Traumatic events damage the mental and emotional processes and affect brain physiology. According to the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; American Psychiatric Association [APA], 2013), people with posttraumatic stress disorder (PTSD) may present with the following:

In recent years, many researchers have focused on trauma and its symptoms, obtaining important results concerning the understanding of traumatic memory and how it affects the brain and human behavior.

Through neuroimaging techniques such as positron emission tomography (PET), single photon emission tomography (SPECT), electroencephalography (EEG), and functional and structural magnetic resonance imaging (fMRI, MRI), it has been possible to identify the brain circuits involved in the pathophysiology of PTSD. Changes in metabolism, brain morphology, and networking have been found in the amygdala, the medial prefrontal cortex (mPFC), and the hippocampus (Martin, Ressler, Binder, & Nemeroff, 2009; Shin, Rauch, & Pitman, 2006; Wager, Lindquist, & Kaplan, 2007; Yehuda & LeDoux, 2007), which together form the so-called neural model of PTSD (Shin et al., 2006).

These are the types of changes that occur in the different areas of the brain in PTSD patients:

A few functional studies on traumatized patients have disclosed the impact of various psychotherapies, such as cognitive behavior therapy, brief eclectic therapy, and mindfulness, on the neurobiology of PTSD as investigated before and after therapy. In this respect, research on the efficacy of EMDR therapy in psychological trauma has identified that post intervention, there is a significant normalization of blood flow, mainly in the limbic and the frontal cortex areas, thus determining a higher control over the amygdala. In turn, this normalization decreases the pathological cortical hyperactivation, resulting in the disappearance of PTSD symptoms, including a reduction in anxiety, somatosensory symptoms, flashbacks, intrusive memories, and the feeling of reliving the trauma with persistent sensations even at a somatic level (Lansing, Amen, Hanks, & Rudy, 2005; Oh & Choi, 2007; Pagani et al., 2007).

In a study where traumatized subjects suffering with PTSD were compared to traumatized subjects not developing PTSD, Nardo et al. (2010) found a decrease in gray matter density in several limbic regions, such as the posterior cingulate, para-hippocampal, and insular cortex in those subjects with PTSD. These regions are implicated in processes such as integration, encoding and retrieval of autobiographical and episodic memories, self-referential conscious experience, emotional processing (i.e., classical conditioning, cognitive appraisal, experience of feeling states), and interoceptive awareness (Pagani, Högberg, Fernandez, & Siracusano, 2013), and are the typical target regions of EMDR therapy. The same investigation highlighted that the subjects not responding to EMDR therapy showed significantly lower neuronal density in the same areas, suggesting that the therapeutic failure might be due to a previous atrophic state not allowing for any neurobiological effect of EMDR therapy.

Most recently, EEG investigations, performed during the bilateral stimulation phase of EMDR sessions, have deepened the knowledge on the neurobiological processes occurring during the therapy. The comparison between the prevalent cortical activation during the first and last EMDR therapy sessions showed a significant deactivation of the orbitofrontal and subcortical limbic structures and an increased activation of the temporo-occipital cortex, mainly on the left side (see Figure 1).

Figure 1.

Prevalent cortical activation comparing first and last EMDR therapy sessions.

Source: Images from Pagani, M., Di Lorenzo, G., Verardo, A. R., Nicolais, G., Monaco, L., Lauretti, G., & Fernandez, I. (2012). Neurobiology of EMDR—EEG imaging of treatment efficacy. PloS One, 7(9), e45753. doi:10.1371/journal.pone.0045753

As a result, traumatic experiences and memories move from an implicit subcortical state to an explicit cortical state and are properly processed, reelaborated, and adapted into patients’ semantic memory (Pagani et al., 2011, 2012, 2015; Trentini et al., 2015).

The following are some of the models to explain the mechanisms of action used to elucidate EMDR therapy:

The neurobiological model provides solid foundation in how to unravel the functional and structural correlates of effective treatments. Taking also into account the REM sleep model, a further possible mechanism has been hypothesized (Carletto, Borsato, & Pagani, 2017; Pagani, Amann, Landin-Romero, & Carletto, 2017). During bilateral stimulation in EMDR therapy, the cortical activity as recorded by EEG resembles that of slow wave sleep (SWS), in which fragmented episodic and traumatic memories move from the amygdalar-hippocampus complex to the neocortex, in which they will be further integrated and encoded during REM sleep. Since during EMDR therapy the frequency of bilateral stimulation matches that of SWS (0.5–4 cycles per second, delta waves), the repetition of such stimulation during several sessions might be its “added value,” mimicking the natural physiological memory processes and favoring the traumatic traces to be contextualized in the neocortex. This would make EMDR faster and more effective in treating PTSD than other psychotherapies.

In conclusion, all changes found in EMDR therapy research confirm at various levels a solid neurobiological basis for the psychotherapy, resulting in improved symptoms and quality of life in patients with a PTSD diagnosis.

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