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.