy, 26, 487-499.

Foa, E.B., Rothbaum, B.O., Riggs, D.S. & Murdock, T.B. (1991). Treatment of posttraumatic stress disorder in rape victims: a comparison between cognitive-behavioral procedure and counseling. Journal of Consulting and Clinical Psychology, 59(5), 715-23.

Jaycox, L.H., Foa, E.B., & Morral, A.R. (1998). Influence of emotional engagement and habituation on exposure therapy for PTSD. Journal of Consulting and Clinical Psychology, 66(1), 185-92.

Macrae, C.N., Moran, J.M., Heatherton, T.F., Banfield, J.F., & Kelley, W.M. (2004). Medial prefrontal activity predicts memory for self. Cerebral Cortex, 14(6), 647-654.

Meadows, E.A., & Foa, E.B. (1998). Intrusion, arousal and avoidance. Sexual trauma survivors. In: V.M. Follette, J.I. Ruzek, & F.R. Abueg (Eds.), Cognitive behavioral therapies for trauma (pp. 100-123). New York: Guilford Press.

Resick, P.A., Nishith, P., Weaver, T.L., Astin, M.C., & Feuer, C.A. (2002). A comparison of cognitive-processing with prolonged exposure and a waiting condition for the treatment of chronic posttraumatic stress disorder in female rape victims. Journal of Consulting and Clinical Psychology, 70(4), 867-879.

Van Minnen, A., Wessel, I., Dijkstra, T., & Roelofs, K. (2002). Changes in PTSD patients’ narratives during prolonged exposure therapy: a replication and extension. Journal of Traumatic Stress, 15(3), 255-258.

Vogt, B.A., Berger, G.R., & Derbyshire, S.W. (2003). Structural and functional dichotomy of human midcingulate cortex. European Journal of Neuroscience, 18(11), 3134-44. pdf

White, N.M., & McDonald, R.J. (2002). Multiple parallel memory systems in the brain of the rat. Neurobiology of Learning and Memory, 777, 125-184.

Concluding Thoughts

This portion of the web site sought to examine the nature of PTSD trauma memory within the context of neuroscience findings. In its analysis it was found that patients with PTSD tend to develop memory gaps for traumatic memory that affect the trauma narrative’s coherence and temporal order. These symptoms are also associated with the syndrome and constellation of documented PTSD symptoms. Trauma avoidance and thought suppression-induced impairments in trauma coherence and temporal order result in the development of characteristic symptom progression and disrupt the development of personally meaningful trauma narrative. PTSD trauma memory may be characterized as implicit memory, as its memory’s personal meaningfulness is not voluntarily accessible and is modality specific with perceptual triggers. It like implicit memory is behaviorally inferred in symptoms. Unlike implicit memory and more like explicit memory, there is a reliving quality to traumatic perceptions and behaviors. It is also characterized by fast, one trial learning.

According to neuroimaging findings PTSD trauma memory also shares similar neural activity as human fear conditioning during its unpairing phase. Thought suppression and neural activity in the dorsal anterior cingulate and dorsolateral prefrontal cortex may likely play roles in locking personally meaningful trauma memory into place and disrupt consolidation traumatic retrieval processes. These processes may serve to inhibit hippocampal-mediated voluntary and intentional retrieval and reexperiencing processes. Moreover thought suppression-mediated inhibition may progressively impair trauma memory retrieval over time and support its inhibition and lack of access. Understanding that PTSD is a manifestation of traumatic memory that gets locked into hippocampal consolidation processes may offer an explanation as to its persistence, enduring physiological arousal, and “indelible subcortical conditioned response, held in check?” (Shalev, Ragel-Fuchs, & Pitman, 1992, p. 864).

PTSD trauma memory’s extinction and fear conditioning’s extinction are associated with activity in the medial prefrontal cortex, which is functionally specialized for declared emotion. Developing a declared trauma narrative during the course of cognitive therapy which is imputed with personal meaning may transform implicit trauma memory to declarative memory, thus reducing abnormal amygdala-mediated brainstem arousal. This process may allow emotional and medial prefrontal cortical expression (Gilboa, Shalev, Laor, Lester, Louzoun, Chisin, & Bonne, 2004) and not vice versa, i.e. traumatic processing may force the mPFC’s functional integrity in response to initial amygdaloid involvement. Successful completion of cognitive therapy for PTSD probably works with both structures to allow for later mPFC expression and mediated extinction.

This concept is supported in the findings of another study (Lieberman, Eisenberger, Crockett, Tom, Pfeifer, & WAy, 2007), which found the early stages of “affect labeling” during a fear-arousing task initially activated the amygdala and ventrolateral prefrontal cortex. This allowed later expression of healthy emotion and activations in the dorsal medial prefrontal cortex or rostral midcingulate cortex (2,18,32). This supports Gilboa and colleagues (2004)  assertion noted above, that temporally sequenced amygdala activity allows for the later expression of the medial prefrontal cortex.

This model has the capacity at enhancing our understanding of how initial coping mechanisms of thought suppression may disrupt the progression and expression of consolidation processes necessitating traumatic memory retrieval. This process may or may not be associated with initial PTSD symptom expression in response to trauma; however subsequent perceived traumas may reinforce neural components underlying thought suppression and input into intermediate consolidation processes. This may predispose one to the later development of PTSD symptom expression in response to future traumatic experience depending upon one’s genetic vulnerability (Segman & Shalev, 2003).

This is an exciting time for the study of PTSD because the study of stress related brain structures is starting to zero in on consolidation, reconsolidation and extinction processes in fear conditioning. It is important for psychotherapists to study neuroscience findings to modify current psychotherapies for PTSD and make them more exact and measurable in their methodology. With emerging neuroscience research and knowledge of brain structures someday psychotherapy methods will be standardized for use by all therapists, irrespective of skill level. This may result in more effective and predictable psychotherapy methods with diverse client populations irrespective of genetically determined symptom expression. Certainly one can conclude ventilating emotion at source promotes medial prefrontal activity, which is a necessary and needed CNS component for later stress-resiliency.

References

Gilboa, A., Shalev, A.Y., Laor, L., Lester, H., Louzoun, Y., Chisin, R., & Bonne, O. (2004). Functional connectivity of the prefrontal cortex and the amygdala in posttraumatic stress disorder. Biological Psychiatry, 55(3), 263-272.

Lieberman, M.D., Eisenberger, N.I., Crockett, M.J., Tom, S.M., Pfeifer, J.H., & Way, B.M. (2007) Putting feelings into words: affect labeling disrupts amygdala activity in response to affective stimuli. Psychological Science, 18(5), 421-8.

Phelps, E.A., Delgado, M.R., Nearing, K.I., & LeDoux, J.E. (2004). Extinction learning in humans: role of the amygdala and vmPFC. Neuron, 43(6), 897-905.

Segman, R.H., & Shalev, A.Y. (2003). Genetics of posttraumatic stress disorder. CNS Spectrum, 8(9), 693-698.

Shalev, A.Y., Fagel-Fuchs, Y., & Pitman, R.K. (1992). Conditioned fear and psychological trauma. Biological Psychiatry, 31(9), 863-865.