Several traditional PTSD therapies give concerted attention to changing irrational thoughts about traumatic experiences to more rational characterizations of what transpired. Other therapies favor addressing the sensory and somatic symptoms associated with traumatic experiences, believing it’s more important to help clients work through those negative reactions, rather than focus on an event’s cognitive aspects. One way of differentiating trauma methods is by categorizing them as either “top-down” or “bottom-up.” (NICABM, 2018). “Top-down” approaches (e.g., cognitive behavioral therapies) emphasize the restructuring of negative, trauma-related thoughts processed in the upper brain into more rational internal narratives. “Bottom-up” approaches (e.g., MEMI, yoga and neurofeedback), on the other hand, focus on sensory reactions regulated by limbic structures at the base of the brain. This commentary explores whether the use of one of these paradigms makes more sense than the other, particularly in light of recent discoveries about the limbic system’s role in the development of PTSD.
Underlying top-down PTSD approaches like cognitive and behavioral therapies is a theory that negative emotions and behaviors are the result of irrational thoughts. If clients can be taught to identify faulty thinking related to traumatic experiences, and replace those thoughts with more self-affirming internal narratives, it’s believed their emotional and physical symptoms will improve. Although these therapies use both cognitive techniques such as thought stopping and cognitive restructuring and behavioral methods like reciprocal inhibition and systematic desensitization, the primary focus of this commentary is on their cognitive aspects.
Of all the PTSD treatment types—whether narrative, somatic, cognitive, cognitive behavioral, eye movement, exposure, or neuro-sensory—only three cognitive behavioral therapies with exposure (Prolonged Exposure, Cognitive Processing Therapy, and Cognitive Behavioral Therapy) have received a “strong recommendation” from the American Psychological Association (APA, 2019). This decision has resulted in heated disagreements over the actual effectiveness of these “evidence-based practices.” The marriage of the cognitive and behavioral theoretical models was thought to bring the best of each to bear on mental health issues—in this case PTSD treatment. But from an evaluation perspective, a growing body of research suggests these PTSD methods endorsed by the APA as most effective and “evidence-based” are neither (Van der Kolk, 2015). The reasons for this are summarized in a previous commentary on this website entitled “Why evidence-based treatments for PTSD are not!” and explained in greater detail in Chapters 2 & 3 of Multichannel Eye Movement Integration: The Brain Science Path to Easy and Effective PTSD Treatment (Deninger, 2021).
Moreover, given the importance of research into the limbic brain’s role in the development and persistence of PTSD symptoms, cognitive techniques for PTSD may not be as valid as they were once thought to be. Serious questions are now being raised about cognitive techniques for PTSD following the discovery of neurological reactions that occur in the limbic system following traumatic events. Cognitive therapeutic models were conceived decades ago—long before we had the technical ability to examine the traumatized brain up close and in real time. In view of what is now known about limbic reactions following traumatic events, I contend that cognitive behavioral therapies are less efficient at quelling limbic reactions and resulting PTSD symptoms than “bottom-up” approaches like MEMI that use eye movements as the principal change mechanism.
Limbic System Research
Multiple studies, a few of which are presented here, have confirmed that the fight or flight response is initiated by the amygdala after receiving sensory input about threats to survival from the thalamus and hippocampus. In rapid succession, approximately 1,400 biochemical and psychophysiological changes are activated by the sympathetic nervous system: blood pressure elevates, heart rate and blood flow to the muscles increase, pupils dilate, saliva production is restricted, breathing becomes rapid, digestion deactivates, and immune capabilities are enhanced—all in order to bring us to a hyper-alert state. (Deninger, 2021).
