Consistently, one of the first experiences arising from neurofeedback that clients especially note is a growing awareness that they are reacting less to things that in the past had been serious triggers. This is not always the case with highly traumatized individuals but typical of modestly traumatized clients who initially respond well to neurofeedback and don’t go on to do intense alpha theta sessions. However, even the worst cases of trauma eventually report this same phenomena as they advance through alpha theta training.
This reduced reactivity has been reported as a positive therapeutic outcome in different forms throughout the history of the literature in psychology. Traumatized individuals tend to over react or under react to triggering events but their response constitutes two sides of the same coin. Re-experiencing and retrieval of autobiographical memories related to trauma, often referred to as “triggering” and “exposure” events, activates the Default Mode Network (DMN) in experimental subjects differently than in the control subjects (Thome et al., 2019; Fenster et al., 2018). This arises partly from a loss of inhibitory control in the prefrontal cortex as well as an overactive amygdala. This loss of inhibitory control has EEG markers and is the subject of ongoing co-registration studies involving EEG and fMRI investigations (Nicholson et al., 2020; 2022)
This phenomena has been recently published in JAMA where they found individuals with PTSD over reacted at the physiological level and under reacted at the psychological level in attempt to control their expression of emotions and physiology (Korem et al., 2024). A tug of war between networks in response to a threat. Whether they were successful at this or not, subjects with PTSD reacted much faster than subjects without significant trauma. Ironically, those subjects who were capable of controlling this over reaction typically experienced intense delayed reaction and over time developed general emotional numbness.
As you can imagine, this level of emotional reactivity is a centerpiece of experience for clients with trauma. They are in a constant struggle with their over reaction to triggers. When this reactivity dissipates as a result of prefrontal training, it makes a dramatic impression upon them and persuades them in regard to the efficacy of neurofeedback. They often make statements like “I feel bullet proof” or “things that used to really upset me, don’t bother me so much”. These comments should be noted and immediately explored. Often clients will keep this observation to themselves, so it is often necessary to prompt them with specific probes. I make enquiries every session regarding this without being too explicit.
The reduction in frontal inhibitory control is a key feature of the disorder but training the prefrontal cortex directly is not always the solution to the problem. Again, we are dealing with highly distributed networks when attempting to determine the best location for intervention with neurofeedback protocols. There is increased activity around the parietal location Pz according to Nicholson in conjunction with the reduced frontal inhibitory control. The increased activity within the posterior DMN involves increased connectivity between the posterior cingulate cortex (PCC) and the precuneus which is just posterior to it. The PCC is also reportedly overactive in terms of BOLD signal. This results in excessive synchronization with reduced alpha in relation to increased beta. This increased activity was reported Engels et al (2007) connecting it also with the rumination associated with anxiety involving the precuneus and inferior parietal cortex, especially in the right hemisphere. This presents as a decrease in alpha and increased beta, especially at sites Pz and P4 which are picking up the parietal cortical regions (Soutar, 2025). I have consistently seen this pattern in sLORETA map analyses of war veterans who come to my office with PTSD. I have seen other patterns to trauma as well, but that is for another post.
The brain grows into patterns of anxiety and depression that are consolidated in network pathways and it is necessary to grow new pathways in order to compensate for them. That growth involves insight and integration of the experiences that precipitated the anxiety to begin with (LeDoux, 2015). The outcome of that integration process results in a return to an internal locus of control and a renewed sense of empowerment. An imperative aspect of this process is that clients need to learn to draw on their own spontaneously generated internal resources in order to emit novel behaviors which help them adapt to what were once overwhelming challenges (Soutar, 2025). Neurofeedback provides the recovery of the capacity for creative response that is required as well as providing reduced reactivity to allow that creative response to surface. A healthy emotional latency is a part of that response and allows the individual to react with innovation rather than over react in fear with a stereotypical behavior that is socially inaccurate. This type of behavior is intuitive and productive of better outcomes in challenging situations.
Although the correct emotional latency is crucial, it is not always enough. Increasing connectivity between cortical and subcortical networks of affect is also vital to the process. This can be done with alpha theta training. Alpha theta training amplifies this type of positive response because it makes the creative response more accessible in addition to the training done to improve prefrontal inhibitory control. The alpha theta protocol was designed specifically to increase creativity and was documented to do just that by Green and Green (1977). There are apparently involuntary subcortical processes which we have yet to understand that don’t involve conscious voluntary intent as the research on task learning has recently revealed.
To reiterate, network changes have to be initiated and consolidated with prefrontal inhibitory controls re-established and fine tuned with regard to the amygdala and central grey area (Terpou et al., 2020). This can be done very effectively through the process of neurofeedback in conjunction with proper counseling. In addition, in the NewMind clinics, we have found that supportive supplementation was frequently necessary in addition to neurofeedback. This might involve methyl folate for depression and magnesium for anxiety due to genetic methylation snips associated with physiological deficiencies and tendencies toward both. This is consistent with the literature in physiology.
References
Engels, A. S., Heller, W., Mohanty, A., Herrington J. D., Banich, M. T., Webb, A. G., Miller, G. A. (2007). Specificity of regional brain activity in anxiety types during emotion processing. Psychophysiology, 44, 352-363
Fenster, R. J., Lebois, L. A. M., Ressler, K. J., & Suh, J. (2018). Brain circuit dys-function in post-traumatic stress disorder: From mouse to man. Nature Reviews Neuroscience, 19(9), 535–551.
Green, E. E. & Green, A. M. (1977). Beyond Biofeedback. San Francisco: Delacarte.
Korem, N., Duek, O., Spiller, T., Ben-Zion, Z., Levy, I., & Harpaz-Rotem, I. (2024). Emotional State Transitions in Trauma-Exposed Individuals With and Without Posttraumatic Stress Disorder. JAMA network open, 7(4), e246813. https://doi.org/10.1001/jamanetworkopen.2024.6813
Nicholson, A. A., Ros, T., Densmore, M., Frewen, P. A., Neufeld, R., Théberge, J., Jetly, R., & Lanius, R. A. (2020). A randomized, controlled trial of alpha-rhythm EEG neurofeedback in posttraumatic stress disorder: A preliminary investigation showing evidence of decreased PTSD symptoms and restored default mode and salience network connectivity using fMRI. NeuroImage. Clinical, 28, 102490. https://doi.org/10.1016/j.nicl.2020.102490
Nicholson, A. A., Rabellino, D., Densmore, M., Frewen, P. A., Steryl, D., Scharnowski, F., Théberge, J., Neufeld, R., Schmahl, C., Jetly, R., & Lanius, R. A. (2022). Differential mechanisms of posterior cingulate cortex downregulation and symptom decreases in posttraumatic stress disorder and healthy individuals using real-time fMRI neurofeedback. Brain and Behavior, 12(1), e2441. https://doi.org/10.1002/brb3.2441
Terpou, B. A., Densmore, M., Théberge, J., Frewen, P., McKinnon, M. C., Nicholson, A. A., & Lanius, R. A. (2020). The hijacked self: Disrupted functional connectivity between the periaqueductal gray and the default mode network in posttraumatic stress disorder using dynamic causal modeling. NeuroImage: Clinical, 27, 102345.
Thome, J., Terpou, B. A., McKinnon, M. C., & Lanius, R. A. (2019). The neural correlates of trauma-related autobiographical memory in posttraumatic stress disorder: A meta-analysis. Depression and Anxiety, 37(4), 321–345.