Hormonal secretions alter the functions of the amygdala, hippocampus, and the frontal lobe’s prefrontal cortex, all of which play a role in memory formation (Wlassoff, 2015). The neurohormones norepinephrine and corticosterone change interactions between the amygdala and the hippocampus in ways that impair memory encoding of traumatic events (Richter-Levin and Akirav, 2002). Brain imaging studies have reported heightened amygdala reactivity following traumatic experiences as well as a failure of the ventromedial prefrontal cortex to activate, leading researchers to hypothesize that these limbic reactions cause cognitive distortions and correlate with an inability to extinguish PTSD symptoms (Bremner et al., 2008; Stevens et al., 2017). The study by Stevens and her colleagues also reports a relationship between decreased anterior cingulate cortex (ACC) activity and the persistence of PTSD symptoms over time. The lead author summarized the team’s findings in this way:
“People with a greater amygdala response to fearful faces had greater initial symptom severity and were more likely to maintain PTSD symptoms over the following year. Additionally, those with a sharper decrease in ventral ACC activity over repeated viewing of fearful images, called habituation, showed a poorer recovery trajectory. The findings suggest that amygdala reactivity and ventral ACC habituation to a threat predict the emergence of PTSD symptoms after trauma.” (Stevens, 2017).
Not surprisingly, Stevens recommends the development of new treatments designed to reduce amygdala reactivity and re-stimulate ACC function immediately following traumatic incidents.
Sweeton reports that the hippocampus absorbs cortisol during the stress response and ceases functioning properly; images become distorted, blurry, no longer panoramic, and PTSD is more likely to develop. She also observes that therapeutic eye movements act as a “memory reconsolidation tool” for the hippocampus and help to restore its normal function (J. Sweeton, personal communication, November 4, 2019). It’s also suspected that eye movements help to return the amygdala to its normal activity level, but this needs further investigation. Given these findings, and the above recommendation from Stevens, interventions delivered immediately after traumatic incidents should be evaluated for their ability to resolve hippocampus, ACC and amygdala irregularities. And because the prefrontal cortex is deactivated during the stress response, new therapies that have the potential to reverse PFC deactivation should also be investigated.
Considered as a whole, these findings, and others not reported here, confirm the existence of a biological relationship between limbic system overreactions following traumas and the development of PTSD. Although not biomarkers of the disorder such as blood pressure readings for diagnosing heart disease or body temperature to detect infection, their clinical relevance when assessing the validity of PTSD treatments should not be discounted. Given that the amygdala’s initiation of the stress response impedes the accurate encoding of trauma-related thoughts by the hippocampus and prefrontal cortex, should we not attempt to rectify the limbic irregularities first, rather than address trauma-related thoughts formed in the aftermath? Addressing cognitions first assumes that working backwards from thoughts (linguistic in nature) to amygdala dysregulation (neuro-hyperactivity) is a more expedient approach. But isn’t that like thinking the best way to fix a breach in a dam is to channel the rushing water back upstream instead of repairing the dam problem? Although not explicitly stated, these are questions Stevens and others (2017) are implying with their recommendation for new PTSD interventions that target limbic abnormalities. And because the blunting of ACC activity following traumatic events correlates with poorer client recovery trajectories, does it not make sense to target ACC dysregulation before cognitions as well?
Extending this logic, I would argue that bottom-up therapeutic techniques that use eye movements as the principal treatment mechanism are a more sensible alternative. And because eye movements are considered a “memory reconsolidation tool” for the hippocampus and possibly the amygdala as well, researchers should give attention to PTSD therapies like MEMI—models more responsive to recent brain science. Early interventions targeting limbic system abnormalities with eye movements, if proven successful, could foster a paradigm shift and revolutionize PTSD treatment. If this were to occur, cognitive behavioral therapies for PTSD might lose favor, given what is now known about PTSD and the brain.
Multichannel Eye Movement Integration
Multichannel Eye Movement Integration (MEMI) is a bottom-up method that addresses PTSD symptoms at their source in the limbic system using an unparalleled eye movement approach. Brain research and clinical results suggest this treatment offers a more direct and effective path to PTSD symptom resolution than cognitive methods. In fact, I have found that thought restructuring is completely unnecessary when using MEMI, because irrational cognitions are automatically reorganized when somatic and sensory reactions to recalled traumas are desensitized:
“Cognitive restructuring can be thought of as an active strategy, whereas changing thoughts in MEMI should be considered a more “passive” one. Changing irrational thinking in MEMI is not a goal, a strategy, or a perquisite for memory reorganization. Neither is it assumed that thought distortions are the sole cause of physical or mental distress. Instead, clinical evidence has confirmed that thoughts naturally self-adjust in response to changes in somatic and sensory reactions following eye movements and accompanying interventions. In other words, cognitions become more rational without redirection after the visual, auditory, physical and emotional reactions to a problem state are desensitized.
MEMI is not considered cognitive or behavioral, but more aptly described as organic, limbic, neurological, linguistic and systemic. All modalities are engaged as a memory is reflexively desensitized during the eye movements and spoken commands. MEMI presuppositions assume that the body’s cognitive and neurological systems will achieve desensitization naturally, as a result of strategic pattern interruptions in the form of eye movements, reframes, and embedded commands.” (Deninger, 2021).
MEMI is derived from the original Eye Movement Integration (EMI) methodology developed by Connirae and Steve Andreas (1993) and a later adaptation by Ron Klein (2015) he called Eye Movement Integration™. The Andreases are recognized leaders in the Neuro-linguistic Programming (NLP) field with several acclaimed books, many articles, innovative training modules and commentaries about NLP to their credit. Klein has been an outstanding NLP trainer for many years. MEMI represents an expansion of earlier EMI techniques into a fully-formed, multisensory PTSD therapy with a simple theoretical model, five guiding presuppositions, a 10-step protocol, assessments, procedures and scripts for therapists. Unlike other PTSD therapies, MEMI is an easy-to-learn multifaceted approach that addresses all aspects of traumatic experiences, not just its cognitive representations. Everything a therapist needs to know is contained in Multichannel Eye Movement Integration: The Brain Science Path to Easy and Effective PTSD Treatment. For more information about this bottom-up approach with predetermined eye movements order the book now or email drmikelpc@comcast.net.
References
American Psychological Association. (2019). Clinical practice guideline for the treatment of posttraumatic stress disorder. http://apa.org/ptsd-guideline.
Andreas, C., & Andreas, S. (1993). Eye Movement Integration applied with a Vietnam veteran experiencing traumatic memories. Video recorded at the 5th International Congress on Ericksonian Approaches to Hypnosis and Psychotherapy and print instructions. Orlando, FL. http://j.mp/3ulsxV.
Bremner, J. D., Elzinga, B., Schmahl, C., and Vermetten, E. (2008). Structural and functional plasticity of the human brain in posttraumatic stress disorder. Progress in Brain Research, 167: 171-186. https://www.ncbi.nlm.nih.gov/pmc/articles//PMC3226705
Deninger, M. (2021). Multichannel Eye Movement Integration: The brain science path to easy and effective PTSD treatment. Gracie Publications: Tucson, AZ. https://www.Multichanneleyemovementintegration.com
Klein, R. (2015). Eye Movement Integration™ manual. American Hypnosis Training Academy: Silver Spring, MD. https://www.ahtainc.com/index_files/Page673.htm
National Association for the Clinical Application of Behavioral Medicine. (2018). Brain-based approaches to help clients after trauma. http://www.nicabm.com.
Richter-Levin, G. & Akirav, I. (2002). Mechanisms of amygdala modulation of hippocampal plasticity. The Journal of Neuroscience, 22 (22): 9912-9921. https://www.jneurosci.org/content/22/22/9912
Stevens, J. S., Kim, Y. J., Galatzer-Levy, I. R., Reddy, R., Ely, T. D., Nemeroff, C. B., Hudak, L. A., Jovanovic, T., Rothbaum, B. O., and Ressler, K. J. (2017). Amygdala reactivity and anterior cingulate cortex habituation predict posttraumatic stress disorder symptom maintenance after acute civilian trauma. Biological Psychiatry, 2017; 81 (12): 1023-1029. https://doi.org/20.2026/j.biopsych.2016.11015
Van der Kolk, B. (2015). The body keeps the score: Brain, mind and body in the healing of trauma. New York: Penguin Books. https://www.amazon.com/s?k=van+der+kolk+body+keeps+the+score&hvadid=78065460842546&hvbmt=be&hvdev=c&hvqmt=e&tag=mh0b-20&ref=pd_sl_9ekjsmv93_e.
Wlassoff, V. (2015). How does posttraumatic stress disorder change the brain? http://brainblogger.com/2015/01/24/how-does-post-traumatic-stress-disorder-change-the-brain/.